Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241715EnglishN2015August11HealthcareCOMPARISON OF CONVENTIONAL CERVICAL CYTOLOGY IN WOMEN WITH HEALTHY AND UNHEALTHY LOOKING CERVIX
English0107Lalji G. ValiyaEnglish Seema N. BaxiEnglishObjectives: To compare conventional cervical cytology in women with healthy/unhealthy looking cervix.
Methods: A prospective study on conventional cervical cytology was performed including 340 women, 174 with healthy looking cervix, 160 with unhealthy looking cervix and 6 with absent cervix (post hysterectomy), attending the Gynecologic outpatient department at a tertiary care hospital in Bhavnagar district of Gujarat state. Cytological findings including incidence of inflammatory smears and epithelial abnormalities were compared between the two groups.
Results: The demographic profile difference between the two groups was statistically non-significant. Overall incidence of squamous cell abnormality was 4.1 % and of glandular cell abnormality was 1.2%. Incidence of squamous cell abnormalities increases as the age of patients increases, highest incidence were seen in 61-70 years age-group. Inflammatory smears were common in women with unhealthy cervix (p=0.0001), however difference in epithelial abnormalities between the two groups were statistically non-significant (p=0.248).
Conclusion: Inflammatory smears were higher among the women with unhealthy cervix in comparison to healthy cervix but the differences in epithelial abnormalities between the two groups were statistically non-significant. Hence this study emphasizes on the importance of universal screening of both the groups.
EnglishPap smear, Bethesda, Cervical erosion, Squamous Intraepithelial Lesion (SIL).INTRODUCTION
Cancer of the uterine cervix is the second most common cancer among women in the world after breast cancer. Cervical cancer accounted for 493 000 new cases and 273 000 deaths in 2002 worldwide. More than 80% of the cervical cancer cases occurred in developing countries.1 Taking the lives of 75,000 women each year, cervical cancer is the leading cause of death for women in India. This number accounts for a third of all cancers that affect women in India. The age-specific incidence rates (ASIR) for cervical cancer revealed that the disease increases from 35 years and reaches a peak between the ages 55 to 64 years2 . The differential pattern of cervical cancer and the wide variation in incidence are possibly related to environmental differences. Etiologic association and possible risk factors for cervical carcinoma have been extensively studied. The factors are: Sexual and reproductive factors, socio-economic factors (education and income), viruses e.g., herpes simplex virus (HSV), human papilloma virus (HPV), human immunodeficiency virus (HIV) and other factors like smoking, diet, oral contraceptives, hormones, etc.3 Indian study found that about two thirds of women with invasive cancer were detected through visual inspection of cervix using a speculum and light source. Cancer indicators are small growths, cervical erosion that bleeds on touch, ‘suspicious’ looking cervix. It primarily identifies invasive cancer, not precancerous conditions.4 Historical study has found a positive correlation between the decrease in mortality from carcinoma cervix and the rate of cytological screening.5,6,7 The overall results of various studies reaffirm that cervicovaginal cytology (Pap smear) remains the most inexpensive and effective tool for the elimination of cervical cancer.6
Since data from Gujarat is not well documented and since no other previous study of Pap smears was ever conducted in Bhavnagar district, the present study was conducted on the patients having various symptoms related to lower genital tract and/or having unhealthy looking cervix, attending the outpatients department of gynecology at Sir T. Hospital, Bhavnagar, to compare the incidence of intraepithelial neoplasm and invasive carcinoma of cervix and various genital tract infections in women with healthy/unhealthy looking cervix.
MATERIALS AND METHODS
Study was conducted over a span of 16 months at a tertiary care hospital in Bhavnagar on women attending the Gynaecologic outpatient department having various symptoms related to lower genital tract and/or having unhealthy looking cervix. Three patients of physical fitness with no complaints were also included in this study. Unhealthy and healthy cervix was judged during per speculum examination. The cervix was considered healthy if it didn’t had any abnormalities in terms of size, shape, position, colour and surface irregularity, otherwise it was considered as unhealthy. As antimicrobial therapy was given according to clinical suspicion and followed up if symptoms and/or signs persisted, such patients were also taken up for this study. Complete history including complaints, personal and marital history was noted. Material was collected from the ecto cervix by cervical scrapping with the help of an Ayre’s wooden spatula and from endocervix with cytobrush and immediately smeared on a clean glass slide that was premarked as ‘ecto’ or éndo’ with patient’s identity. Smears were stained by rapid Pap method and reported according to the Bethesda system (2001). The patients with abnormal Pap smear findings and unsatisfactory Pap smears were further evaluated by repeat Pap smear examination or cervical biopsy. Statistical analysis: The P -value was calculated using Chisquare and Student’s T tests.
RESULTS
Out of a total 340 patient between the ages of 20-103 years examined, 174 had healthy looking cervix, 160 had unhealthy looking cervix and 6 were of total hysterectomy without cervix. All except one were married, with mean age at marriage being 19 years. 6 patients were of total hysterectomy in which vaginal vault smears were taken. 111 were post menopausal. Follow up Pap smear examination was done in 6 patients and the follow up Pap smear findings were same as the first diagnosis in all cases except in one in whom previous unsatisfactory result became satisfactory on follow up. Overall incidence of different Bethesda’s reporting categories was shown in Figure 1. Age-wise incidence of various Bethesda’s reporting categories was shown in Figure 2. It was evident from Fig.-2 that in present study incidence of squamous cell abnormalities increases as the age of patients increases. It increased from 1.72% in the 31-40 years age group to 25% in the 61-70 years age group. Although it appears low in >70 years age group, it can’t be concluded; it could be due to the reason that total number of patient in >70 years age-group were only 7. Glandular cell abnormalities were detected only in age group 41-50 and 61-70 years. Highest incidences of epithelial cell abnormalities (squamous as well as glandular) were seen in 61-70 years age-group. Difference in various demographic profile like age, age at marriage, parity between women with healthy and unhealthy cervix were statistically non significant as shown in Table-1. Chief complaint wise distribution of women with healthy and unhealthy cervix was shown in Table 2. It is evident from Table-2 that, common histories among both the groups include excessive white discharge, post menopausal bleeding, uterine prolapse and menorrhagia. A history of excessive white discharge was more often present in women who had unhealthy cervix (61.2%) than healthy cervix (32.8%). The difference was statistically significant (pEnglishhttp://ijcrr.com/abstract.php?article_id=476http://ijcrr.com/article_html.php?did=4761. Gynaecological Cancer Screening and Prevention, Best Practice and Research Clinical Obstetrics and Gynaecology; Volume 29, Issue 2, April 2006, Pages 207-225.
2. Murthy, Nandagudi Srinivasa, Chaudhry Kishore, Saxena Sunita: Trends in cervical cancer incidence - Indian scenario. European Journal of Cancer Prevention: Volume 14, Issue 6, December 2005, Pages 513-518.
3. Shanta V, Krishnamurthi S, Gajalakshmi CK, Swaminathan R, Ravichandran K, Epidemiology of cancer of the cervix: global and national perspective. J Indian Med Assoc. 2000 Feb; 98(2):49-52.
4. Suresh Bhambhani: Gynecological Cytology – Cervix, 1st edition, New Delhi, Interprint, 1996, Pages 141-152.
5. Elizabeth A Warner and Anna K. Parson, Screening and early diagnosis of gynecological cancers. The Medical Clinics of North America. Vol. 80, No. 1, Jan. 1999.
6. Michael J. Costa, Cyngiear Grimes et al: Cervicovaginal cytology in an indigent population – comparison of results for 1964,, 1981 and 1989. Acta Cytol, 1991, Vol. 35, No. 1, PP 51.
7. Cramer DW: The role of cervical cytology in the declining morbidity and mortality of cervical cancer. Cancer 34: 2018, 1974.
8. D. Pandit, R. Prabha, S. Shanbhag, R. Mayekar : Morbidity Pattern of Women Attending Screening Program in an Urban Slum in Mumbai; Indian Journal of Community Medicine, Vol. 30, No. 4 (2005-10 - 2005-12).
9. Kavatkar AN, Nagwanshi CA, Dabak SM. Study of a manual method of liquid-based cervical cytology. Indian J Pathol Microbiol 2008; 51:190-4.
10. Kalavathy, Veena, Binu, Nirmala : RTI control programme by Pap smear screening among tribal women in Palakkad district, Kerala, India. Asian Pacific Journal of Cancer Prevention, Vol. 1, No.1, 2001.
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241715EnglishN2015August11HealthcareSTUDY OF CLINICAL PROFILE OF CD4 COUNT AND OUTCOME IN CHILDREN WITH HIV/ AIDS BELOW 12 YEARS
English0811A.M. LingayatEnglish Prathamesh KambleEnglishStudy: To study clinical profile CD4 count and outcome in children with HIV/AIDS below 12 years of age.
Aims and Objective: To study, in children with HIV/AIDS Clinical profile, CD4 count and Out-come.
Material and Methods: The study was carried out in ART OPD and pediatric ward over one year duration. All children who were HIV reactive below 12 years were enrolled. Detail history examination and investigation done clinical profile, symtomatology, staging CD4 count and outcome studied in these cases.
Result: Males (79%) are affected more than females, while common age of presentation was 8.2yrs. Majority of patients were in WHO staging of Stage III (33.6%) and Stage IV (29.6%), most common symptom was weight loss in 50 cases and commonest sign was generalized lymphadenopathy in 57 cases. Tuberculosis was the most common opportunistic infection in 18.4%.
Baseline CD4 count was EnglishHIV, Childrens < 12 years, CD4 Count, OutcomeINTRODUCTION
The UNAIDS report on the global AIDS epidemic estimated that approximately 4,20,000 (3,50,000-5,40,000) new HIV infections occurred in children below 15 years of age in year 2007.90% of them through me other to child transmission. The global impact of HIV epidemic has been 50 dramatic and devastating that it has been described as the “epidemic of current century”1 . The first case of HIV infection in India was diagnosed among sex workers in Chennai, Tamil Nadu in 19862 . The clinical manifestation of HIV infection in children is different from those in adults. The immune system of young children who are infected perinatally is immature and hence dissemination throughout the various organs may occur very early3 . Antiretroviral therapy (ART) has been scaled up in Africa over the past year (UNAIDS and WHO 2003, 2007). At the end of 2007, 30% of the estimated 7 million people in need of treatment were receiving it (WHO, 2009)4 . We have studied clinical manifestations staging and outcome of these HIV infected cases.
AIMS AND OBJECTIVE
To study in children with HIV/AIDS clinical profile, CD4 count and out come
MATERIAL AND METHODS SETTING: The study was carried out in ART centre and pediatric ward at Govt. Medical College, Aurangabad. STUDY
PERIOD: January 2009 to Dec 2009.
STUDY DESIGN: Prospective observational study
SAMPLE SIZE: All children who were HIV reactive attending ART OPD and IPD below age of 12 years
INCLUSION CRIETERIA: All children who were HIV reactive attending ART OPD and IPD below age of 12 years.
EXCLUSION CRITERIA: Children above 12 years.
METHOD
Written and informed consent of all parents and caretakers was taken before performing the tests and examination. All children who were thus confirmed seropositive using three rapid tests (Tridot, coombed and immunochromatography) were included in the study. A detailed history including family history, birth history and immunization history noted. A detailed physical was examination done. Investigations like hemoglobin, total WBC count, platelets count, CD4 Cell count by standard flow cytometric method using FACS count, done. Other tests like tuberculin test, LFT, KFT, CSF exam. Blood culture was done as per the indication. All patients were treated with ART as per NACO 2006 guidelines. All cases were followed up to 6 months and outcome was studied.
RESULT
Total 125 cases of HIV/AIDS attending ART OPD or admitted in ward during study period were studied. Out of total 125, 79 (63.2%) cases were of males and 46 (36.8%) were of females. Mean age of presentation was 8.2 years. Most common symptom was weight loss (50 cases) and most common sign detected in this case was generalized lymphadenopathy (in 57 cases) as shown in fig. 1 and Fig. 2 According to WHO staging 33.6% were in stage III and tuberculosis was the most common opportunities infection (18.4%). Baseline CD4 count wasEnglishhttp://ijcrr.com/abstract.php?article_id=477http://ijcrr.com/article_html.php?did=4771. Padmapriyadarsinic, Pooranagangadevi N, Chandrasekaran K, Sudha S, Tiruvalluvan C, Bhani PK et al. Prevalence of underweight, stunting, and wasting among children infected with Human Immunodeficiency Virus in South India, Int J Pead 2009;2009:1-5.
2. Gallo RC, Sahalludin SZ, Papovic M, Shearer G, Mark K, Barton F. Frequent Detection and Isolation of cytopathic Retrovirus from patient with AIDS and risk of AIDS.AIDS 1984;224:500- 03.
3. Ira Shah, Nitin Shah, Mamta Manglan. IAP Speciality Series On Peadiatric HIV: National Guidelines Of Peadiatric HIV. NACO and IAP 2006 Pg.1-114.
4. Megan McGuire1, Tamika Munyenyembe1, Elisabeth Szumillin, Annette H,Mickael LP, Nenette B. Vital status of pre-ART and ART patients defaulting from care in rural Malawi. Trop Med Int Heath 2010;(1):55-62.
5. Agrawal D, Chakrabvarty J, Sunder S, Gupta V, Bhatia BD. Correlation between clinical features and degree of immunosuppression in HIV infected children: Indian Peadiatr2008;45:140-43.
6. Shet A, Mehta S, Rajgopalan N, Dinkar C, Elango R, Samuel NM. HIV –associated anemia in children: A systematic review from a global perspective. Peadistrics 2009;9:37-40.
7. Addy Kekitiinwa, Kathrine J.Lee. Walkar A. Albert M. Katja D. Initial growth, CD4, and viral load responses to HAART in Ugandan compare to UK/Irish HIV –Infected children. J Aqure Immune Deffic syndrome,2007;49:384-94.
8. Lodha R, Thorkild T, Robert D, James KT. Severe Malnutrition with and without HIV-1 infection in hospitalized children in Kampala, Uganda: Differences in clinical features, haematological findings and CD4+ cell counts. Nutr J 2006;5:27-32.
9. Ranbir Singh L, National guidelines of Peadiatric HIV.NACO and IAP 2006 Pg.13-20.
10. Sharma S, Dhungana GP, Pkherel BM,Rajal BP.Clinical features of HIV/AIDS various Oppurtunistic infection in relation to antiretroviral status among HIV seropositive individual from central Nepal: Kathmandu University Med J 2009;7(4):355-9.
11. Mwangelwa Mubiana-Mbewe1, Carolyn Bolton-Moore, Yolan Banda, Namwingo C, Mutinka N. Causes of morbidity among HIV-infected chiidren on retroviral therapy in primary care facilities in Lusaka.Trop Med Int Health 2009;14(10);1190-8.
12. Soumya Swaminathan, Sangeetha M, Arunkumar M, Menon PA, Thomas B, Shibi K et al. Pulmonary tuberculosis in HIV positive individuals: Preliminary report on clinical features and responses to treatment. Indian J Tubercle 2002;49;189-94.
13. Shah SR, Tullu MS, Jaishree K. Clinical profile of Pediatric HIV infection from India. Arch Med Res 2004;36(1):24-36.
14. Hamid MZA, Aziz NA, Syed Z, Morlijah O, Kumar R. Clinical features and risk factors for HIV Encephalopathy in children: South Asian J Trop Med 2008;39:266-71.
15. Carolyn Bolton Moore, Mwangelwa Mubiana- Mbewe, Ronal A, Cantrell clinical outcomes and CD4 cell response in children receiving antiretroviral therapy at primary health care facilities in Zambia : JAMA.2007;298(16):1888-99.
16. Pol RR. Sherpur T. Ratageri V. To study the clinical manifestations and incidence of opportunistic infections in HIV/AIDS, Indian J pediatr 2007;74:1072-74.
17. Kumarasamy N, Vallabhaneni S. clinical profile of HIV in India. Indian J Med Res 2005;121:377-94.
18. Devi PG Padampriydarshini C. Persistence of stunting after highly active antiretroviral therapy in HIV infected children in South India 2009 Pg.1-12.
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241715EnglishN2015August11HealthcareA RARE COMBINATION OF SYNCHRONOUS DOUBLE PRIMARY MALIGNANCIES - A CASE REPORT WITH LITERATURE REVIEW
English1216Balasubramanian A.English N. S. Kannan English C. P. Ganesh BabuEnglish M. PalaniappanEnglish A. S. MughilanEnglishAim: Aim of this study is to report a rare combination of synchronous double primary malignancies and to review the literature with reference to so far reported cases.
Case Report: A 48 years old male patient presented to us with lower abdominal pain and burning micturition of one month duration. Based on clinical presentation and investigation reports he was diagnosed as a case of synchronous double primary malignancies of ascending colon and urinary bladder. After complete workup for both the malignancies, he underwent Trans Urethral Resection of Bladder Tumour (TURBT) and radical right hemicolectomy.
Discussion: The term Multiple Primary Malignant Neoplasms (MPMNs), was first used by Billroth in 1889. They can be synchronous or metachronous. Extensive literature search shows only four cases of synchronous double primaries involving urinary bladder and colon. We are reporting a rare combination of synchronous double primary malignancies of urinary bladder and ascending colon. This is the fifth case report of synchronous double primaries involving bladder and colon and third case report involving bladder and ascending colon to the best of our knowledge.
Conclusion: MPMNs are still elusive for want of proper guidelines regarding correct terminology and classification encompassing varying presentations of chronological, aetiological, clinical and histopathological combinations. Our case adds up to literature for further research. The possibility of occurrence of synchronous multiple primary malignancies should be considered during workup for any malignant condition to institute early intervention to achieve good outcome.
EnglishColonic adenocarcinoma, Synchronous primaries, Urothelial carcinomaINTRODUCTION
The term Multiple Primary Malignant Neoplasms (MPMNs), was first used by Billroth1 in 1889. MPMNs are referred by some authors as multiple primary cancers (MPCs), or as Multiple primary malignacies (MPMs). Though the occurrence of multiple primary cancers has risen due to improvements in diagnostic techniques and treatment, the diagnostic criteria for multiple primary cancers remain the same as advocated by Warren and Gates2 in 1932. i.e. 1) Each cancer must be definitively malignant by histopathology, 2) they must be histologically different and 3) the possibility of metastasis among the cancers must be excluded. Differentiation between multiple primary and multicentric cancers was addressed in the classification by Moertel CG3 : I MPMNs of multicentric origin: a) The same tissue and organ. b) A common, contiguous tissue shared by different organs. c) The same tissue in bilaterally paired organs. II MPMNs of different tissues or organs. III MPMNs of multicentric origin plus a lesion (s) of a different tissue or organ.
In 2002, Howe in ‘A review of the definition for multiple primary cancers in the United States’ classified the association of different cancers in two categories depending on the timing of their discovery; a) synchronous in which the cancers occur at the same time or within two months and b) metachronous in which the cancers follow in sequence of more than two months apart4 . Vaamonde et al. reckoned the time factor as six months5 . In 2005, International Agency for Research on Cancer working Group has come out with International Rules for Multiple Primary Cancers6 .
CASE DETAILS
A 48 years old male patient presented to us with lower abdominal pain and burning micturition of one month duration and was evaluated for the same with ultrasonography abdomen, which revealed well defined isoechoic lesion in the left lateral wall of urinary bladder. Further evaluation with CT Urogram showed well defined heterogeneous enhancing lesion with speculations in the urinary bladder suggestive of carcinoma of bladder and incidentally discovered circumferential wall thickening involving the distal part of ascending colon causing partial obstruction with presence of multiple enlarged lymph nodes seen adjacent to the lesion. (Figure 1a and 1b). His serum CEA level was 38 ng/ml. Evaluation with colonoscopy showed circumferential proliferative growth in the distal ascending colon (Figure 2a). Biopsy taken from the growth at colonoscopy reported as adenocarcinoma. He was planned for cystoscopy, which showed a large (6x5cm) papillary growth in the left lateral wall of bladder and rest of the bladder normal (Figure 2b). Transurethral resection of bladder tumour (TURBT) was done and sent for Histopathological examination, which was reported as papillary urothelial carcinoma, low grade with focal invasion and bladder muscle free of tumour (T1G1) (Figure 3a and 3b). Patient was taken up for radical right hemicolectomy. At laparotomy found to have circumferential growth involving distal ascending colon with few enlarged lymph nodes at the adjacent mesocolon. Radical right hemicolectomy with ileotransverse anastomosis was carried out. Right hemicolectomy specimen is shown in (Figure 4a and 4b). Histopathological examination of the postoperative specimen was reported as well differentiated adenocarcinoma involving muscularis, pT2pN0 (Figure 5a and 5b). Postoperative period went uneventful and patient was advised regular follow up including periodic cystoscopy.
DISCUSSION
MPMNs/MPCs/MPMs, whether synchronous or metachronous are rare as such. Of late, the occurrence of multiple primary cancers has risen due to improvements in diagnostic techniques and treatment. According to study by Suzuki et al., most diagnosed synchronous double primary malignancies (SDPM) were lung cancer and head-neck cancers; metachronous double primary malignancies (MDPM) were lung cancer and breast cancer7 . They labelled the first of the MDPMs as MDPM-F and second one as MDPM-S. Double primary malignancies occurring at the same time or at the interval of 2-6 months apart are labelled as SDPMs4,5. Our case presented as synchronous double primary malignancies presenting at the same time. MPMNs prevalence ranged from 0.7 to 11.7% in various publications8-13. According to SEER (Surveillance, Epidemiology and End Results) data, the risk of developing subsequent MPMN varies from 1% for an initial liver primary diagnosis to 16% for bladder cancer primaries14. Ishimaro et al. published that at least 1.2% of patients referred to PET/CT with cancer diagnosis have a second cancer15. Although the mechanism involved in the development of multiple primary cancer has not been clarified, some factors such as heredity, constitution, environmental and immunological factors, oncogenic viruses, radiological and chemical treatments have been implicated16. Hereditary susceptibility explains only a small proportion of all second cancers though many hereditary cancer syndromes have been described17. MPMNs can occur at any age. However, from the reviewed series, patients with MPMNs tend to be older than those with a single primary malignant neoplasm. In many autopsy series and clinical reports, the median age of 50-94% of MPMN patients was over 50 years1,2,3,18,19 . Our case is a 48 years old male. The ratio of male/female patients with MPMNs in several publications varies between 0.9 and 3.5 with male predominance3,4,19-21. There are no established therapeutic rules for multiple primary cancers, but the type, progression, response to therapy and patient’s general health status should be considered. If each of the cancers has the possibility for cure, radical therapy is indicated. If radical therapy of the one primary cancer is impossible, conservative therapy is indicated for the other cancers22,23. Multiplicity of primary malignancies itself does not necessarily indicate a poor prognosis as long as adequate diagnosis and treatment are performed24. A review of 837 cases of colorectal carcinoma showed 32 cases (3.8%) of colorectal multiple primary malignant tumors and 11 cases (1.3%) of colorectal primary malignant tumour associated with extra colonic primary malignant tumour25. There are many reports in literature about double synchronous malignancies. In addition, there are many reports relating to MPMNs of more than two, up to eight MPMNs in the same patient26-30, but almost all of them are metachronous. Colonic primary with extra colonic primary along with other multiple primaries have reported earlier in the literature31,32. They are all metachronous in nature. In 2001 Sari R et al., has reported a case of synchronous double primary malignant neoplasms of colon and bladder33. In 2014, Liu Z et al. reported five patients diagnosed with synchronous bladder cancer and ColoRectal Cancers (CRCs) between May 1997 and September 2010. In this series, the primary colorectal tumors included three sigmoid cancers, one ascending colon cancer and one rectal cancer34. All the patients in this report underwent simultaneous radical cystectomy and CRC resection. Out of three sigmoid cancers, one was associated with recurrent bladder cancer. Hence, up to date literature search reveals only four cases of synchronous double primaries involving bladder and colon. Our case is unique due to its rare combination of synchronous primaries of urinary bladder (T1 N0 M0 ) and ascending colon (T2 N0 M0 ) presenting at the same time in 48 year old male, treated with transurethral resection of bladder tumour and radical right hemicolectomy in immediate consecutive sittings.
CONCLUSION
We have reported a rare combination of synchronous double primary malignancies of urinary bladder and ascending colon. This is the fifth case report of synchronous double primaries involving bladder and colon and third case report involving bladder and ascending colon to the best of our knowledge. MPMNs are still elusive for want of proper guidelines regarding correct terminology and classification encompassing varying presentations of chronological, aetiological, clinical and histopathological combinations. Influence of one primary over other and suggestions for best possible management are also yet to be defined properly. Our case adds up to the previously available ones for further research. The possibility of occurrence of synchronous multiple primary malignancies should be considered during workup for any malignant condition. As long as appropriate early interventions are performed in the synchronous multiple malignancies, good outcome is expected.
ACKNOWLEDGMENT
Authors acknowledge the immense help received from the scholars whose articles are cited and included in references of this manuscript. The authors are also grateful to authors/ editors/publishers of all those articles, journals and books from where the literature for this article has been reviewed and discussed. Authors are grateful to IJCRR editorial board members and IJCRR team of reviewers who have helped to bring quality to this manuscript.
Source of funding: Nil
Conflict of interest: Authors declare that they do not have any conflict of interest.
Englishhttp://ijcrr.com/abstract.php?article_id=478http://ijcrr.com/article_html.php?did=4781. Billroth T. General surgical pathology and therapeutics in: A textbook for students and physicians in fifty-one lectures. 14th ed. Berlin, DE: G. Rerimer; 1889.
2. Warren S, Gates O. Multiple primary malignant tumors; Surgery of literature and statistical study. Am J Cancer 1932;16:1358– 1414.
3. Moertel CG Multiple primary malignant neoplasms: historical perspectives. Cancer 1977;40(4 Suppl):1786-92.
4. Howe HL (Ed) A review of the definition for multiple primary cancers in the United States In Workshop Proceedings from December 4-6, 2002, in Princeton North American Association of Central Cancer Registries: New Jersey, Springfield (IL) 2003.
5. Vaamonde P, Martin C, del Rio M, LaBella T. Second primary malignancies in patients with cancer of the head and neck. Otolaryngol Head Neck Surg 2003;129:65-70
6. International Association of Cancer Registries. International rules for multiple primary cancers. Asian Pac J Cancer Prev. 2005;6(1):104-6.
7. Suzuki T, Takahashi H, Yao K Multiple primary malignancies in the head and neck: a clinical review of 121 patients. acta otolaryngol suppl 2002;547:88-92.
8. Demandante CG, Troyer DA, Miles TP Multiple primary malignant neoplasms: case report and a comprehensive review of the literature. Am J Clin Oncol. 2003;26(1):79-83.
9. Spratt JS Jr, Hoag MG. Incidence of multiple primary cancers per man-year of follow up: 20-year review from the Ellis Fischel State Cancer Hospital. Ann Surg 1966;164: 775-84.
10. Hajdu SI, Hajdu EO. Multiple primary malignant tumors. J Am Geriatr Soc 1968;16:16-26.
11. Berge T, Cederqvist L, Schonebeck J. Multiple primary malignant tumours. An autopsy study of a circumscribed population. Acta Pathol Microbiol Scand 1969;76:171-83.
12. Lee TK, Myers RT, Scharyj M, Marshall RB. Multiple primary malignant tumors (MPMT): study of 68 autopsy cases (1963- 1980). J Am Geriatr Soc 1982;30:744-53.
13. Aydiner A, Karadeniz A, Uygun K Tas S, Tas F, Disci R et al. Multiple primary neoplasms at a single institution: differences between synchronous and metachronous neoplasms. Am J Clin Oncol 2000;23:364-70
14. Hayat MJ, Howlader N, Reichman ME, Edwards BK. Cancer statistics, trends, and multiple primary cancer analyses from the Surveillance, Epidemiology, and End Results (SEER) Program. Oncologist 2007;12:20-37.
15. Ishimori T, Patel PV, Wahl RL. Detection of unexpected additional primary malignancies with PET/CT. J Nucl Med 2005;46:752-7.
16. Tamura M, Shinagawa M, Funaki Y: Synchronous triple early cancers occurring in the stomach, colon and gallbladder. Asian J Surg 2003;26(1):46-8.
17. Hawley AT, Pandolfi PP. Cancer susceptibility syndromes (Ch 12). In: De Vita VT, Hellman S, Rosenberg SA (Eds): Cancer: Principles and Practice of Oncology (8th Edn). Lippincott Williams and Wilkins, Philadelphia, Baltimore, New York, London, Buenos Aires, Hong Kong, Sydney, Tokyo, 2008, pp 157- 168.
18. Lee TK, Barringer M, Myers RT, Sterchi JM. Multiple primary carcinomas of the colon and associated extracolonic primary malignant tumors. Ann Surg 1982;195: 501-7.
19. Vyas JJ, Deshpande RK, Sharma S, Desai PB. Multiple primary cancers in Indian population: metachronous and synchronous lesions. J Surg Oncol 1983;23:239-49
20. Gürsel DM, Ozbek N, Ozdemir O, Odabas E. Multiple PrimaryMalignant Neoplasms from the Black Sea Region of Turkey. J Int Med Res 2011;39:667-74.
21. Ueno M, Muto T, Oya M, Ota H, Azekura K, Yamaguchi T. Multiple primary cancer: an experience at the Cancer Institute Hospital with special reference to colorectal cancer. Int J Clin Oncol 2003;8:162-7
22. Noh S K, Yoon J Y, Ryoo U N, Choi C H, Sung C O, Kim T J. A case report of quadruple cancer in a single patient including the breast, rectum, ovary, and endometrium. Journal of gynecologic oncology, 2008;19(4):265-69.
23. Yoshino K, Asanuma F, Hanatani Y, Kumai K, Ishibiki K: Statistical studies on multiple primary cancers including gastric cancers. Gan No Rinsho 1984;30(12 Suppl):1514-23.
24. Kim JW, Han JW, Jung SY, Jung JP, Kim JW. Synchronous double primary malignant tumor of the gallbladder and liver: a case report. World Journal of Surgical Oncology. 2011;9:84.
25. Iar?mov N, Toshev S, Angelov K, Lukanova Ts, Gribnev P, Sokolov M. Multiple primary carcinomas of the colon and associated extracolonic primary malignant tumors. Khirurgiia (Sofiia). 2007;(4):5-9.
26. Cercato M C, Colella E, Ferraresi V, Diodoro M G, Tonachella R. Report of two cases of quintuple primary malignancies and review of the literature. Anticancer research, 2008;28(5B):2953- 8.
27. Sommers, G. M., Logan, S., and Camel, H. M. Six independent neoplasms in one woman. A case report. The Journal of reproductive medicine, 1988;33(1):82-3.
28. Baigrie, R. J. Seven different primary cancers in a single patient. A case report and review of multiple primary malignant neoplasia. European journal of surgical oncology: the journal of the European Society of Surgical Oncology and the British Association of Surgical Oncology, 1991;17(1):81-3.
29. Cigna E, Gradilone A, Sorvillo V, Scuderi N. ABCB5 in peripheral blood of a patient affected by multiple primary malignancies. Ann. Ital. Chir, 2011;82(1):49-53.
30. Zhao J, Tan Y, Wu Y, Zhao W, Wu J, Ji M et al. A rare case of eight multiple primary malignant neoplasms in a female patient: A case report and review of the literature. Oncology Letters, 2015;9(2):587-90.
31. Weingartner K, Melekos MD, Gerharz EW, Kohl U, Neumann K, Riedmiller H. Multiple (five) synchronous primarymalignant neoplasms of dissimilar histogenesis including a malignant fibrous histiocytoma of the bladder. Inter Urol Nephrol 1995;27:157-66.
32. Yakushiji H, Mukai S, Matsukura S, Mukai S, Matsukura S Sato S et al: DNA mismatch repair deficiency in curatively resected sextuple primary cancers indifferent organs: a molecular case report. Cancer Lett 1999;142:17-22,
33. Sari R, Buyukberber S, Sevinc A, Mizrak B. Synchronous primary malignant neoplasms of colon and bladder. Indian J Gastroenterol. 2001;20(4):156-7.
34. Liu, Z., Chen, G., Zhu, Y., and Li, D. Simultaneous radical cystectomy and colorectal cancer resection for synchronous muscle invasive bladder cancer and cT3 colorectal cancer: Our initial experience in five patients. Journal of research in medical sciences: the official journal of Isfahan University of Medical Sciences, 2014;19(10):1012-5]
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241715EnglishN2015August11HealthcareASSESSMENT OF BOHLER'S AND GISSANE’S ANGLES OF THE CALCANEUM IN A GROUP OF SOUTH INDIAN POPULATION - A RADIOLOGICAL STUDY
English1720Rahe RamachandranEnglish Shailaja ShettyEnglishCalcaneus is the largest tarsal bone designed to withstand the daily stresses of weight bearing. Bohler’s and Gissane’s angles are subtended by the Calcaneus, these angles are used in the assessment of Calcaneal fractures.
Objective: Measuring the Bohler’s and Gissane’s angles from computed ankle radiographs and comparing the results with previous studies.
Materials and Methods: This study was done in M.S. Ramaiah teaching hospital and M.S. Ramaiah memorial hospitals, Bangalore, India. Study was conducted on 92 patients older than 17 years. The angles were measured and the variation in range was compared with that of the previous studies.
Observation and Results: From this study it was observed that the Bohler’s angle ranges between 18.7 – 46.2 degrees. Gissane’s angle ranges between 87.5 – 137.8 degrees. The normal international reference values are; Bohler’s angle 280 to 400 and Gissane’s angle 1200 to 1400. The lower limit of Bohler’s angle in our study group, like few other studies is found to be much less than the reference values which is used to diagnose Calcaneal fractures.
Conclusion: The range of Bohler’s and Gissane’s angles in the Indian population is much less when compared to the standard reference values, indicating that range of the angles is variable in different population groups. Hence knowledge of the exact range of the angles in a specific population group aids in accurate diagnosis and meticulous treatment of Calcaneal fractures.
EnglishCalcaneal angle, Measurement, Ankle fracturesINTRODUCTION
Foot has evolved over many million years to attain the human type. Foot has 28 bones and 31 articulations to support daily biomechanical loads of up to three to seven times the body weight. One of the key bones supporting the body weight is the calcaneus. Fracture of the calcaneus is common in fall from height and slipping from stairways. Imaging plays major role in the diagnosis, treatment and prognosis of Calcaneal fractures. Radiological measurement of Bohler’s angle and Gissane’s angles of the calcaneum are important parameters in Calcaneal fracture diagnosis, management and assessment of prognosis. Bohler’s and Gissane’s angles are subtended by the Calcaneal bone. Bohler’s angle is also known as Calcaneal angle, Tuber joint angle or Salient angle. It is used for assessing the loss of Calcaneal inclination (or ankle dorsiflexion impingement). It is measured at the intersection of a line drawn between the posterior superior aspect of calcaneal tuberosity and the highest point in the posterior talar facet, to another line drawn to the anterior process of the calcaneus. It normally ranges from 280 to 400 1,2 . Fracture through the calcaneus with displacement causes reduction of angle to less than 280 1 . Measurement of Bohler’s angle plays a key role in diagnosis of Calcaneal fractures and its intra operative reduction and fixation. Gissane’s angle or Critical angle of Gissane is the angle subtended between the anterior and posterior talar facets of the calcaneus. The angle normally ranges between 1200 and 1400 2 .
Since the calcaneum is a weight bearing bone the Calcaneal angles can possibly be variable in different races due to variation in built and load bearing. The objective of the study is to measure the Bohler’s and Gissane’s angles of the calcaneum from computed radiographs of lateral view of ankle joint in a group of South Indian population and look for deviations from the present international reference values. The study also includes comparison of results with previous studies conducted in different racial groups. The study was done on radiographs as they are the most common tools used for the measurement of the Calcaneal angles pre-operatively and intra-operatively.
MATERIALS AND METHODS:
This is a hospital based cross sectional study done in M.S. Ramaiah Medical college hospital, Bangalore from September 2011 to May 2013. By analysing the previous studies the minimum sample size was calculated as 84. In this study computed radiographs of 184 normal ankles of 92 patients, older than 17 years were obtained and analysed . The study population included 61 males and 31 females. Ethical clearance was obtained. Patients referred to the radiology department were randomly included for the study. Patients with ankle deformities, Calcaneal fractures, congenital anomalies and arthritis were excluded. Radiograph of the lateral view of both right and left the ankles were taken in a single exposure. A medio-lateral view was taken. The digital radiograph was obtained and the Bohler’s and Gissane’s angles were measured using the angle tool in software called Dicom Viewer (Fig;1,2). Each angle was measured thrice and the mean was calculated and tabulated.
RESULTS
In the present study done in the Indian population, 184 ankle radiographs were taken (118male and 66 female ankles). The mean Bohler’s angle was found to be 31.3±5SD. Minimum and maximum values were 18.7° and 46.2° (Table:1). The lower limit which is diagnostically significant, is lower than that observed in Nigerians (28 to 38 degrees) 3 , Ugandans (20 to 50 degrees) 4 and Egyptians (22 to 40 degrees) 5 and higher than that observed in Americans (14 to 50 degrees)6 and Saudi Arabians (16 to 47 degree)7 (Table:2). The mean Gissane’s angle in the present study was 108.5 degrees. The maximum and minimum values for Gissane angle were 86.3° and 137.8° (Table:1). The minimum angle was found to be lower than that observed in all the previous studies (Table 3).
DISCUSSION Calcaneum is the most vulnerable bone of the ankle region. It is the tarsal bone most commonly prone for fractures and accounts for about 2% of the total fractures1 . Various studies have been conducted on Bohler’s and Gissane’s angles on different races. There is no literature suggestive of such a study done in South India. The tuber angle of Bohler ranges from 28 – 40 degrees. A decrease in angle indicates that the posterior facet i.e. the weight bearing surface of the calcaneus has collapsed, this leads to shifting of the weight of the body anteriorly. The reduction of Bohler’s angle indicates mainly the degree of proximal displacement of the Calcaneal tuberosity. Hence the angle is reduced in both intra-articular and extra-articular fractures of the calcaneus 11. The study conducted in 1991 in the American population concluded that if 28 degree is taken as the lower limit of normal for Bohler’s angle, 37 cases (31%) would be false-positive abnormal. The use of 20 degree as the lower limit may decrease the number of false-positive to three cases (2.5%); using 18 degree (mean − 2 SD) reduces the false-positive rate to less than 1% (one case) 6 . in studies conducted in most of the above mentioned races (Table:2,3), the lower limit of Bohler’s angle is less than 28 degrees. The Bohler’s and Gissane’s angles are the most frequently assessed angles in the interpretation of Calcaneal fractures 12. Radiographic evaluation for a suspected Calcaneal fracture should include the 4 views : (i)Antero posterior view / dorsoplantar view, (ii) Oblique view / medial oblique axial projection, (iii) Broden’s view and the lateral view 13,14. Among these the lateral view includes assessment of height loss (using Bohler’s angle) and assessment of rotation of posterior facet (using Gissane’s angle). Bohler’s angle and Gissane’s angle are used also in classification of Calcaneal fractures. Bohler’s angle also plays a role in the surgical management of Calcaneal fractures15. Bohler’s angle of 15 degrees or less is an indication for surgical reduction of the fracture15. During the surgical procedure the displaced fragment is reduced in such a way that the Bohler’s angle is restored16. The initial value of Bohler’s angle at the time of trauma guides the treatment 17. Literature affirms that Bohler’s angle serves as a guide in assessing outcome following surgical or non surgical treatment of Calcaneal fractures 18. The angle escalates towards near normal values with appropriate management.
CONCLUSION
Calcaneus, the weight bearing bone of the lower limb handles the stresses of the upright human posture. Fracture of this bone leads to hindrance in his or her day to day activities. The evaluation of Bohler’s and Gissane’s angles plays an important role in the diagnosis, treatment and prognosis of Calcaneal fractures. The range of Bohler’s and Gissane’s angles in the present study group of south Indian population is much less when compared to the standard reference values, indicating that range of the angles is variable in different population groups. The study of Bohler’s and Gissane’s angles in many such groups in a particular race helps in standardisation of range to that population. Hence this study helps the radiologist and orthopaedic surgeons to achieve accurate diagnosis, deliver apt treatment and in better assessment of prognosis.
Englishhttp://ijcrr.com/abstract.php?article_id=479http://ijcrr.com/article_html.php?did=4791. Sonin AH, Boles CA, Roger LF. Skeletal Trauma. In: Grainger RG, Alleson DJ, Adam A, Dixon AK, editors. Diagnostic Radiology. 4th ed. Vol 3. London, UK: Elsevier Churchill Livingstone; 2001. p. 1813.
2. Yochum TR, Rowe LJ. Essentials Of Skeletal Radiology. 3rd ed. Vol 1. Philadelphia: Lippincott Williams And Wilkins; 1996. p. 241.
3. Didia BC, Dimkpa JN. The calcaneal angle in Nigerians. Relationship to sex, age, and side of the body. J Am Podiatr Med Assoc 1999;89:472-4.
4. Igbigbi PS, Mutesasira AN. Calcaneal angle in Ugandans. Clin Anat 2003;16:328-30.
5. Shoukry FA, Aref YK, Sabry AE. Evaluation of the normal calcaneal angl
6. Chen MY, Bohrer SP, Kelley TF. Boehler’s angle: a reappraisal. Ann Emerg Med 1991;20:122-4.
7. Khoshhal KI, Ibrahim AF, Al-Nakshabandi NA, Zamzam MM, Al-Boukai AA, Zamzami MM. Bohler’s and Gissane’s angles of the calcaneus in the Saudi population. Saudi Med J 2004;25:1967-70.
8. Seyahi A, Uludag S, Koyuncu LO, Atalar AC, Demerhan M. The calcaneal angles in the Turkish population. Acta Orthop Traumatol Turc 2009;43:406-11.
9. Boyle MJ, Walker CG, Crawford HA. The paediatric Bohler’s angle and crucial angle of Gissane: a case series. Journal of Orthopaedic Surgery and Research 2011;6:2-5.
10. Daftary A, Haims AH, Baumgaertner MR. Fractures of the calcaneus: a review with emphasis on CT. Radiographics. 2005;25(5):1215–26.
11. Sanders R. Displaced intra-articular fractures of the calcaneus. The Journal Of Bone And Joint Surgery 2000;82a:225-50.
12. Schepers T, Ginai AZ, Mulder PG, Patka P. Radiographic evaluation of calcaneal fractures; To measure or not to measure. Skeletal Radiol 2007;36(9):847-52.
13. Canale ST. Campbell’s operative orthopaedics, 10th edition. Fractures and dislocations of foot. Murphy GA. Philadelphia, Pennsylvania: Mosby, Elsevier; 2003: 4231- 47.
14. Gupta MK. An outcome evaluation of operative compared with non operative management of intra-articular Calcaneum fractures [unpublished dissertation]. M.S.Ramaiah medical college: Rajiv Gandhi University Of Health Sciences; 2011.
15. Schepers T, Patka P. Intra-articular calcaneal fractures; A review of the literature. Ned Tijdschr Trauma 2008;16(2):40-7.
16. Meraj A, Zahid M, Ahmad S. Management of intra-articular calcaneal fractures by minimally invasive sinus tarsi approachearly results. Malay Orthop J 2012;6:13–17.
17. Bakker B, Halm JA, Van Lieshout EM, Schepers T. The fate of Böhler’s angle in conservatively treated displaced intra-articular calcaneal fractures. Int Orthop 2012 Dec;36(12):2495-9.
18. Schepers T, Vogels LMM, Schipper IB, Patka P. Percutaneous reduction and fixation of intra-articular calcaneal fractures. Oper Orthop Traumatol 2008;20(2):168-175.
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241715EnglishN2015August11HealthcareFUNGAL INFECTIONS - A CLINICOMORPHOLOGICAL SPECTRUM
English2125Thamil Selvi RamachandranEnglish K. SivakamiEnglish Prakash H. MuddegowdaEnglish P. VenukeerthanEnglishIntroduction: Fungal infections at different sites are showing increasing incidence in both healthy and Immunocompromised individuals. Among the fungal infections, Aspergillus and Mucormycosis are the common infections, involving maxillary sinus, oral cavity, lung followed by each case of maduramycosis of foot and mucormycosis of forearm in this study.
Aims: To study the clinical and pathological profile of fungal infections at various sites.
Settings and Design: A Retrospective observational study conducted in Department of Pathology from Jan 2011- Dec 2012, VMKV medical college, Salem.
Material and Methods: Seventeen cases were analyzed in this study with respect to clinical history, physical examination and neuroimaging [computed tomography (CT) or magnetic resonance imaging (MRI)] wherever necessary. Operated specimens were received in 10% formalin for histopathological examination.
Results: Male:female ratio was 11:6. Mean age of 49 years. The common clinical presentations were nasal discharge followed by oral ulcer and foot ulcer. Commonest site of lesion was nasal cavity (59%). Mucormycosis was the commonest fungus.
Conclusions: Early diagnosis and prompt treatment can reduce the mortality and morbidity of this lethal fungal infection.
EnglishFungal infections, Mucormycosis, Aspergillus, Oral ulcerINTRODUCTION
Fungal infections at different sites are now-a-days showing increasing incidence in both normal and Immunocompromised individuals. Mucormycosis, a fulminant fungal infection, invades the arteries, forms thrombi within the blood vessels that reduces blood supply and causes necrosis of hard and soft tissues (1,2). Once within the arteries, the fungus may spread to orbital and intracranial structures. Aspergillus species are the most common cause of fungal sinusitis. (3,4)
AIMS
To study the clinical and pathological profile of fungal infections at various sites.
MATERIAL AND METHODS
A Retrospective observational study from Jan 2011- Dec 2012 was conducted in the Department of Pathology, VMKV medical college, Salem. Seventeen cases were analyzed in this study with regards to clinical history, physical examination, and radiological examination( like X-Ray paranasal sinus view, neuroimaging [computed tomography or magnetic resonance imaging (MRI)] studies). Operated specimens were received in 10% formalin for histopathological examination. Routine Haematoxylin and Eosin stain and, when necessary, special stains like Periodic Acid Schiff stain(PAS) and Silver stains were done.
RESULTS
A total of seventeen cases were studied, with age range of 15 to 80 years. Mean age was 49 years and Male:Female ratio was 11:6. Most common presenting symptom was nasal discharge and clinical diagnosis was nasal polyp/growth. In six cases, the underlying disease was diabetes mellitus. (Table 1). X-ray paranasal sinus showed haziness of maxillarysinus in all cases. MRI revealed Orbital pseudo tumor in 3 cases and one case showed air filled cavity in the lung. In this study, Mucormycosis (Fig 1-4) was the commonest fungi (seven cases), followed by five cases of Aspergillosis (Fig 5 and 6) , two cases each of candida (Fig 7 and 8) and Rhinosporidosis (Fig 9 and 10). Only one case of maduramycosis was present in this study (Fig 11 and12). Periodic Acid Schiff (PAS) and Silver methenamine special staining technique demonstrated the fungus. Microbiology culture was positive in 7 cases.
DISCUSSION
In this study, histopathological examination with hematoxylin and eosin (H and E) stained sections showed various types of fungal infection with their characteristic feature, like abscess , necrotic material, inflammatory cells or granuloma composed of epithelioid cells, giant cells, surrounding the thin ribbon like fungal hyphae. The most common fungal infection in the present study was Mucor, an aggressive, opportunistic infection in the class of Phycomycetes, first described in 1885 by Paultauf. (5) Rhinocerebral mucormycosis is a rare opportunistic infection. It is mostly seen in association with immunosuppression as in this study, underlying conditions were diabetes mellitus and malignancy. (5,6,7) Ferry et al in 1983 and Yohai et al (8) in 1994, reported sinus involvement in 69% - 79% of mucormycosis respectively. In our study, it was 59%. Aspergillus species is the most common fungal infection of the paranasal sinuses. (6) Allergic Aspergillus sinusitis was first described as a form of fungal sinusitis by Katzenstein et al in 1983. (7) The typical presentation is nasal polyp associated with thick mucin and scanty fungal hyphae. However, culture is usually negative in most of the cases.(7,8) In our study, out of five cases of aspergillosis, only two cases showed positive culture. The next common fungal infection was candidiasis. Candida species, most often C. albicans, are the most frequent cause of human fungal infections. Diabetics patients are particularly susceptible to superficial candidiasis. Candidiasis takes the form of a superficial infection on mucosal surfaces of the oral cavity (thrush), oesophagitis, vaginitis, mucocutaneous and Invasive candidiasis. 9 We reported two cases of Rhinosporidiosis. It is characterised by hyperplastic polypoidal lesion of the nasal cavity. The organism of Rhinosporidiosis are huge, thick walled sporangia containing several thousands of spores. They elicit inflammatory response composed of neutrophils, lymphocytes and plasma cells. 10 In our study, we had only one case of maduramycosis. 13 species of fungi have been identified as causes of mycetoma. These include madurella mycetomi and Allescheria boydii . The condition occurs mainly in Tropical countries like India. The foot is most commonly involved, as in this study. 11
CONCLUSION
The early diagnosis and recognition of invasive fungal infection is very important, to prevent progression of the disease and avoid the high morbidity and mortality with this destructive disease.
Englishhttp://ijcrr.com/abstract.php?article_id=480http://ijcrr.com/article_html.php?did=4801. Leitner C, Hoffmann J, Zerfowski M, Reinert S. Mucormycosis: necrotizing soft tissue lesion of the face. J Oral Maxillofac Surg 2003;61:1354-8.
2. Pogrel MA, Miller CE. A case of maxillary necrosis. J Oral Maxillofac Surg 2003;61:489-93.
3. Zapico ADV, Suarez AR, Encinas PM, Angulo CM, Pozuelo EC. Mucormycosis of the sphenoidal sinus in an otherwise healthy patient. Case report and literature review. J Laryngol Otol 1996;110:471-3.
4. Jones AC, Bentsen TY, Fredman PD. Mucormycosis of the oral cavity. Oral Surg Oral Med Oral Pathol 1993;75: 455-60.
5. Paulltauf A. Mycosis mucorina. Virchows Arch [A]. 1885, 102- 543.
6. Stammberger M,Jakes R, Beaufort, Austria G. Aspergillosis of the paranasal sinuses: X-ray diagnosis, histopathology and clinical aspects. Ann Otol Rhino Laryngol 1984; 93:251-6.
7. Katzenstein AA, Sale SR, Greenberger PA. Allergic Aspergillus sinusitis. A newly recognized form of sinusitis. The Laryngoscope 1983;72:89-93.
8. Yohai RA, Bullock JD, Aziz AA et al, Survival factors in Rhinoorbito-cerebral mucormycosis. Surv opthalmol:1994; 39:3-22
9. Achkar JM, Fries BC. Candida infections of the genitourinary tract. Clin Microbiol Rev. 2010;23(2):253-73.
10. Sinha A, Phukan JP, Bandopadhyay G, Sengupta S, Bose K, Mondal RK, et al. Clinicopathological study of rhinosporidiosis with special reference to cytodiagnosis. J Cytol 2012;29(4):246- 9.
11. Bonifaz A, Tirado-Sánchez A, Calderón L, Saúl A, Araiza J, Hernández M, et al. (2014) Mycetoma: Experience of 482 Cases in a Single Center in Mexico. PLoS Negl Trop Dis 8(8): e3102. doi:10.1371/journal.pntd.0003102
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241715EnglishN2015August11HealthcareINVASIVE LOBULAR BREAST CARCINOMA (ILC) IN AN ELDERLY MALE ON PROLONGED RANITIDINE THERAPY
English2631Srikantaiah HiremathEnglish Nikhil Nanjappa B. A.EnglishBreast carcinoma in men is an exceedingly rare entity, contributing to 1% of all breast cancers [1], of which invasive lobular carcinoma (ILC) accounts for 1.5% [2]. The average age at diagnosis is usually five years older compared to women [1, 3]. Although the exact aetiology remains unknown, hyperestrogenic states are attributed as the most likely cause [4]. Men with family history of female breast cancer are at 2.5 times more increased risk when compared to those with no family history [5]. Lobular histologic subtype of breast carcinoma in males is rare due to the lack of acini and lobules [6]. Some medications, such as cimetidine
[7, 8] are thought to multiply the risk of male breast cancer because they induce a hyperestrogenic state. The authors report a rare case of ILC in a 75 year old man, with no known risk factors for breast cancer. However, he had a history of prolonged self-prescribed ranitidine use for dyspeptic symptoms. Although there isn’t enough evidence to suggest that ranitidine, like its predecessor cimetidine, may cause male breast cancer. The authors would like to draw attention to this possibility.
EnglishMale breast carcinoma, Male breast cancer, Invasive lobular carcinoma males, Ranitidine induced male breast cancerINTRODUCTION
Breast carcinoma in men is an exceedingly rare entity. As the incidence is very low, the exact aetiology remains unknown; however, it is largely attributed to oestrogen excess states. Men who have family history of female breast cancer are at 2.5 times increased risk when compared to those with no family history [5]. The average age at diagnosis is five years older compared to women [1, 9]. Most of the breast cancers in men are of ductal (in situ and invasive) type. Invasive lobular cancer is an extremely rare histopathological type of male breast cancer because lobular and acinar components are rarely found in the normal male breast [10]. Breast cancer in men carries a worse prognosis when compared to women, although the principles of management remain the same. We present an extremely rare case of invasive lobular carcinoma (ILC) in an elderly gentleman with no other risk factors but for prolonged ranitidine therapy. Although there is not enough evidence to suggest that ranitidine, like its predecessor cimetidine, may cause male breast cancer, the authors would like to draw attention to this possibility.
CASE REPORT
A 75 year old male fruit vendor presented with complaints of a lump in the right breast since 7 months. The lump developed insidiously and was associated with pain that led him to seek medical intervention. He did not have any associated medical co-morbidities and was not on any chronic medications. He did not have any history of gynaecomastia and was not on any form of hormone replacement therapy. His scrotum was normal on examination. He did not have any family history of breast or ovarian cancers. On retrospective questioning he admitted that would often consume ranitidine tablets for symptoms of gastritis which was easily available over the counter. On examination he had a 3*3 cm hard lump in the central quadrant of the right breast; the mobility ofwhich was restricted indicating fixity to the pectoralis muscle (Fig. 1). There was another hard 1*1 cm solitary lump lateral but separate from the aforementioned lump. One hard solitary central group lymph node was palpable on examination of the right axilla. Clincal AJCC stage of the tumour was T4cN1M0. Ultra sonogram of the breast and axilla complimented the clinical findings. A whole body PET-CT did not reveal any evidence of distant metastasis. Fine needle cytology evaluation confirmed the diagnosis of carcinoma breast in the primary lump, the satellite nodule as well as in the axillary lymph node. The patient underwent a modified radical mastectomy of the right breast (Fig. 2 and 3). Histopathological examination of the specimen showed invasive malignant tumour comprising of tumour cells arranged in nests and trabeculae. The tumour cells possessed round nuclei with minimal atypia, vesicular chromatin and prominent nucleoli. Stromal desmoplasia was seen along with mild lymphocytic infiltration. Multiple microcalcifications were present along with some perineural involvement. The overlying skin and underlying skeletal muscles were involved. Metastasis was present in 3 of the 9 lymph nodes studied along with extranodal spread. These findings were consistent with invasive lobular carcinoma (Fig. 4 and 5). Pathological AJCC stage was IIIB (pT4N1M0). The tumour was both estrogen and progesterone receptor positive on immunohistochemistry. The patient was advised to receive adjuvant chemotherapy but was not compliant. However, he has been on Tamoxifen (100 mg) for the last four years and has had no recurrence.
DISCUSSION
Breast carcinoma in men is an exceedingly rare entity. The prevalence of which is one per 100,000 persons and accounts for less than 1% of all breast cancers. It is responsible for less than 1% of all male malignancies [1]. The average age at diagnosis is usually between 63 and 71 years which is five years older compared to women with a range of 58 to 93 years [1, 2, 3]. This gentleman was 75 years old at the time of diagnosis which is a little more than the average, but consistent with the fact that male breast cancers occur in the 7th and 8th decades of life. Since male breast carcinomas have a low rate of incidence the exact aetiology remains largely unknown. However, some risk factors have been elucidated. Androgen aromatisation, obesity and alcoholic liver disease all of which are associated with increased levels of sex steroid binding globulin. These in turn incite a state of oestrogen excess and remain the most probable aetiologies [4]. Undescended testes, orchitis, orchiectomy, and sterility are other risk factors, albeit a causal association is yet to be determined. Some medications, such as cimetidine, are thought to multiply the risk of male breast cancer due to hyperestrogenism [5, 6]. A few controlled studies in animals and man have shown no stimulation of any pituitary hormone by ranitidine hydrochloride and no antiandrogenic activity. Studies have even claimed that cimetidine-induced gynaecomastia and impotence reduced when cimetidine was substituted with ranitidine [7]. However our patient was on long term over the counter ranitidine treatment. Whether ranitidine also has the same properties of its predecessor cimetidine remains unknown. Anecdotal evidence such as this may not be sufficient to justify our claim, but there certainly is a possibility that should be looked at. Men who have a family history of female breast cancer are at 2.5 times increases risk when compared to those with no family history [8]. Some studies attribute mutations in the genes BRCA1 and BRCA2 to male breast cancer but with a lower absolute risk and frequency compared to women [9]. Data from SEER (Surveillance, Epidemiology, and End Results cancer registry) of 2000 patients showed that 93.7% of breast cancers are ductal man or unclassified, 2.6% were papillary, 1.8% is mucinous and only 1.5% are lobular [2]. The ductal carcinoma in situ (DCIS) accounts for 10% of male breast cancers [2]. The in situ lobular carcinoma (LCIS) is rare due to the absence of terminal lobules, although it is found in association with ILC [10]. Goss et al. reported 1.9% of all male breast cancers as ILC [11]. Nahleh et al. reported the highest percentage of ILC when they analysed the Veterans Affairs Central Cancer registry with 612 male breast cancer patients [12]. ILC is completely different entity from the much more common invasive ductal carcinoma (IDC). Although ILC accounts for 12% of all female breast cancers, they are exceedingly rare in the male breast [13]. Lobular histologic subtype of breast carcinoma is due to the lack of acini and lobules in the normal male breast [14]. Endogenous or exogenous estrogenic stimulation may incite the development of acini and lobules in the male breast; this is referred as ‘lobulization’of the male breast. This could theoretically increase the risk of development of ILC in males [14]. ILC displays a wide variety of histologic subtypes from classical through solid to pleomorphic forms. The classical variant is found to have better prognosis. Male breast cancers are strongly hormone dependent tumours. Almost 90 and 81% are estrogen and progesterone receptor positive respectively [2, 15]. But overexpression and/or amplification of the Her2 gene is less than IDC [16]. Our patient was both oestrogen and progesterone receptor positive and has been on Tamoxifen daily for the last 4 years.
ILC characteristically lacks E-cadherin expression on immunohistochemical (IHC) staining and this property is now used as a diagnostic aid [10]. We were unable to carry out IHC staining due to cost constraints and hence reserve any judgements. Male breast cancer carries a worse prognosis than female [2]. This could be attributed to the lack the lobular component allowing the tumour to invade local structures like the chest wall more rapidly and also distant spread occurs sooner due to the same reason. Tumour size and the lymph node involvement are important prognostic factors just like in females [2]. Men with T2 tumours have a 40% increased mortality risk compared to those with T1 tumours [5]. Our patient presented with a T4a tumour for which he underwent a modified radical mastectomy. Despite having chosen not to receive adjuvant chemotherapy he has no evidence of recurrence and has survived for 4 years after the surgery. We do not wish to enter the debate on the need for adjuvant chemotherapy as the evidence is only anecdotal.
CONCLUSIONS
• The first case of ILC without known estrogen exposure was reported in 1989 [13], and about 30 cases have been reported since. Hence we felt the need to report this case.
• This gentleman had no history of gynaecomastia, no evidence of testicular abnormalities, no liver cirrhosis, no family history of breast or ovarian cancer, and was not on any hormone replacement therapy, but still developed invasive lobular breast carcinoma.
• The only possible contributory factor was chronic consumption of ranitidine.
• Ranitidine is easily available over the counter at a fraction of the cost compared to proton pump inhibitors. Dyspeptic symptoms are easily attributed to gastritis, especially in the elderly.
• Although there is isn’t sufficient evidence to suggest that ranitidine is a potential risk factor, there lies a pressing need to study this association further.
Englishhttp://ijcrr.com/abstract.php?article_id=481http://ijcrr.com/article_html.php?did=4811. Tunon de Lara C, G Goudy, MacGrogan G, M Durand, JM Dilhuydy, Avril A, E Stoeckle, I Bussieres, Debled M, De Mascarel I, Mauriac L. Breast cancer in humans: about 52 If supported in BergoniéInstitute of Bordeaux between 1980 and 2004. Obstetrics and Gynecology Fertility 2008 Apr; 36 (4): 386-394.
2. Giordano SH, DS Cohen, Buzdar AU, Perkins G, Hortobagyi GN. Breast carcinoma in men: a population-based study. Cancer. 2004 Jul 1; 101 (1): 51-7.
3. Goss PE, Reid C, Pintilie M, Lim R, N Miller. Male breast carcinoma: a review of 229 patients who presented to the Princess Margaret Hospital Pendant 40 years: 1955-1996 Cancer. 1999 Feb 1; 85 (3): 629-39.
4. JR Weiss, Moysich KB, Swede H. Epidemiology of male breast cancer. Cancer Epidemiol . Biomarkers Prev 2005; 14 (1): 20- 26.
5. Sorensen HT, Friis S, Olsen JH, Thulstrup AM, Mellemkjaer L, Linet M, Trichopoulos D, Vilstrup H, Olsen J. Risk of breast cancer in men with liver cirrhosis. Am J Gastroenterol. 1998;93:231–233.
6. San Miguel P, Sancho M, Enriquez JL, Fernandez J, GonzalezPalacios F. Lobular carcinoma of the male breast associated with the use of cimetidine. Virchows Arch. 1997;430: 261–263.
7. The Internet Drug Index (RxList). California: The Internet Drug Index [Cited 2015 March 1]. Available from: http://www.rxlist. com/zantac-drug/side-effects-interactions.htm
8. Laabadi K, Jayi S, Alaoui FF, et al. Breast Cancer man: about 6 cases. The Pan African Medical Journal 2013; 16: 70.
9. Sverdlov RS Barshack I, Bar Sade RB, RG Baruch, Hirsh-G Yehezkel, Dagan E, Feinmesser M Freeze A, Friedman E. Genetic analysis of male breast cancer in Israel. Genet Test. 2000; 4 (3): 313-7.
10. Espiémillion Gorins A. Breast normal to pathological: state of the art. Oxford University Press; 2001.
11. Goss PE, Reid C, Pintilie M, Lim R, Miller N. Male breast carcinoma: a review of 229 patients who presented to the Princess Margaret Hospital during 40 years: 1955-1996. Cancer. 1999;85:629–639.
12. Nahleh ZA, Srikantiah R, Safa M, Jazieh AR, Muhleman A, Komrokji R. Male breast cancer in the veterans affairs population: a comparative analysis. Cancer. 2007;109: 1471–1477.
13. Giordano SH. A review of the diagnosis and management of male breast cancer. Oncologist. 2005;10(7):471–479.
14. Zahir MN, Minhas K, Shabbir-Moosajee M. Pleomorphic lobular carcinoma of the male breast with axillary lymph node involvement: a case report and review of literature. BMC Clinical Pathology 2014;14:16.
15. Maly B, Maly A, Pappo I, Meir K, Pappo O. Pleomorphic variant of invasive lobular carcinoma of the male breast. Virchows Arch. 2005;446(3):344–345.
16. Varga Z1, Mallon E. Histology and immunophenotype of invasive lobular breast cancer. Daily practice and pitfalls. Breast Dis. 2008-2009; 30:15-9.
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241715EnglishN2015August11HealthcareNATURAL RESISTANCE ASSOCIATED MACROPHAGE PROTEIN 1 POLYMORPHISM SUSCEPTIBILITY TO MULTI DRUG RESISTANCE TUBERCULOSIS IN SOUTH INDIAN POPULATION: A CASE -CONTROL
STUDY
English3235Rooth Vasantha M.English G. SudhakarEnglish S. SrideviEnglishAim: To know the association of NRAMP1 gene polymorphisms in MDR-TB Patients.
Methodology: Studies on NRAMP1 (Natural Resistance Associated Macrophage Protein1 or SLC11A1 revealed its function on macrophage activation and its association with infectious diseases. A case-control study was carried out to find the association of NRAMP1 gene with MDR-TB belonging to Visakhapatnam district of Andhra Pradesh, India. Genetic polymorphisms of NRAMP1 gene 3’UTR and 274 CT were analysed using Polymerase Chain Reaction-Restriction Fragment Length Polymorphism
(PCR-RFLP).
Results: Significant statistical difference in the 3’UTR polymorphism between MDR-TB patients and healthy controls was observed. (P=0.001, OR=0.691,95%CI=0.077-6.208). But no significant association was found between the disease and 274 CT polymorphism (P>0.05).
Conclusion: Significant association of MDR-TB with 3’UTR polymorphism of NRAMP1 gene was identified, while no significant association was observed in 274CT polymorphism of NRAMP1 gene. Further study with large sample size is required to confirm the above results.
EnglishNRAMP1, 3’UTR, 274CT, MDR-TBINTRODUCTION
According to World Health Organisation Global Tuberculosis report 2014, nine million people developed TB in 2013 and 1.5 million died of the disease(WHO, 2014(1)). The number of people developing the disease is declining by an average of 1.5% a year. However the report underlines that many lives are being lost to a curable disease and confirms that TB is the second largest killer disease from single infectious agent-Mycobacterium tuberculosis. Although routine surveillance efforts are increased yet millions of people who fall ill from TB are missed by health system each year, because they are not diagnosed or they diagnosed but not reported. The association of tuberculosis with HIV and increasing multi-drug resistant tuberculosis (MDR-TB) frames a serious issue especially in the developing nations (WHO 2014(2)) Increase in population rate along with disorders, linked with several socio-economic factors are operational in India, than in any other developing country. The proportion of patients with MDR-TB is increasing day by day due to insufficient treatment facilities. The progression of molecular study up to gene level in research has attributed much to the identification of the individual strains of MTB. The reason that many TB patients who are in the course of anti-TB treatment are stopping to take medicines, is that after seven weeks of using the drug, major symptoms of TB reduce and the patients assume that their health has improved. Thus a man made public hazard has become prominent (3). Treatment of MDR-TB has become difficult as the MTB became resistant to two most powerful anti-TB drugs Rifampicin and Isoniazid. MDR-TB patients who are not responding to the treatment are a constant source of transmission of multi-drug resistant MTB. In India many people have the habit of spitting the sputum in public places. If patients with TB and MDR-TB cough and spit in public places then the infection is transmitted by air through droplets of sputum dispersed into the environment. The amount of germs in the phlegm is also massive. Molecular study on Tuberculosis affected patients reveals that acquisition of TB does not occur due to horizontal transfer of resistance bearing genetic elements, but due to mutations (nucleotide substitution, insertions, or deletions in specific resistance determining region of the genetic targets. In humans, drug-resistance mutation in MTB occurs mainly within the lung cavities, where high loads of bacteria are present. Here active mycobacterial replication and reduced exposure to host defence mechanism was reported. Chromosome 2q35 was mapped with NRAMP1 gene (4). Many polymorphisms in this gene alter its function.NRAMP1 controls the replication of intracellular parasites by altering the intra vacuolar environment of the microbe containing phagolysosome (5,6). Mutations in this gene may play an important role in rapid screening of drug resistance among MDR-TB patients and early treatment can be initiated.
MATERIALS AND METHODS
33 In patients diagnosed with multidrug resistant TB were taken into study. Diagnosis was based on clinical and laboratory data retrieved from the clinical records maintained by Chest and Tuberculosis Hospital in Visakhapatnam between the time periods of July 2012 to Dec 2012. Diagnosis of the patients was done within the hospital laboratory using Lowenstein Jensen (L-J) medium. All the patients were under Anti-TB therapy. Patients were identified to have MDRTB if they were resistant to both Isoniazid and Rifampicin anti TB drugs. Data of these patients on basis of age, gender, drug resistance, habitual smoking and drinking, irregular treatment, details of prior treatment with anti-TB medication were recorded. Among the 33 MDR-TB patients, 27 were males and 6 were females. 100 healthy contacts were taken as controls. Written consent was obtained from all individuals taken into study. This study was carried out only after getting ethical approval from Institutional ethical committee, Andhra University.
DNA extraction
Isolation of Genomic DNA using salting out procedure was done in the Human Genetics Department laboratory of Andhra University, Visakhapatnam. After quantity and quality analysis using spectrophotometer and Agarose Gel electrophoresis, the isolated DNA was stored at -4o c.
Molecular analysis
3’UTR and 274 CT genotype analysis of NRAMP1 gene was carried out using Thermocycler. Primers used for the detection of SNP’s were purchased from Thermo scientific, restriction enzymes Fok1(NEB) and Mnll (Thermo scientific). PCR was performed in a total volume of 20µl of a solution containing 2µl of genomic DNA, 2.0 µl of 10×PCR buffer, 0.8 µl dNTPs, 0.5 µl of recombinant Taq polymerase (Invitrogen), 1 µl of Forward primer, 1 µl of reverse primer and 12.7 µl of sterile water. PCR amplification was carried out by operating the thermal cycler for 3’UTR NRAMP1/SLC11A1 polymorphism using the following conditions. 95o c for 5 mins,30 cycles of 95 oc for 30s, 52 oc for 30s and 72 oc for 30 sec with a final extension at 72 oc for 10 min. Primer sequence for 3’UTR, Forward: GCA TCT CCC CA TTC ATG GT. Reverse: AAC TGT CCC ACT CTA TCC TGC (Rahayu Anggraini et al., 2010(7). A region of 240 bp was amplified and genotyping was performed using restriction fragment length polymorphism analysis. The amplified PCR product was digested at 37o c for 2 hours with Fok1. The digested products were run on 2% agarose gel which is stained with Ethidium bromide and visualised under UV transilluminator. Primer sequence for 274 CT of NRAMP1 gene Forward: TGC CAC CAT CCC TAT ACC CAG. Reverse: TCT CGA AAG TGT CCC ACT CAG (Rahayu Anggraini et al., 2010). A region of 167 base pairs was amplified with annealing temperature of 56o c for 30 sec. The amplified PCR product is then digested at 37o c for 2 hours with Mnll restriction enzymes. The digested products were then run on 2% agarose gel stained with Ethidium bromide and visualised under UV transilluminator.
RESULTS
The observed results in Agarose gel electrophoresis for 3’UTR show genotype TGTG++ at 211bp and 33bp;TGTG+/ del genotype at 244bp,211bp, and 33bp;genotype TGTG del/ del at 244bp. Here the normal allele is TGTG+ and the mutant allele is TGTG del. For 274 CT polymorphism CC genotype at 102bp, 65bp, 37bp, and 12bp; CT genotype at 167bp, 102bp, 65bp, 37bp and 12bp; TT genotype at 167bp, 37bp, and 12bp.Here C is the normal allele and T is the mutant allele. Some of the PCR samples did not get amplified due to unseen reasons, so the sample size decreased to 29 MDR-TB and 89 healthy controls. A significant difference between the genotype frequencies of 3’UTR polymorphism of NRAMP1 gene in patients with MDR-TB and those in control group was observed.
Among the MDR TB patients, about 83 percent are found to be homozygous for the genotype TGTG/TGTG for the 3’UTR region of NRAMP1gene. The frequency of heterozygous type (TGTG/TGTG del) is only 3 percent among MDR TB patients, The remaining 14 percent are homozygous for TGTG del/TGTG del type.(P= 0.001;Odds ratio0.691;95%CI=0.077-6.208)
Among the MDR TB patients, 79 percent are found to be homozygous for the genotype C/C for the 274 CT SNP of NRAMP1 gene. The frequency of heterozygous type (C/T) is 21 percent among MDR TB patients. The homozygous type T/T is not found in the present patient sample. (P=0.533;odds ratio=1.500;95%CI=0.505-4.451)
DISCUSSION
MDR-TB is a severe health problem in the world today. Nearly estimated 29% of the global tuberculosis cases come from India. Out of which 0.5% to 3.2% have MDR-TB. Gujarat state showed high rate of prevalence in India (8, 9, 10). The reason for MDR-TB emergence is due to drug discontinuation in middle of the treatment and the bacteria becoming susceptible to TB drugs. Hence Anti-TB drugs should be individually tailored for each MDR-TB patient as the standard treatment for drug-resistant TB is not known. And even after administering the treatment less percentage of cases showed favourable outcome. HIV is also expected to cause an increase in the percentage of MDR-TB (11, 12, 13) But HIV patients were not included in the present study. Natural mutation in NRAMP1 gene impairs early immunity to several intra cellular pathogens including mycobacterium. Increased frequency of specific NRAMP1 mutation among patients and control is observed in various studies. The distribution of NRAMP1 3’UTR polymorphism did not deviate from the Hardy Weinberg Equilibrium (P>0.05) the frequency of 3’UTR in MDR TB patients was 17.2% and that of controls is 5.7%. No significant association was found between MDR-TB patients and controls in 274 CT polymorphism of NRAMP1.3’UTR of NRAMP1 studies on Thais,(14) Chinese,(15) and Koreans(16) show significant difference in Pulmonary TB patients. Polymorphisms of SLC11A1 /NRAMP1 gene are known to influence phagolysosomal function of macrophages in iron transport, maintenance of acidity, and production of nitric oxide(NO)(17-20). The change in the phagolysosomal function of NRAMP1 gene may affect the viability of phagocytosed MTB leading to the development of drug resistant strains of MTB. Variations in 3’UTR leading to mutations could be one of the independent risk factor for MDR-TB and possible basis for drug penetration. This study suggests that NRAMP1/ SLC11A1 polymorphisms in part are associated with the emergence of multi drug resistance and extensive pulmonary involvement. Further study is necessary to confirm the association of 3’UTR of NRAMP1 gene with more number of MDR-TB patient samples.
CONCLUSION
The results obtained in the study suggest that variation in the NRAMP1/SLC11A1 gene is associated with the emergencef Susceptibility to multidrug resistance TB. Further study with larger sample size is required to confirm the association.
ACKNOWLEDGEMENTS
The authors are thankful for the UGC RGNF fellowship from the government of India, for funding of the research work. The author also acknowledges the published articles of the scientists and other dignitaries on Tuberculosis.
Conflict of interest: The authors declared no conflict of interest
Englishhttp://ijcrr.com/abstract.php?article_id=482http://ijcrr.com/article_html.php?did=4821. WHO .2013.Global tuberculosis report.
2. WHO.2014.Multi Drug and Extensively drug-resistance TB 2014. Global Report on Surveillance and Response 2014.
3. Article on Tuberculosis in Hindu Newspaper Magazine dated March 15/2015.Pg:4
4. Blackwell J et al., 1995. Genomic Organisation and Sequence of the Human NRAMP gene: Identification and mapping of a promoter region polymorphism. Mol Med.1:194–205.
5. Gruenheid S et al., Natural resistance to infection with intracellular pathogens; the NRAMP1 protein is recruited to the membrane of the phagosome. J. Exp Med 1997; 4:717-30.
6. Hackam D et al., Host resistance to intracellular infection: mutation of natural resistance associated macrophage protein 1(Nramp1) impairs phagosomal acidification. J.Exp Med 1998; 188:351-64.
7. Rahayu Anggraini et al., 2010. Polymorphism of Natural-resistance-Associated Macrophage Protien1 (NRAMP1)D543N gene and expression of NRAMP1 on Lung Tuberculosis Patients and Nurses in Surabaya. Folia Medica Indonesiana.Vol.46 No.2:78- 87.
8. Mendez AP et al., Global Surveillance for anti tuberculosis dug resistance, 1994-1997. N.Eng J Med.1998; 338:1641-49.
9. Jawahar MS. Multi drug resistance tuberculosis. ICMR bull 1999. 29:10-11.
10. Ramachandran R, Balasubramanian R. Chemotherapy of Resistant tuberculosis; the tuberculosis research center experience over 40 years. Indian J Tub 2000;47:201-10.
11. H.S. Subhas et al., Clinical characteristics and treatment response among patients with multi drug resistant tuberculosis; A retrospective study. India chest Dis Allied Sci 2003, 45:97-103.
12. Gilad J, Borer A, Riesenberg K, Peled N, schlaeffer F. Epidemiology and ethnic distribution of multidrug resistant tuberculosis in southern Israel,1992-1997. Chest 2000;117:738-43.
13. Suchindran S, Brouwer ES, Van Rie A .2009. Is HIV Infection a Risk Factor for Multi-Drug Resistant Tuberculosis? A Systematic Review PLoS One 4 (5): e5561.
14. Vejbaesya S, Chierakul N, Luangtrakool P, Sermduangprateep C. 2007. NRAMPI and TNF-Alpha polymorphisms and susceptibility to tuberculosis in Thais. Respiratory.12:202-206.
15. W. Liu, W.C. Cao and et al. 2004. VDR and NRAMP1 gene polymorphisms in susceptibility to pulmonary tuberculosis among the Chinese Han population: a case-control study. The international journal of tuberculosis and lung disease: the official journal of the International Union against Tuberculosis and Lung Disease. Vol: 8:428.
16. Ryu S et al., 2000. 3’UTR Polymorphisms in the NRAMP1 gene are associated with susceptibility to tuberculosis in Koreans. Int J Tuberc Lung Dis.4:577-580.
17. Govoni G, Gros P. Macrophage NRAMP1 and its role in resistance to microbial infections. Inflamm Res 1998.47:277–84.
18. Kuhn DE, et al., Iron transport into Mycobacterium aviumcontaining phagosomes from an Nramp1 (Gly169)- transfected RAW264.7 macrophage cell line. J Leukocyte Biol 2001.69:43– 9.
19. Hackam DJ et al., Host resistance to intracellular infection: mutation of natural resistance-associated macrophage protein 1(Nramp1) impairs phagosomal acidification. J Exp Med 1998.188:351–64.
20. Barton CH, Whitehead SH, Blackwell JM. Nramp transfection transfers Ity/Lsh/Bcg-related pleiotropic effects on macrophage activation: influence on oxidative burst and nitric oxide pathways. Mol Med 1995.1:267–79.
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241715EnglishN2015August11HealthcarePREDICTION OF SIGNIFICANT HYPERBILIRUBINEMIA IN TERM NEWBORNS USING CORD BLOOD BILIRUBIN
English3639Ram Prasad BanasiaEnglish Hemant JainEnglishAims: The present study was done to assess the usefulness of the cord blood bilirubin estimation as a predictor of subsequent neonatal hyperbilirubinemia in a healthy term infants who require phototherapy.
Setting and Design: A prospective cohort study was conducted at tertiary care centre. 100 term newborn delivered by LSCS was included in this study.
Methods and Materials: 5ml of blood was collected from umbilical cord during delivery. It was used for estimation for conjugated, unconjugated, total serum bilirubin levels and blood group. All enrolled babies were followed up for 5 days and clinically assessed for jaundice according to Kramer dermal scale. In these babies, bilirubin estimation was done on samples collected at birth (cord blood), at 72 hrs. of life (3rd day), at 120 hrs. of life (5th day).
Results: Cord blood bilirubin level of more than 2.15mg/dl has a sensitivity of 65% and specificity of 65% % in prediction of neonatal hyperbilirubinemia. Babies having serum cord bilirubin level of >2.15mg/dl can be followed up in the hospital for 5 days, the time of peak neonatal hyperbilirubinemia to prevent the babies discharged early and later readmission for neonatal hyperbilirubinemia.
Conclusion: It is recommended to have cord blood bilirubin estimation of all healthy term babies delivered in an institution to prevent the dangerous consequences of neonatal hyperbilirubinemia like Kernicterus6
EnglishNeonatal hyperbilirubinemia, Cord blood bilirubinINTRODUCTION
Neonatal Hyperbilirubinemia1 is one of the most common cause for admissions in neonatal unit. Early discharge of healthy term babies from the hospitals is increased due to medical, social and economic reasons. The risk of readmission22 due to jaundice is increasing. The recognition, follow up and early treatment of jaundice has been difficult as a result of early discharges. The American Academy of Pediatrics5 recommends that newborns discharged within 48 hours should have a follow-up visit after 2-3 days to detect significant jaundice and other problems. This recommendation is not possible in our country due to limited follow up facilities in the community. The concept of early prediction of jaundice would facilitate safe and cost- effective targeted intervention and follow-up. The timely detection of neonatal hyperbilirubinemia9-12 and optimal management are crucial to prevent brain damage and subsequent neuromotor retardation due to bilirubin encephalopathy6 . Examination of newborns, cord blood bilirubin level is a non invasive procedure and can increase early detection to prevent severe hyperbilirubinemia.
MATERIAL AND METHOD
A prospective cohort study was conducted in department of pediatrics at tertiary care centre. 100 term newborn delivered by LSCS was included in this study. Newborn with congenital malformation were excluded. Other exclusion criteria include infant born to diabetic mother, neonatal sepsis, Rh incompatibility13 and conjugated jaundice.5ml of blood was collected from umbilical cord during delivery. It was used for estimation for conjugated, unconjugated, total serum bilirubin levels and blood group. All enrolled babies were followed up for 5 days and clinically assessed for jaundice according to Kramer dermal scale2 . In these babies, bilirubin estimation was done on samples collected at birth (cord blood), at 72 hrs. of life (3rd day), at 120 hrs. of life (5th day). Maternal variables like history of jaundice, first trimester bleeding, gestational hypertension, mode of delivery and uses of drugs during pregnancy were collected. Medication during labour, details of delivery, APGAR score and maternal blood group were recorded. Babies were examined daily and looked for evidence of jaundice, sepsis, illness or birth trauma. Weight of the newborn was recorded and gestational age calculated. All the babies were followed up daily for first 5 postnatal days. Serum bilirubin estimation was done within 12 hours of collection of sample by Diazotized sulfanilic test (Jendrassik modified method). The main outcome of the study was inferred in terms of hyperbilirubinemia. Serum bilirubin ≥12.9 mg/dl after 72 hours of life was taken as hyperbilirubinemia needing phototherapy and treatment is advised to all those full term healthy babies as per the American academy of pediatrics practice parameter. So in the present study babies with serum bilirubin level of ≥12.9 mg/dl are considered hyperbilirubinemia. ANALYSIS AND
RESULTS
Statistical analysis- Statistical data were analyzed with the independent sample t test and the descriptive analysis and chi-square tests. Sensitivity, specificity, negative and positive predictive value of the test was calculated. The critical cord bilirubin level having the highest sensitivity and specificity was determined with the Receiver operating characteristics (ROC) curve analysis. Cord serum bilirubin concentration was used for developing ‘prediction test’. The sensitivity and specificity were calculated for predicting hyperbilirubinemia. The present study infers that cord serum bilirubin level of babies with neonatal hyperbilirubinemia (>12.9mg/dl on 5th day) is significantly higher (mean-2.36 mg/dl) than without hyperbilirubinemia (mean-1.91 mg/dl). Out of 100 newborn 23 newborn had significant hyperbilirubinemia on 5th day (mean-15.16 mg/dl). Bilirubin profile of first 5 days of post natal life (table 1) infers that babies with neonatal hyperbilirubinemia has significantly higher bilirubin level compared to babies without hyperbilirubinemia. Cord bilirubin level of >2.15 mg/dl cut off value is chosen based on the receiver operating characteristics (ROC) analysis. In the present study cord serum bilirubin level of >2.15 mg/ dl (table 2) has sensitivity and specificity both 65%, positive predictive value 65% and the negative predictive value of 64% in prediction of neonatal hyperbilirubinemia. So the cord serum bilirubin level of >2.15 mg/dl can be used as an early predictor of neonatal hyperbilirubinemia (p=0.004125). 3rd day bilirubin level of >10.15 mg/dl cut off value is chosen based on the receiver operating characteristics (ROC) analysis. In the present study 3rd day serum bilirubin (table 3) level of >10.15 mg/dl has sensitivity 87%, specificity 80%, positive predictive value 86% and negative predictive value of 81%. So the 3rd day serum bilirubin level of >10.15 mg/dl can also be used as an early predictor of neonatal hyperbilirubinemia (> 12.9mg/dl).
DISCUSSION
In this study, study group is uniformly distributed with 53 male and 47 female babies. There is no significant correlation (p 0.200) in the serum bilirubin levels and the sex of the newborn. Hence the present study infers that the neonatal hyperbilirubinemia (≥ 12.9mg/dl) is independent of the sex of the newborn. In this study, the timing of initiation of breast feeding is significantly (P=0.0183) associated with neonatal hyperbilirubinemia. Early introduction have less chance of hyperbilirubinemia. There is no significant association between the neonatal hyperbilirubinemia and maternal gestational hypertension with p value=0.476. On ROC curve analysis critical cord bilirubin level (≥2.15mg/ dl) with high sensitivity and high specificity is selected. The probability that a neonate with cord bilirubin ≥2.15mg/dl would later become hyperbilirubinemia (positive predictive value) was 65%. The negative predictive value, the probability of non-hyperbilirubinemia given a cord bilirubin lower than 2.15mg/dl was 64%. If a child become hyperbilirubinemic, the probability that the cord bilirubin was ≥2.15mg/ dl was 65% (sensitivity). Given a non-hyperbilirubinemic child, the probability that the cord bilirubin was 2.15mg/dl) and neonatal hyperbilirubinemia (>12.9mg/dl) on 5th day (p = 0.0041)18-21.
In this study, on ROC curve analysis critical 3rd day bilirubin level with high sensitivity and high specificity ≥10.15mg/dl is selected. The probability that a neonate with 3rd day bilirubin higher than ≥10.5mg/dl would later become hyperbilirubinemia (positive predictive value) was 86%. The negative predictive value, the probability of non-hyperbilirubinemia given a 3rd day bilirubin lower than ≥10.15mg/dl was 81%. If a child become hyperbilirubinemic, the probability that the 3rd day bilirubin was ≥10.15mg/dl was 87% (sensitivity). Given a non-hyperbilirubinemic child, the probability that the 3rd day bilirubin was Englishhttp://ijcrr.com/abstract.php?article_id=483http://ijcrr.com/article_html.php?did=4831. MacDonald, Mhairi G.; Seshia, Mary M. K.; Mullett, Martha D. Chapter 35-Jaundice, Physiologic Mechanisms of Neonatal Jaundice, Avery’s Neonatology. 6th Edition. Lippincott Williams and Wilkins; 2005: 773.
2. Kramer LI et al, advancement of dermal icterus in jaundiced newborn. Am J Dis Child 1969; 118: 454-458.
3. Martin CR, Cloherty JP, Eicchenwald EC, Stark AR. Manual of neonatal care: 7th ed: Wolters Kluwer, 2012; 304-339.
4. Niki papavramidou, Elizabeth Fee and Helen ChristopoulouAletra. Jaundice in the Hippocratic Corpus. Springer New York, Journal of Gastrointestinal Surgery 2007; 11(12) : 1728-1731.
5. American Academy of Pediatrics Subcommittee on Hyperbilirubinemia: Management of hyperbilirubinemia in the newborn infant 35 or more weeks of gestation. Pediatrics. 2004; 114: 297- 316
6. Brown AK. Kernicterus past, present and future. Neoreviews. 2003; 4: e33.
7. Bracken H. The Midwives Companion. Book 3, London 1737.
8. Gottlieb R. Bilirubin formation and the reticuloendothelial system, The Kupffer cells and their relation to the reticuloendothelial system. CMAJ 1934 Mar: 256-58.
9. Murchison C. Clinical Lectures on Diseases of the Liver, Jaundice and Abdominal Dropsy. Third Edition. William Wood and Co. New York 1885.
10. Hansen TWR. Pioneers in the Scientific Study of Neonatal Jaundice and kernicterus. Pediatrics. Aug 2000; 106(2):e15
11. Holt LE. Diseases of Infancy and Childhood. First Edition, D Appleton Co. New York 1897.
12. Ottenberg R. The etiology of eclampsia : historical and critical notes. J Amer Med Ass 1923; 81: 295.
13. Diamond LK, Allen FII, Thomas WO. Isoimmunisation Fetalis, VII Treatment with exchange transfusion. N Eng J Med. 1951: 244.
14. Landsteiner K. Wiener AJ. An agglutinable factor in human blood recognized by immune sera for rhesus blood. Proc Soc Exp Biol and Med 1940; 74: 309.
15. Hart AP. Familial icterus gravis of the newborn and its treatment. Canad Med Assn J 1925; 15: 1008.
16. Halbrecht I. Icterus precox: Futher studies on its frequency, etiology, prognosis and the blood chemistry of the cord blood. J Pediatr. 1951 Aug; 39:185-90.
17. Cremer RJ, Perryman PW, Richards DH. Influence of light on hyperbilirubinemia of infants. Lancet. 1958; 1094-97.
18. Amar Taksande, Krishna Vilhekar, Manish Jain, Preeti Zade, Suchita Atkari, Sherin Verkey. Prediction of the development of neonatal hyperbilirubinemia by increased umblical cord blood bilirubin. Ind Medica 2005; 9(1): 5-9.
19. Risenberg HM, Mazzi E, Macdonald MG, Peralta M, Heldrich F. Correlation cord bilirubin levels with hyperbilirubinemia in ABO incompatibility. Arch Dis Child 1977; 57: 219-222.
20. Rosenfeld J. Umbilical cord bilirubin levels as predictor of subsequent hyperbilirubinemia. J Fam Pract 1986; 23: 556-58.
21. Knudsen A. Prediction of the development of neonatal jaundice by increased umbilical cord blood bilirubin. Acta Paediatr Scand 1989; 78: 217-221.
22. Maisels MJ, Kring E Length of stay, Jaundice and hospital readmission. Pediatrics 1998; 101: 995-998.
23. Shally Awasthi and Hasibur Rehman. Early Prediction of Neonatal Hyperbilirubinemia. Indian J Pediatr 1998 ; 65 : 131-139.
24. Bhutani VK, Johnson L, Sivieri EM. Predictive ability of a predischarge hour specific serum bilirubin for subsequent significant hyperbilirubinemia in healthy term and near-term newborns. Pediatrics 1999; 103: 6-14.
25. IAP-NNF Guidelines 2006 on Jaundice in Newborn. 188-209.
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241715EnglishN2015August11HealthcarePREVALENCE OF ANEMIA AMONG RURAL SCHOOL CHILDREN OF RAJASTHAN
English4043Sanjay MandotEnglish Subhash BamnawatEnglishAims: To study the prevalence of anemia among rural school children of Rajasthan.
Study Design: A prospective cross sectional study was conducted in 8 government schools in tribal villages of Sirohi district over a period of 6 months. 1462 school children between 5 to15 years of age were clinically examined. Hemoglobin estimation was done using cynmethemoglobin method and peripheral blood smear were also examined. Anemia was diagnosed according to the WHO standard for the given age and sex.
Materials and Methods: Hemoglobin estimation was done using cynmethemoglobin method. Peripheral blood film was prepared and stained by Leishman’s stain using standard technique. Peripheral smear was examined by Pathologist to know the type of anemia and eosinophilia.
Results: Overall prevalence of anemia was 83.6%. Girls had a higher prevalence of anemia than boys except at 10 years of age. Menarcheal age group girls (11 to15 years) were more anemic than boys and lesser age group girls (EnglishAnemia, Iron deficiency, Peripheral blood smear, Prevalence, School childrenINTRODUCTION
Anemia in children, especially iron deficiency is the commonest and widespread health problem in India with an estimated prevalence of 50%. Nearly one-fifth of the population comprises of the school children. Nutritional disorders in the school children account for the majority of morbidity and school dropout. The children of tribal community due to their low socio-economic status, poor hygiene and poor awareness are more vulnerable to anemia. Iron deficiency along with anemia causes impaired growth, behavioral abnormalities and impaired cognitive function leading to poor school performance. It also adversely affects the immune system of the growing child. The main cause of iron deficiency is inadequate iron intake and low bioavailability of iron in the diet. During adolescence, the overall iron requirement of the body increases and in girls repeated menstrual blood loss also adds to iron deficiency. Intestinal parasitic infections are widely prevalent in many developing countries including India. These parasitic infections especially hookworms are particularly important in the school children as they aggravate malnutrition including iron deficiency. Numerous studies have shown prevalence of anemia between 22-94% as the methodology and criteria for diagnosing anemia has been variable (1-6).
MATERIALS AND METHODS
The study was conducted on 1462 children aged 5-15 years of government schools in villages namely Ker, Issara, Daanava, Kacholi, Delwara, Torna, Phula Bai Kheda and Panchdeval of Sirohi district. Children in selected schools were from low socioeconomic status and majority of them were scheduled tribes. A detailed proforma which included data regarding socioeconomic status, medical history and consent was given to school children to be completed by parents/guardians. A detailed medical examination including anthropometry was done by medical officer and recorded on the proforma. For hemoglobin estimation and peripheral smear examination blood was drawn by finger prick using 26G needle. Hemoglobin estimation was done using cynmethemoglobin method. Peripheral smear was examined by Pathologist to know the type of anemia and eosinophilia. Anemia was diagnosed and the children were grouped under different grades of anemia by adopting WHO guidelines (7). Analysis of the results was done using the statistical method – chi square test and p value.
RESULTS
Out of 1462 school children studied only 239 (16.4%) were normal and 1223 (83.6%) were affected with various grades of anemia i.e. 664 (56.1%) mildly anemic, 525 (42.9%) moderately anemic and 11 (0.89%) severely anemic. The mean hemoglobin, number and percentage prevalence of anemia according to age in both sexes is shown in Table I. Girls had high prevalence of anemia (87%) compared to boys (81.5%) [Chi-square test value: 7.5 (df =1); p value ≤ 0.05, significant] at all ages except at 10 years age (Fig. I). A higher proportion (89.7%) of menarcheal girls (11-15 years age) had anemia. Moderate degree of anemia was more common in girls (45.4%) than boys. The commonest blood picture was microcytic hypochromic seen in 56.4% followed by normocytic normochromic and dimorphic in only 0.5%. Eosinophilia (>6%) on peripheral smear was observed in 21.6% school children.
DISCUSSION
The present study shows a high prevalence of anemia among school children of lower socio-economic status from tribal/ rural background .Occurrence of anemia in children from poor socio-economic status is a well fact and many studies have reported high prevalence of anemia among rural/tribal school children (8-11). It is apparent from Table I that out of 1462 children studied, only 16.3% were normal and 83.6% were affected from various grades of anemia. Iron deficiency is common in healthy, non anemic and high socio-economic status children also as reported by Thavraj et al3 . These children may have latent iron deficiency and possible reason for this could be the poor bio-availability of iron in the Indian diets. Male to female ratio was 1.6:1 which suggests that the lesser number of girls are enrolled in schools for education. Reasons could be due to gender bias as males are given better care over females. The girls had a higher prevalence of anemia except at 10 years of age. More menarcheal age group girls were anemic as compared to others because of increased iron requirement during adolescence and repeated menstrual blood loss .Various studies have also observed a high prevalence of iron deficiency anemia among adolescent girls of urban and rural areas (12-14). Predominantly Microcytic hypochromic (55.4%) blood picture was also reported in a study by Verma. M et al. on urban school children of Punjab (15). Eosinophilia was observed in 21.6% school children. This could be due to intestinal helmenthiasis especially hookworm infestation. Other common causes of eosinophilia like allergy and drug intake could not be applied to these school children at the same time. Filariasis is also commonly associated with eosinophilia but it is rare in this part of the country.
CONCLUSION
The present study shows that anemia is a major health problem among rural school children belonging to poor socioeconomic status. Dietary modification, routine iron supplementation, improvement in hygiene and awareness are the key strategies recommended for prevention.
Conflict of Interest: None.
Source of funding: By Investigator
Ethical Clearance: Obtained
ACKNOWLEDGEMENT
We acknowledge the immense help received from the scholars whose articles are cited and included in references of this manuscript. We are also grateful to authors / editors / publishers of all those articles, journals and books from where the literature for this article has been reviewed and discussed.
Englishhttp://ijcrr.com/abstract.php?article_id=484http://ijcrr.com/article_html.php?did=4841. Sundaram VM, Sankaranaraynan VS, Rajendran S, Varalakshmi, Sarasa. Health profile of school children in Madras City. Indian Pediatr 1978; 15: 586-725.
2. Gopaldas T, Kale M. Prophylactic Iron supplementation for underprivileged school boys. Indian Pediatr 1985; 22: 731- 743.
3. Thavraj VK, Reddy V. Serum Ferritin in healthy school children. Indian Pediatr 1985; 22: 51-57.
4. Goyal RC, Chavan VA. Health status of school children in Ahmednagar City. Indian J Maternal and Child Health 1993; 4: 81-83.
5. Aggarwal KN, Khanduja PC, Aggarwal PK, Madhavan S, Tarkar AD. Normal hematological levels for school children (5- 16 years). Indian Pediatr 1972; 9: 785- 795.
6. Malhotra AK, Srivastava RN. A study on impact of socio-economic status on hemoglobin levels of rural school children of district Wardha. Indian J Prev Soc Med 1982; 13: 95-99.
7. WHO. Indicators for assessing iron deficiency and strategies for its prevention. WHO/UNICEF/UNU 1998 Technical workshop. Geneva, World Health Organization 1998.
8. Gupta VM, Shukla KK. Epidemiology of anemia in preschool children from a rural and a slum community, Varanasi. Indian J Prev Soc Med 1985; 15: 85-89.
9. Aggarwal DK, Bhardwaj B, Singla PN, Tripathi AM, Aggarwal KN. Etiology of maternal and early childhood deficiency anemia. Indian J Pediatr 1986; 53: 389-396.
10. Sharma A, Sharma SK, Grover AK, Tewari AD, Abrol P. Anemia in protein energy malnutrition. Indian Pediatr 1985; 22: 841- 843.
11. Desai N, Chaudhry VP. Nutritional anemia in protein energy malnutrition. Indian Pediatr 1993; 30: 1471-1483.
12. Vasanthi G, Pawashe AB, Susie H, Sujatha T, Raman L. Iron nutritional status of adolescent girls from rural area and urban slum. Indian Pediatr 1994; 31: 127- 132.
13. Kapoor G, Aneja S. Nutritional disorders in adolescent girls. Indian Pediatr 1992; 29: 969-973. 1
4. Aggarwal K.N. Assessment of prevalence of anemia and iron in response to daily/weekly iron folate supplement in adolescent girls (10-18) from urban slums of North Delhi. UNICEF Contract No. 95/0075/1998, 1-9(1998).
15. M. Verma, J. Chhatwal and Gurmeet Kaur . Prevalence of anemia among urban school children of Punjab. Indian Pediatr 1999; 36: 1181-1186.
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241715EnglishN2015August11HealthcareCOMPARISION OF TRANSCUTANEOUS ELECTRICAL NERVE STIMULATION AND KATI BASTI FOR PATIENTS WITH SCIATICA
English4448Sabnam HashmiEnglish Abdul Rahim ShaikEnglish Padma Kumar Somasekharan PillaiEnglishStudy Design: Experimental study.
Background: The majority of the people experience low back pain at some point in their life. World data reveals 40 % or more people have sciatica due to lumbar disc prolapse mostly in younger adults in association with 50-70% lifetime incidence of low back pain.
Objective: To compare the effectiveness of Transcutaneous Electrical Nerve Stimulation and Kati Basti in reducing the Sciatica.
Method: Fifty Eight patients with chronic pain were recruited for the study. Investigator explained the study to the patients and obtained an informed consent form and they were divided into two groups such as group A (Transcutaneous Electrical Nerve Stimulation) and group B (Kati Basti).Twenty nine patients were given Transcutaneous Electrical Nerve Stimulation and 29 patients were given Kati Basti for two weeks. Outcome measures were assessed before and after the treatment in both groups.
To measure the angle of movement and intensity of pain Straight Leg Raise Test and Visual Analogue Scale were administered respectively before and after the treatment for both groups.
Results: The study shows that after two weeks of intervention, there was a significant reduction of pain and improvements in Straight Leg Raise Test in both the groups from baseline. Thus, both interventions were found to be effective in reducing pain for patients with sciatica. However, Transcutaneous Electrical Nerve Stimulation was more effective than Kati Basti in relieving the pain.
Conclusion: Both the interventions, Transcutaneous Electrical Nerve Stimulation and Kati Basti, were effective in improving Straight Leg Raise Test and reducing the pain. However, patients in Transcutaneous Electrical Nerve Stimulation have improved more in terms of reduction of pain than in patients who were treated with Kati Basti after two weeks of treatment.
EnglishStraight leg raising test, Transcutaneous electrical nerve stimulation, Kati basti intensity of pain, SciaticaINTRODUCTION
World data reveals 40 % or more people have sciatica due to lumbar disc prolapse mostly in younger adults in association with 50-70% lifetime incidence of low back pain. Sciatica involves compression of the sciatic nerve roots caused by a herniated (torn) or protruding disc in the lower back that causes radiating pain in the distribution along the course of sciatic nerve in the hip, thigh lower leg and reaches up to the foot. The prevalence of sciatic symptoms reported in the literature varies considerably ranging from 1.6% in the general population to 43% in a selected working population1, 2. There are number of treatment options available for sciatica. However, Transcutaneous Electrical Nerve Stimulation (TENS) is a simple, non-invasive analgesic technique that is used extensively in health-care settings by physiotherapists for sciatica3 . The use of conventional (high-frequency) Transcutaneous Electrical Nerve Stimulation is originally based on the gate-control theory of pain, which suggested that counter stimulation of the nervous system could modify the perception of pain. Later studies suggested that with lowfrequency, high-amplitude (acupuncture-like) stimulation, TENS could also raise endorphin levels in the spinal fluid4,5. Kati Basti is one of the treatments of Keraliya Panchakarma for Gridrashi (sciatica) in ayurveda. The word Kati Basti is formed by combining two letters ‘Kati’ and ‘Basti and it is the procedure in which Dough-well is formed bywarm medicated oil which is placed on Kati (lumbo-sacral region) for a specified period of time (40 to 45 minutes) while the patient is lying prone position6,7. A study conducted by Khagram RV (2004) showed that the patients treated with Kati Basti had relief in the symptoms of pain and Straight Leg Raising Test8 . Transcutaneous Electrical Nerve Stimulation was significantly effective in decreasing the pain9 . In order to find the outcome measures, Visual Analogue Scale (VAS) scores and Straight Leg Raise Test (SLRT) were used. The Visual Analogue scale(VAS) is a simple and frequently used method for the assessment of variations in intensity of pain. The Straight Leg Raising Test (SLRT) is a useful measure because immediate effects of treatment can be determined. However, studies have been conducted using Kati Basti and other modalities in physiotherapy to find out the effectiveness in reduction of pain in sciatica, but studies on effectiveness of Kati Basti and TENS in sciatica have not been conducted in this region. Hence, the current study was undertaken to find the effectiveness between TENS and Kati Basti in reducing pain in sciatica patients caused by herniated or protruding disc.
MATERIALS AND METHODS
The present study is an experimental study conducted in 60 Sciatica patients of age group ranging from 18 to 50 years. The inclusion criteria were patients with Sciatica more than six weeks, and SLRT positive between 30º to 70º. Patients with the history of piriformis syndrome, spinal stenosis, spondylolisthesis, tuberculoma causing cord compression, diabetic neuropathy, and contraindicated for TENS and Kati basti were excluded. Participants were divided into two groups such as group A and B. The sciatica patients admitted in Yenepoya Medical College Hospital and Shaffi Ayurvedic Nursing Home constituted the population of the study.
PROCEDURE
The approval from the University ethical committee was obtained prior to the commencement of the study. Total of 75 patients with history of chronic lumbar radiculopathy were screened those who are admitted in Yenepoya Medical college Hospital and Shaffi Ayurvedic Nursing Home Mangalore. Out of 75 patients 15 patients were not met the inclusion criteria, hence a total of 60 patients were included as participants for the study. The patients were assigned into two groups by a convenience sampling method. Each group consisted of 30 patients. Group A - Patients admitted in Yenepoya Medical Hospital and given treatment Transcutaneous Electrical Nerve Stimulation for 2 weeks. Group B - Patients admitted in Shaffi Ayurvedic Nursing Home taking treatment Kati Basti for 2 weeks. However, one patient from Group A did not participate in this study due to severe pain and undergone surgery and one patient from Group B due to hypersensitivity of heat. Hence, a total 29 patients in each group have undergone a procedure. Patients were explained about the study in their local language and informed consent was taken from each patient. Patients in the Group A, received TENS with frequency of 2Hz pulse duration of 0.2 ms and intensity was given until getting visible muscle contractions for 20 minutes daily for two weeks by the same researcher. Electrodes were placed and secured with Velcro straps on the affected leg as well as back in the course of Sciatic nerve. Patients in Group B received Kati Basti treatment by the Ayurvedic physician, in the presence of researcher, in which warm medicated oil was applied to the lumbo-sacral region daily for 45 minutes for two weeks. After administration of two weeks of treatment, outcome measures of Group A, was assessed by another Physiotherapist in the presence of researcher, whereas Ayurvedic physician in the presence of the researcher assessed Group B.
OUTCOME MEASURES
Straight Leg Raising Test was administered prior to the treatment by using goniometer to find the angle of movement. To measure the angle of SLRT, patients were asked to lie down on his or her back on an examination table. The examiner lifts the patient’s leg passively while the knee is straight until patient experiences pain in course of sciatic nerve and the angle was measured by goniometer. Intensity of Pain was measured by Visual Analogue Scale.
DATA ANALYSIS
The Data was analyzed by using SPSS version 17 software. Demographics were done by using Unpaired t test(age and duration), Fishers exact test(Gender) and between the two groups Paired t test was used. P value less than or equal to 0.05 was considered to be significant.
RESULTS
Baseline characteristics of the 58 patients in two treatment groups are presented in following Tables. The two groups were considered comparable for all measured baseline characteristics.
DISCUSSION The Study was conducted to compare the effectiveness of Transcutaneous Electrical Nerve Stimulation (TENS) and Kati Basti in 58 Sciatica patients (29 in each group) by means of Visual Analogue Scale(VAS) and Straight Leg Raise Test(SLRT). Physiotherapy and Ayurveda modality are most commonly used as conservative treatments in India for Sciatica patients. Result of the study shows that the degree of SLRT was improved in both right and left lower extremity in TENS group (p< 0.001) and Kati Basti group (p< 0.001). A study by Melzack R et al revealed that SLRT for left and right leg after TENS treatment was improved (pEnglishhttp://ijcrr.com/abstract.php?article_id=485http://ijcrr.com/article_html.php?did=4851. Conditions of the Spine. Lumbar Radiculopathy. [Updated 2010; Cited 2012 Dec 3]. Available from http://www.njpcc.com/conditions-of-the-spine/lumbar-radiculopathy-sciatica.html.
2. Konstantinou K, Dunn KM. Sciatica: review of epidemiological studies and prevalence estimates. Spine. 2008; 33: 2464–2472.
3. Pope G, Mockett S, Wright, J. A survey of electotherapeutic modalities: ownership and use in the NHS in England physiotherapy. 1995; 8:82-91.
4. Sjolound BH, Eriksson MBE. Endorphin and analgesia produce by peripheral conditioning stimulation. Adv Pain Res Ther. 1979; 3:587-90.
5. Melzack R, Wall PD. Pain mechanisms: a new theory. Science. 1965; 150:971–9. 6. Shridhr BS. Managemnt of Gridhrasi w.s.r. to Basti- G.C.I.M. Mysore; 1991.
7. Bharati, Kumar A, Bhikshapati T. Kati Basti - A Clinical Study. AYU. 2008; 29(1): 42-45.
8. Khagram RV. A comparative study of Kati basti and Matra bati in management of sciatica. Gau jam. 2004.
9. Ghoname EA, White PF, Ahmed HE, Hamza MA, Craig WF, Noe CE. Percutaneous electrical nerve stimulation: an alternative to TENS in the management of sciatica. Pain. 1999; 83(2):193-9.
10. Melzack R, Vetere P, Finch L. Transcutaneous electrical nerve stimulation for low back pain: A comparison of TENS and massage for pain and range of motion. Phys Ther. 1983;63(4):489- 93.
11. Hughes GS Jr, Lichstein PR, Whitlock D, Harker C. Response of plasma beta-endorphins to transcutaneous electrical nerve stimulation in healthy subjects. Phys Ther.1984;64(7):1062-6.
12. Han JS, Chen XH, Sun SL, Xu XJ, Yuan Y, Yan SC et al.Effect of low- and high-frequency TENS on Met-enkephalin-Arg-Phe and dynorphin A immunoreactivity in human lumbar CSF. Pain. 1991 Dec;47(3):295-8.
13. Salar G, Job I, Mingrino S, Bosio A, Trabucchi M. Effect of transcutaneous electrotherapy on CSF beta-endorphin content in patients without pain problems. Pain. 1981;10(2):169-72.
14. Sudesh G, Muralidhara S, Bhawana G. Effect of Matra Basti and Katibasti in the Management of Lumbar Disc Disease. IJPBA. 2012; 3(5):1271-1277.
15. Peter F. J, Harvey E J, Arcaro N, Kaczorowski J. Transcutaneous Electrical Nerve Stimulation for Short-Term Treatment of Low Back Pain–Randomized Double Blind Crossover Study of Sham versus Conventional TENS, Journal of Musculoskeletal Pain.2005;13( 2) :11-17.
16. Padmakiran C, Ramachandra R, Prasad U. N, Rao N. Role of Kati Basti in gridhrasi (lumbago sciatica syndrome) .IAMJ.2013;1(4):1-5.
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241715EnglishN2015August11HealthcareANATOMIC VARIATIONS OF PARANASAL SINUSES IN PATIENTS WITH CHRONIC SINUSITIS AND THEIR CORRELATION, WITH CT SCAN STUDY
English4955Kate Sarika P.English Mandke N. D. English Bahetee B. H.EnglishThe study of anatomic variation of paranasal sinuses is important to understand the pathophysiology of chronic sinusitis. The rate of anatomic variations in chronic sinusitis varies according to different studies but the data in Indian population is lacking. The purpose of this study is to assess the frequency of anatomic variations in chronic sinusitis in the subset of Indian patients presented to Medical Colleges and hospitals from 2011 to 2013. A total of 90 patients were included. We found concha bullosa
in 23% patients with higher incidence in inferior turbinate, nasal septal deviation in 65% patients with higher incidence on right side. 85% patients suffered from maxillary sinusitis. Haller cell was found only in 1 patient while Onodi and Agger nasi cells were not seen in any patient. To conclude, in view of the presence of these significant variations, we reemphasize the need for proper preoperative assessment in every patient in order to accomplish a safe and effective endoscopic sinus surgery. The present
study is a step to provide suggestive findings to surgeons regarding various parameters involved and our contribution to the enormous work of other research workers.
EnglishParanasal sinuses, Chronic sinusitis, Computed tomographic (CT) scanINTRODUCTION
Complications are always a proven risk in any surgery, but location of few structures or relations make things still worst in the human body. This is well implicated to the location of ethmoids which is so complex and has always been an area of challenge to the operating surgeon. This very fact interested me to explore the anatomy and its variations in the region of paranasal sinuses through my proposed present study. Drainage and ventilation of paranasal sinuses are important for the normal function which in turn depends on effective mucociliary clearance. (1) Drainage of secretions in paranasal sinuses follows definite course.(2) The frontal and maxillary sinuses communicates with middle meatus through prechambers. Mucosa of prechambers are closely opposed and clearance of is through ciliary action. These narrow prechambers are blocked by mucosal inflammation which affects ciliary clearance. It establishes a vicious cycle of infection and stasis causing chronic sinusitis.(2) The key region for these changes is that part of the lateral nasal wall that encloses the sinus ostia and their adjacent mucosa and prechambers. There is considerable anatomical variation in this area that may interfere with normal nasal function and predispose to recurrent or chronic sinusitis(3) Functional endoscopic sinus surgery restores normalcy by working on the key regions rather than on the larger sinuses. Good knowledge of anatomy is required for effective surgery. This is most true during endoscopic sinus surgery because of the intimate association with such vital structures as the orbit, optic nerve, anterior and posterior ethmoidal vessels, skull base and internal carotid artery. Anatomical variations in paranasal sinuses is more common in patients with chronic sinusitis which may be due to improper drainage. CT scan is standard imaging for detecting diseased paranasal sinuses along with their anatomical variations.(4)
AIMS AND OBJECTIVES
The complex anatomy of paranasal sinuses was explored by many researchers. The present study is an effort to contribute to their works. Our study is proposed to -
1. Evaluate the anatomical variations of paranasal sinuses by CT scan in chronic sinusitis patients
2. Study the proportion of anatomical variations of paranasal sinuses in patients with chronic sinusitis.
MATERIAL AND METHODS
The study was conducted at Medical colleges and Hospitals in Pune. We included patients who were referred for CT scan of PNS during a period of 18 months from December 2011 to May 2013. Unenhanced CT of the PNS was performed for 90 patients in the coronal plane, complemented by axial views. The investigations were performed by using SIEMENS SOMATOM SPIRIT single slice spiral CT machine. For coronal studies, patients were put in prone position. Taking the hard palate as reference axis, the plane of section was perpendicular to this structure. Direct scans 3 mm in thickness were made, from the anterior walls of the frontal sinuses to the posterior wall of the sphenoid sinus. For the axial scans, which were 5 mm thick, the orbitomeatal line was taken as reference with the patient in supine position. The exposure settings used were 130 kVp and 80 to 100 mAs. In all cases, systematic studies of the nasal sinus region were performed in coronal complemented by axial views in selected cases. Analysis of anatomical variants was performed both using a soft parts window and a bone density window
INCLUSION CRITERIA
Adult patients presenting with history of nasal obstruction, headache and who are subjected to radiological investigations after a clinical examination and diagnosis as chronic sinusitis were included in the study.
EXCLUSION CRITERIA
1. Paediatric age group( 0-15 years)
2. Patients with history of road traffic accidents of head, neck and face, sinonasal malignancy or past history of surgery in the paranasal region were not included in this study.
PARAMETERS RECORDED
The scans procured from various hospitals were then saved and evaluated for following structures and anatomical variations.
1. Turbinates: superior concha bullosa, middle concha bullosa, inferior concha bullosa
2. Nasal septum: septal deviation.
3. Sinus involved: Frontal ,maxillary, Anterior ethmoid, Middle ethmoid and Posterior ethmoid, Sphenoid.
4. Ethmoid air cells: Agger nasi cells, Haller’s cells, Onodi cells (extramural sphenoid cells).
STATISTICAL METHODS
Percentage is taken into consideration in sex distribution, the presence of concha bullosa, incidence of deviated nasal septum, distribution of sinusitis, correlation of anatomic variants with mucosal changes.
RESULTS
1. Patients included in our study ranges between16 -76 years old. More patients lie in 21 to 30 years of age.
2. Out of 90 patients ,males were 52 (57.77%) while females were 38 (42.23%). So the present study has limitation of sex wise co-relation.
3. Out of 90 patients evaluated, averagely 23% patients show concha bullosa. Higher incidence is seen in Inferior turbinate (41%) while Superior turbinate was least involved.
4. Out of 90 patients evaluated, right sided nasal deviation was seen in 33 (36%) patients. No deviation seen in 32 (35.52%) patients.
5. Out of 90 patients evaluated, the highest incidence of sinusitis was seen in maxillary sinus which was 85%(77 patients) while middle ethmoid 2%(2 patients) was least involved.
6. Anatomical variations were seen in 73(81.11%) patients out of which 67(74.44%) had mucosal changes. While Anatomical variations were absent in 17(18.84%) patients but they still suffered from chronic sinusitis.
7. Onodi cells and Agger nasi cells were not found in any patient.
8. Pansinusitis is present in 5 patients out of 90
9. Haller cell found only in1 patient out of 90.
DISCUSSION
In a study done in 90 subjects, paranasal region shows high percentage of anatomical variability, the variations most often observed were, in order, deviation of the nasal septum, the presence of a concha bullosa.
In our study patients age ranged from 16 to 76 years which was consistent with study done by Gliklich RE.
More patients lie in age group between 21 to 30 years.
Concha bullosa (pneumatised turbinate) has been implicated as a possible aetiological factor in the causation of recurrent chronic sinusitis. It is due to its negative influence on PNS ventilation and mucociliary clearance in the middle meatus region. The presence of a concha bullosa has ranged between 4% and 80% in different studies; our data gave 71% which is more compared to Bolger(53.6%) ,Zinreich S et al (36%) and Dua K (16%) and Peres et al (24.5%). Such a wide range of incidence is due to the criteria of pneumatization adopted(1,5,11). 3)
DEVIATED NASAL SEPTUM –
In our study deviated nasal septum seen in 58 patients( 64.44%) which is somewhat consistent with Peres Pinas et al while incidence seen by Dua K et al and Zinreich et al lies on lower side. Finding of Bolger et al lies on higher side.
Various studies have reported the incidence of sinusitis in paranasal sinuses. In our study maxillary sinus was involved in 85 %, anterior ethmoids in 51%, sphenoid sinus in 25.55%, posterior ethmoids in 16.66 % and frontal sinus in 33.33% patients. The extent of involvement reported by other authors was also in the same range. Zinreich published maxillary sinus involvement in 65%, posterior ethmoids in 40%, frontal in 34%and sphenoid sinus involvement in 29%(9).Bolger reported maxillary sinus involvement in 77.7%, posterior ethmoids in 38.6%, frontal sinus in 36.6% and sphenoid sinus in 25.4%(5).
Pansinusitis was seen in 5.55 %.
Haller’s cells are ethmoid air cells that project beyond the limits of the ethmoid labyrinth into the maxillary sinus. They are considered as ethmoid cells that grow into the floor of orbit and may narrow the adjacent ostium. The Haller’s cells in our study was seen in 1 patient (1.11%).It is less than that reported by Kennedy and Zinreich (10%) ,Bolger(45.9%) and Asruddin (28%)(5, 11, 12). The clinical significance of anatomical variants of the nasal sinus region is controversial. Most CT anatomical studies of the sinus region have been made in patients suspected of a clinical syndrome suggesting inflammatory sinus pathology.
Zinreich found that 62% of his patients presented at least one anatomic variant, against 11% in the normal control group(5). These findings seem to suggest a positive correlation between anatomical variants and the appearance of inflammatory sinus pathology. However, Bolger et al., in a series of 202 patients studied by CT, observed 131 anatomical variants, but found the incidence in patients with sinus pathology was similar to that in persons studied for other reasons(7). Bolger et al. and Stammberger and Wolf detected the presence of anatomical variants both in patients studied for sinus problems and in those studied for other reasons(8,6). They concluded that the simple presence of variants does not mean a predisposition to sinus pathology, except when other associated factors are present. This opinion is not shared by Yousem, who claimed that the anatomical variants may be predisposing factors, depending on their size (9). Anatomical variation were seen in 73(81.11%) patients out of which 67(74.44%) had mucosal changes.17(18.84%) patients showed absence of Anatomical variations but still suffered from chronic sinusitis. This suggests that patients may have mucosal changes without the presence of Anatomic variations. From this observation our study also reveals that the presence of anatomical variants does not mean a predisposition to sinus pathology. However, it is important for surgeon to be aware of variations that may predispose patients to increased risk of intraoperative complications. The radiologist must pay close attention to anatomical variants in the preoperative evaluation and help avoid possible complications and improve success of management strategies.
CONCLUSION
Computed Tomography of the paranasal sinus has improved the visualization of paranasal sinus anatomy and has allowed greater accuracy in evaluating paranasal sinus disease. It evaluates the osteomeatal complex anatomy which is not possible with plain radiographs. Improvement in Functional Endoscopic Sinus Surgery and CT technology has concurrently increased interest in the paranasal region anatomy and its variations. The present study has it’s own limitations of having less sample size and it is suggested to increase sample size to give significant contribution for clinical implications. Clinical studies shown that prevalence of concha bullosa in general population is more but very few subjects are symptomatic. To conclude, In view of the presence of these significant variations, we reemphasize the need for proper preoperative assessment in every patient in order to accomplish a safe and effective endoscopic sinus surgery. The present study is a step to provide suggestive findings to surgeons regarding various parameters involved and our contribution to the enormous work of other research workers.
ACKNOWLEDGEMENT
Authors acknowledge the immense help received from the scholars whose articles are cited and included in references of this manuscript. The authors are also grateful to authors/ editors/publishers of all those articles, journals and books from where the literature for this article has been reviewed and discussed.
Englishhttp://ijcrr.com/abstract.php?article_id=486http://ijcrr.com/article_html.php?did=4861. Perez-Pinas I, Sabate J, Carmona A, Catalina H C J, Jimenez C J. Anatomical variations in the human paranasal sinus region studied by CT. Journal of Anatomy 2000;197(2):221–227.
2. Kopp W, Stammberger H, Fotter R. Special radiologic image of the paranasal sinuses. European Journal of Radiology 1998;8:152-156.
3. Blaugrund SM. Nasal septum and concha bullosa. Otolaryngol Clinics of North America 1989;22:291-306.
4. Clerico DM. Pneumatized superior turbinate as a cause of referred migraine headache. Laryngoscope 1996;106:874-879.
5. Zinreich S. Imaging of inflammatory sinus disease. Otolaryngol Clin North Am 1993;26:535-547.
6. Stammberger H, Wolf G. Headaches and sinus disease: the endoscopic approach. annals of otology, rhinology and laryngology 1988;97:3-23.
7. Bolger W E, Butzin C A and Parsons D S, Paranasal sinus bony anatomic variations and mucosal abnormalities: CT analysis for endoscopic sinus surgery. Laryngoscope 1991;101:56–64.
8. Bolger W E, Woodruff W and Parsons D S, CT demonstration of pneumatization of the uncinate process. Am. J. Neuroradiol 1990;11:552.
9. Yousem D. Imaging of sinonasal inflammatory disease. Radiology. 1993;188:303-314.
10. Zinreich J, Mattox DE, kennedy DW, Chisholm HI, Diffey DM, Rosenbaum AE. Concha bullosa: CT evaluation. Journal of computer assisted tomography 1988;12:778-784.
11. Dua K, Chopra H, Khurana AS, Munjal M. CT Scan variations in Chronic Sinusitis. Ind J Radiol Imag 2005;15:315-320.
12. Asruddin, Yadav SPS, Yadav RK, Singh J. Low dose CT in chronic sinusitis. Indian Journal of Otolaryngology and Head Neck Surgery 2000; 52: 17-21.
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241715EnglishN-0001November30HealthcareANALYSIS OF FACTORS ASSOCIATED WITH PERITONITIS IN HOLLOW VISCUS PERFORATION
English5661Atif Abdullah C.English Ganesh Babu C.P.English Raghuram K.English Tirou Aroul T.EnglishBackground: Peritonitis due to hollow viscus perforation is one of the causes of acute abdomen warranting emergency laparotomy.
The causes for gastro-intestinal perforation vary between the western countries and Asian countries like India. Though
there are many studies in this regard, very limited studies are available pertaining to southern parts of India. Therefore this study
was carried out to assess the common cause, factors associated and patient outcome in peritonitis due to gastro-intestinal perforation.
Methods: This study was conducted in tertiary care hospital, Pondicherry between July 2012 and July 2014. Fifty five patients who underwent exploratory laparotomy for gastro-intestinal perforation were included in the study and assessed. Appropriate surgeries were performed for the site and cause of the perforation. Patient’s history, clinical examination findings, investigations, intra-operative findings, operative procedure and post-operative complications were recorded and assessed.
Results: In this study, 21.8% patients were in the age group of 51-60 years. Male to female ratio was found to be 6.8:1. The most common symptom was abdominal pain which was present in all the patients. Among patients with peptic ulcer perforation, 73.3% of the patients were smokers and 42.4% of the patients gave history of NSAID intake. Peptic ulcer perforation was found in 60% of the patients. Post-operative complications occurred in 34.5% of the patients. Mortality rate was 7.3% in this study.
Conclusion: Even in the Era of good drugs Peptic ulcer perforation was the commonest cause for perforation. Peptic ulcer perforation was significantly associated with smoking in this study. Alcohol consumption, prior NSAID abuse didn’t significantly affect the outcome of the patients.
EnglishPerforation, Factors associated, PeritonitisINTRODUCTION
Peritonitis due hollow viscus perforation is one of the commonest emergencies faced by general surgeons. Perforation causes exposure of the peritoneum to the gastro-intestinal contents which results in peritonitis. Gastro-intestinal perforation can occur due to various causes but common causes in India is Duodenal ulcer perforation, Typhoid ileal perforation, Perforation due to trauma, Perforation due to malignancy, etc. in the order of frequency1 . However the scenario is different in western countries were distal perforations are more common2 . Emergency surgical intervention is required in most of the patients except few, in whom perforation is contained. Various studies have been conducted to analyze the factors associated with hollow viscus perforation and their outcome. Rajender Singh Jhobta et al in their study concluded that majority of perforation peritonitis in India involve Upper Gastro-Intestinal tract3 . Similar study conducted in Pakistan by Afridi et al found that duodenal ulcer perforation was the commonest cause of perforation followed by Tuberculous perforation of small bowel in their locality4 . Bali et al in their study conducted in Delhi found that 15% of patients gave history for NSAID intake5 . Common cause of peritonitis in their study was peptic ulcer perforation followed by appendicular perforation. Appendicular perforation usually causes localized peritonitis in contrast to perforation at any other site of gastro-intestinal tract. For this reason appendicular perforation was not included in our study. Though there are various studies focused on factors associated with hollow viscus perforation in India, studies pertaining to southern parts of India is limited. Factors contributing to perforation peritonitis in South India can be different from that of North India because of different culture, food habits, health care facilities and awareness. Chatterjee et al conducted a study on ileal perforations in Pondicherry6 , but this study didn’t analyze perforation in other parts of gastro-intestinal tract and this study didn’t include ileal perforation due to typhoid. Hence in order to analyze the factor associated with perforation peritonitis in this part of the world, this study was carried out with the principal aim of calculating the incidence of different types of perforation, assessing the various factors associated with hollow viscus perforation and recording the morbidity and mortality of patients with different types of perforation.
METHODOLOGY
This was a Prospective observational study, which was conducted at the tertiary care hospital, Pondicherry over Two year period. From July 2012 until July 2014 we enrolled patients who were diagnosed with peritonitis due to hollow viscus perforation and underwent Exploratory laparotomy. We excluded all patients who were managed conservatively without exploratory laparotomy. Fifty five patients, who had fulfilled the inclusion criteria, were studied. Preoperative detailed history was noted. Thorough examinations were done to arrive at a preoperative diagnosis. After admission, patients were investigated and resuscitated. Patients were taken for exploratory laparotomy. Intra-operative findings were noted and depending on the type of perforation appropriate surgery was performed. Perforated duodenal ulcers were repaired by simple closure with an Omental Onlay reinforcement or patch. Primary closure, bowel resection and end to end anastomosis or entero-cutaneous stoma was done for perforation due to trauma, perforation due to typhoid etc. Post-operatively patients were followed up for 30 days and complications like surgical site infection, wound dehiscence, anastomotic leak and death were watched evaluated.
RESULTS
This study included fifty five patients. The aim was to calculate the incidence of different types of perforation, assess the various factors associated with hollow viscus perforation and record the morbidity and mortality of different types of perforation. In this study most of the patients with gastrointestinal perforation were in the age group of 51-60 years (21.8%) followed by age group of 41-50 years (20%).(Fig1) The youngest patient in this study was 14 years, who had ileal perforation and the oldest patient was 80 years, who had duodenal ulcer perforation. Perforation peritonitis was found in 48 (87.3%) males and 7 (12.7%) females, in this study. The most common symptom was abdominal pain, which was present in all the patients. Vomiting was second most common symptom and was present in 29 patients (52.7%). Fever was present in 14 patients (25.5%) and was the third most common symptom. Eight patients (14.5%) complained of abdominal distension. Constipation was present in 6 patients (10.9%) and 2 patients (3.6%) had history of malena. Pneumo-peritoneum in chest X-ray of the patients studied was present in 41 (74.5%) patients. Five patients who had enteric perforation of the ileum didn’t have pneumo-peritoneum in the chest X-ray. Four patients who had peptic ulcer perforation of the duodenum and one patient who had peptic ulcer perforation of the stomach didn’t show pneumo-peritoneum. Two patients who had gastrointestinal perforation due blunt trauma abdomen didn’t show pneumo-peritoneum. Out of two patients, one had sigmoid perforation and the other had ileal perforation. One patient who had colonic carcinoma with perforation peritonitis didn’t show pneumo-peritoneum in X-ray. Those patients who didn’t have pneumo-peritoneum in chest X-ray underwent exploratory laparotomy as they had clinical signs strongly suspicious of peritonitis requiring laparotomy. Peptic ulcer disease was the commonest etiology for perforation. It was found in 33 patients (60%). Duodenal ulcer perforation was found in 24 patients and eight patients had gastric ulcer perforation. One patient had stomal ulcer perforation, who had previously undergone truncalvagotomy and gastrojejunostomy (TVGJ). Blunt trauma to abdomen was the cause for gastrointestinal perforation in eight patients (14.5%). Three of the perforation due to blunt trauma to abdomen was in ileum, three were in jejunum, one was in stomach and one was in sigmoid colon. Typhoid enteritis was the cause for perforation in seven patients (12.7.5%). Malignant gastric perforation was found in 2 patients (3.6%). One patient (1.8%) had amoebic perforation of the descending colon. One patient (1.8%) had abdominal tuberculosis with perforation of the ileum.(Table 1) Duodenum(43.6%) was the commonest site for perforation. Other sites in the order of frequency were stomach(20%), ileum(18.2%), jejunum(7.3%), descending colon(1.8%), ascending colon, stomal perforation, sigmoid perforation and transverse perforation.(Table 2) Nineteen patients (34.5%) had post-operative complications. Four patients (7.3%) succumbed to the disease. Superficial surgical site infection was most common complication and was present in 11 patients (20%). Four patients (7.3%) developed burst abdomen out of which two were associated with leak (3.6%). Age, gender and duration of the symptom didn’t affect the outcome of the patient significantly. Twenty patients (66.7%) who had peptic ulcer perforation were alcoholic. Twenty two patients (73.3%) with peptic ulcer perforation were smokers. Smoking was significantly associated with peptic ulcer peforation (P value 0.006).(Table3) Fourteen patients (42.4%) out of 33 patients who had peptic ulcer perforation gave history of NSAID intake. (P value 0.2187).
DISCUSSION
Peritonitis due gastrointestinal perforation is common in developing countries like India. As there are limited studies in this regard pertaining to this part of the world, this study was carried out to assess the factors associated with peritonitis. The commonest age group in this study was 51-60(21.8%) years followed by 41-50(20%) years. Mean age was 44.8 years (range from 14 to 80 years). Afridi et al who conducted similar study found that the mean age of patients with peritonitis due gastrointestinal perforation was 40.5 years4 . Out of 55 patients, 48(87.3%) were males and 7(12.7%) were females with sex of 6.8:1. Bhupender Kumar Jain et al in his study found that sex ratio was 5:17 . However various authors have found varying sex ratio in their study. Abdominal pain was most common symptom and was found in all the patients followed by vomiting which was present in 29 patients (52.7%), fever was present in 14 patients (25.5%) and 8 patients (14.5%) had abdominal distension. Bali et al in their study found that abdominal pain was present in 98% of the patients, 41.5% of the patients had vomiting and 28% of the patients had abdominal distension5 . Thirty eight patients (69.1%) had presented within 1-2 days of onset of the symptoms10 patients (18.2%) had presented between 3-5 days, 6 patients (10.9%) had presented between 6-10 days and 1 patient (1.8%) presented on the 11th day from the onset of the symptom. However, duration of the presentation didn’t significantly affect the outcome of the patient in this study. Thirty patients (54.5%) were smokers. Fourteen patients (42.4%) who had peptic ulcer perforation were smokers and smoking was significantly associated with peptic ulcer perforation in this study. Twenty patients (66.7%) who had peptic ulcer perforation were alcoholic. Fourteen patients (42.4%) who had peptic ulcer perforation had history of NSAID intake. Various studies have shown association between peptic ulcer disease and NSAID. Ohene –yeboah et al in their study they found 47% of patients had history of NSAID intake8 . However in this study NSAID intake was not significantly associated with peptic ulcer perforation. Pneumoperitoneum in X-ray was found in 41 patients (74.5%) and 14 patients (25.5%) didn’t have air under diaphragm. In contrast to this study, Rajender Singh Jhobta et al in their study found only 50% of the patients had air under diaphragm in X-ray. Peptic ulcer disease was the commonest cause of gastrointestinal perforation in contrast to western population where distal gastrointestinal perforations are common9 . The common causes for peptic ulcer disease are H. pylori infection, NSAID abuse and smoking. In the recent times with frequent use of proton pump inhibitors, frequency of surgery for peptic ulcer disease had markedly decreased but emergency surgery for peptic ulcer complications like perforation and bleeding has remained constant. In this study, peptic ulcer disease was the cause of perforation in 33 patients (60%). Duodenal ulcer perforation was present 72.7%, gastric ulcer perforation was found in 24.2% and one patient (3.03%) had stomal ulcer perforation from gastro-jejunostomy site. Dokubo et al in their study found that 88% of the peptic ulcer perforations were found in duodenum and 12% were found in stomach10. Graham’s omental patch repair was the performed in all the patients. Leeman et al in their study 91% of gastric ulcer was treated with graham’s omental patch and large perforations more than 2cm was treated either by simple closure (4.5%) or distal gastrectomy (4.5%)11. Chaudary et al in their study concluded that gastrointestinal ulcer larger than 2 cm can be treated with jejunal loop as serosal patch12. However, in this current study large perforations were not encountered. Three patients (9%) had succumbed to the disease and cause of death in all the three patients was septicemia with multi organ dysfunction syndrome (MODS). Naguiero et al in their study found similar results, 10% of the patients had died because of peptic ulcer perforation13. Blunt trauma abdomen was the second common cause of gastro-intestinal perforation in this study. Eight patients (14.5%) had perforation peritonitis due blunt trauma abdomen. Jhobta et al in their study found 6% patients had gastrointestinal perforation due to blunt trauma abdomen3 . Out of 8 patients, 3 patients (43%) had ileal perforation, 3 patients (28.5%) had jejunal perforation, 1 patient (14.2%) had sigmoid colon perforation, 1 patient (14.2%) has gastric perforation and 1 patient (14.2%) had rectal perforation which was associated with ileal perforation. Sule et al in their study on perforation peritonitis following blunt trauma abdomen found that the site of perforation in the order of frequency was jejunum (16.07%), ileum (14.2%), stomach (3.5%) and colon (3.5%)14. Salmonella typhi causes typhoid or enteric fever and commonly reside in the lymphoid tissue (Peyer’s patch) of small intestine. They cause oval shaped ulcer in the mucosa of the small intestine and perforation usually occurs after two weeks of typhoid fever. In this study, enteric perforation was found in 7 patients (12.7%). Bali et al in their study found that enteric perforation occurred in 12% of the patients and was comparable to the present study5 . Out of 7 patients with enteric perforation, 3 patients were treated with ileostomy, 3 patients were treated with primary closure and 1 patient was treated with resection and end to end anastomosis. In this study all patients with enteric perforation survived. Similar results were obtained by Anupam Pujar et al in their study15. Whereas Edino et al in their study conducted in Nigeria found 15% mortality16. This difference in mortality rate can be variation in severity of the disease in that part of the world. Malignant gastric perforation was found in 2 patients (3.6%). Both patients had malignant growth in the pylorus and perforation was found in the anterior aspect. Both patients under went graham’s omental patch repair and feeding jejunostomy. Definitive procedure was deferred due to poor general condition. Both patients were found to have adenocarcinoma of stomach following histopathological examination of the biopsy from edge of the perforation. Kotan et al in their study found that the incidence of malignant gastric perforation was 4.2% which was similar to this current study17. Intestinal tuberculosis was cause of gastrointestinal perforation in 1 patient (1.8%). Patient had perforation in the ileum and there were multiple tubercles in the ileum which was suggestive of tuberculosis and biopsy from the tubercle was consistent with tuberculosis. Ileostomy was done and closed after 4 weeks. Patient was started on anti-tubercular treatment. Abro et al in their study conducted in Pakistan found that perforation of ileum in intestinal tuberculosis was present in 10% of the patients18. In this study 1 patient (1.8%) had amoebic perforation of the descending colon. Intra-operatively, multiple perforations were present in the descending colon. It was treated with primary closure of the perforation and a diversion ileostomy. Patient expired on the post-operative day 10 due to septicemia and multi organ dysfunction syndrome (MODS). Jain et al in their study 186 patients who underwent exploratory laparotomy 15 patients (8%) had amoebic colonic perforation and also found that mortality was 40% in patients with amoebic perforation of the colon19. In this study colonic cancer perforation was found in 1 patient (1.8%). Intra-operatively patient had malignant growth in the descending colon with perforation of size 5mm. Patient also had liver metastases. Limited resection of the colon with transverse end colostomy and descending colon mucous fistula was done. Afridi et al in their study found colonic cancer perforation was found in 2% of the patients4 . One patient (1.8%) had obstructed left inguinal hernia with perforation of ascending colon. Patient was treated with herniorraphyand primary closure of the perforation of the ascending colon and diversion ileostomy. One patient (1.8%) in this study had strangulated incisional hernia with perforation of the transverse colon. Rajender Jhobta et al in their study found that strangulation of bowel leading to perforation peritonitis was found in 5% of the patients3 . Nineteen patients (34.5%) developed post-operative complications. Eleven patients (20%) developed superficial surgical site infection. Four patients (7.3%) developed burst abdomen and 2 of the patients (3.6%) with burst abdomen had leak from the perforation closure site. Four patients (7.3%) succumbed to the disease. Sharma et al who had conducted similar study in Delhi found similar mortality rate (8%)20. Agarwal et al in his study found burst abdomen in 11% and leak 5 % which was comparable with the present study15. (Table 2) Alcohol consumption and NSAID were not found to be significantly associated with the peptic ulcer perforation. Twenty two patients (73.3%) with peptic ulcer perforation were smokers. Smoking was significantly associated with peptic ulcer peforation (P value 0.006). (Table3) Strength of this study is that, it is one of the few prospective studies which analyzed the factors for gastro-intestinal perforation in this part of the world. Limitation of the study was sample size. The study included only 55 patients.
CONCLUSION
To conclude, peptic ulcer disease was found to be the most common cause of perforation peritonitis followed by blunt trauma abdomen and enteric perforation in contrast to western world where perforation due inflammatory disease and malignancy is common. Gastro-intestinal perforation due to malignancy and obstructed hernia were the least common cause in this study. Surgical site infection was the commonest complication. Smoking was significantly associated with peptic ulcer perforation. Alcohol consumption, prior NSAID abuse and duration of symptoms didn’t significantly affect the outcome of the patient. Morbidity rate was found to be 34% and mortality was 7.3%.
Englishhttp://ijcrr.com/abstract.php?article_id=487http://ijcrr.com/article_html.php?did=4871. Yadav D, Garg PK. Spectrum of Perforation Peritonitis in Delhi: 77 Cases Experience. Indian J Surg. 2013 Apr;75(2):133–7.
2. Chakma SM, Singh RL, Parmekar MV, Singh KG, Kapa B, Sharatchandra KH, et al. Spectrum of Perforation Peritonitis. J Clin Diagn Res JCDR. 2013;7(11):2518.
3. Jhobta RS, Attri AK, Kaushik R, Sharma R, Jhobta A. World Journal of Emergency Surgery. World J Emerg Surg. 2006;1:26.
4. Afridi SP, Malik F, Ur-Rahman S, Shamim S, Samo KA. World Journal of Emergency Surgery. World J Emerg Surg. 2008;3:31.
5. Bali RS, Verma S, Agarwal PN, Singh R, Talwar N. Perforation Peritonitis and the Developing World. IntSch Res Not [Internet]. 2014 [cited 2014 Aug 13];2014. Available from: http://www. hindawi.com/journals/isrn/2014/105492/abs/
6. Chatterjee H, Pai D, Jagdish S, Satish N, Jayadev D, Srikanthreddy P. Pattern of nontyphoidileal perforation over three dec- ades in Pondicherry. Trop Gastroenterol Off J Dig Dis Found. 2003 Sep;24(3):144–7.
7. Nuhu A, Kassama Y. Experience with acute perforated duodenal ulcer in a West African population. Niger J Med J Natl Assoc Resid Dr Niger. 2008 Dec;17(4):403–6.
8. Ohene-Yeboah M, Togbe B. Perforated gastric and duodenal ulcers in an urban African population. West Afr J Med. 2006 Sep;25(3):205–11.
9. Malangoni MA, Inui T. Peritonitis - the Western experience. World J Emerg Surg WJES. 2006;1.
10. Dakubo JCB, Naaeder SB, Clegg-Lamptey JN.Gastro-duodenal peptic ulcer perforation. East Afr Med J. 2009 Mar;86(3):100–9.
11. Leeman MF, Skouras C, Paterson-Brown S. The management of perforated gastric ulcers. Int J SurgLond Engl. 2013;11(4):322– 4.
12. Chaudhary A, Bose SM, Gupta NM, Wig JD, Khanna SK. Giant perforations of duodenal ulcer. Indian J Gastroenterol Off J Indian Soc Gastroenterol. 1991 Jan;10(1):14–5.
13. Noguiera C, Silva AS, Santos JN, Silva AG, Ferreira J, Matos E, et al. Perforated peptic ulcer: main factors of morbidity and mortality. World J Surg. 2003 Jul;27(7):782–7.
14. Sule AZ, Kidmas AT, Awani K, Uba F, Misauno M. Gastrointestinal perforation following blunt abdominal trauma. East Afr Med J. 2007 Sep;84(9):429–33.
15. Agarwal N, Saha S, Srivastava A, Chumber S, Dhar A, Garg S. Peritonitis: 10 years’ experience in a single surgical unit. Trop Gastroenterol Off J Dig Dis Found. 2007 Sep;28(3):117–20.
16. Edino ST, Yakubu AA, Mohammed AZ, Abubakar IS. Prognostic factors in typhoid ileal perforation: a prospective study of 53 cases. J Natl Med Assoc. 2007 Sep;99(9):1042–5.
17. Kotan C, Sumer A, Baser M, K?z?ltan R, Carparlar MA. An analysis of 13 patients with perforated gastric carcinoma: A surgeon’s nightmare? World J Emerg Surg. 2008;3(1):17.
18. Abro A, Siddiqui FG, Akhtar S, Memon AS. Spectrum of clinical presentation and surgical management of intestinal tuberculosis at tertiary care hospital. J Ayub Med Coll Abbottabad JAMC. 2010 Sep;22(3):96–9.
19. Jain BK, Garg PK, Kumar A, Mishra K, Mohanty D, Agrawal V. Colonic perforation with peritonitis in amoebiasis: a tropical disease with high mortality. Trop Gastroenterol Off J Dig Dis Found. 2013 Jun;34(2):83–6.
20. Sharma L, Gupta S, Soin AS, Sikora S, Kapoor V. Generalized peritonitis in India--the tropical spectrum. Jpn J Surg. 1991 May;21(3):272–7.
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241715EnglishN2015August11HealthcareTHE POST-2015 AGENDA: FROM MILLENNIUM DEVELOPMENT GOALS (MDGS) TO SUSTAINABLE DEVELOPMENT GOALS (SDGS)
English6267Suresh P.English Liaquat Roopesh JohnsonEnglishThe Millennium Development Goals (MDGs) are a set of eight Goals, eighteen targets, and 48 indicators that aim to eradicate extreme poverty and hunger, achieve universal primary education, reduce child mortality, improve maternal health, promote gender equality and empower women, combat malaria, HIV/AIDS and other diseases, ensure environmental sustainability, and develop a global partnership for development. The MDGs have an achievement deadline of 2015. The United Nations has developed a comprehensive Post-2015 Development Agenda that hinges around sustainable development. The Sustainable Development Goals (SDGs) will replace the MDGs, and are expected to build upon the achievements of the MDGs. This article outlines the progress towards achieving MDGs, the background behind SDGs, and some of the challenges faced by SDGs.
EnglishMillennium development goals, Post-2015 development agenda, Sustainable development goalsINTRODUCTION
On 6th September2000, 149 Heads of State and Government and high-ranking officials from more than 40 other countries converged at the Millennium Summit in New York. Over the next three days, they declared their commitment to reduce extreme poverty, and established a series of time-bound targets to be achieved by 2015- the Millennium Development Goals.1
MILLENNIUM DEVELOPMENT GOALS (MDGS)
The Millennium Declaration was the main document at the Millennium Summit. Unanimously adopted by the delegates, it established 8 Goals, 18 Targets, and 48 Indicators with a deadline of 2015 for their achievement.2 Popularly known as the Millennium Development Goals (MDGs), these are listed in Table 1. Considerable progress has been made towards the achievement of the MDGs:
Goal 1: Eradicate extreme poverty and hunger
Progress made/ current situation:
By 2010, the proportion of people living in extreme poverty declined by half at the global level- five years ahead of the deadline. However, at the global level, 1.2 billion people are still living in extreme poverty- one-third of this number living in India alone. Globally, the proportion of undernourished people declined from 23.2% (1990-92) to 14.9% (2010-12). However, 870 million people (one in eight globally) are still going hungry.4,5
Goal 2: Achieve universal primary education
Progress made/ current situation:
Literacy rates among adults and youths are increasing and gender gaps are narrowing.
However, at the global level, 123 million youth aged 15-24 years lack basic reading and writing skills- 61% of them are women. In addition, international aid to basic education has fallen, bringing progress to a standstill.6
Goal 3: Promote gender equality and empower women
Progress made/ current situation:
Globally, the share of women employed in non-agricultural sectors rose to 40%; the share of women in parliament reached 20% in 2012. However, disparities persist, and women tend to hold less secure jobs in developing regions. The greater representation of women in parliaments is largely the result of quota systems, rather than true empowerment.7
Goal 4: Reduce child mortality
Progress made/ current situation:
Worldwide, the under-five mortality rate declined from 90 deaths/ 1000 live births in 1990 to 48 deaths/ 1000 live births in 2012- a reduction of 47%. However, about 18,000 children still die each day, mostly from preventable causes.8
Goal 5: Improve maternal health
Progress made/ current situation:
Maternal mortality ratio has declined from 400 maternal deaths/ 100,000 live births in 1990, to 210 maternal deaths/ 100,000 live births in 2010- a reduction of 47% globally. However, only 50% of pregnant women in developing regions receive the recommended minimum of four antenatal care visits. About 140 million married women worldwide have an unmet need for family planning/ contraception.9
Goal 6: Combat HIV/AIDS, malaria and other diseases
Progress made/ current situation:
The MDG target of halting and beginning to reverse the spread of HIV has been met. Globally, there was a 26% fall in estimated malaria deaths between 2000 and 2010. Mortality due to tuberculosis (TB) decreased by 41% between 1991 and 2011, saving an estimated 20 million lives between 1995 and 2011. However, 23 million people are still getting newly infected with HIV each year at the global level. Multi-Drug resistant TB (MDR TB) is a major global challenge, and threatens to jeopardize the progress made so far.10
Goal 7: Ensure environmental sustainability
Progress made/ current situation:
With more than 2.1 billion people gaining access to improved drinking water sources since 1990, the MDG target regarding safe drinking water has been exceeded. 1.9 billion people have gained access to improved sanitation facilities between 1990 and 2011. The MDG slum target has been achieved. However, 2.5 billion people still do not have access to improved sanitation facilities. Due to rapid urbanization, the absolute number of slum dwellers in developing regions has increased to 863 million. Despite an increase in protected areas, more species are at risk of extinction. Forests are disappearing at an alarming rate- especially in South America and Africa.11
Goal 8: Develop a global partnership for development
Progress made/ current situation:
The share of developing countries in world trade stood at 44.4% in 2012, and continues to improve. Mobile-cellular penetration had reached 96%by the end of 2013. Developing countries continue to outpace developed countries in terms of internet user growth rate- 12% in developing countries compared to 5% in developed countries. However, only 31% of the population in developing countries uses the internet, compared to 77% in the developed world. Increasingly, aid is being concentrated in a small number of countries.12
MDGs: What went wrong?
The MDGs have received a fair amount of criticism. Some of the key issues with MDGs are listed in Table 2 below:
SUSTAINABLE DEVELOPMENT GOALS(SDGS)
Background
The most widely quoted definition of the term ‘sustainable development’ is that given by the Brundtland Commission of the United Nations in 1987: “sustainable development is development that meets the needs of the present without compromising the ability of future generations to meet their own needs.”15,16 At the United Nations Conference on Sustainable Development held from 20th to 22nd June 2012 at Rio de Janeiro (henceforth referred to as Rio+20), world leaders renewed their commitment to the achievement of MDGs, sustainable development and eradication of povert The Outcome Document of Rio+20 first described Sustainable Development Goals (SDGs) as a means to furthering the focus and achievements of MDGs in line with the United Nations’ post-2015 development agenda. These goals were to be formulated after extensive discussions with various stakeholders, and a report submitted to the 68th session of the United Nations Assembly, with a proposal for consideration and appropriate action. It was proposed that the SDGs should be action-oriented, easy to communicate, concise, aspirational, limited in number, global in nature and universally applicable to all countries.17,18
Description of SDGs
In all 17, SDGs have been proposed for achievement by 2030. At present, the 17 Goals are accompanied by 169 Targets. The Goals are listed in Table 3. SDGs aim to finish the job of ending poverty in all its forms by building on the success of the MDGs.
Challenges
1. The single most important challenge to the success of SDGs may well be political commitment and good governance. The experience with MDG8 is an indicator of how progress can be impeded by lack of political will.
2. Linked to the issue of political commitment is the problem of communicating the Goals in a language that is simple and easily comprehensible. Failing radical rewording, some of the Goals risk coming across as unduly verbose and complicated. Part of the success of MDGs may be attributed to the simplicity and ease of communication. The MDGs- their flaws notwithstanding, lent themselves to catchy campaigns and rapid dissemination across populations. Inherent in the difficulty to communicate is the aversion that will likely develop amongst policy and decision makers and grassroots workers alike.21
3. Some targets linked to the Goals are vague.
4. There is a lack of consensus regarding implementation, monitoring and evaluation at present. Monitoring requires the development or identification of relevant data points that can be used as indicators. There seems to be little agreement on this matter at present. This includes agreement on which agencies will undertake these tasks.
5. Although an improvement over the MDGs, the SDGs could benefit with some sort of incentivisation.
6. Funding and technical assistance by developed countries.13,21
7. It is challenging to incorporate all pillars of sustainable development within each Goal, as reflected in the corresponding Targets and Indicators.13
8. Data systems will need to be developed to address the needs generated by the SDGs.
9. The convergence of MDGs and SDGs within the post 2015 development agenda is another area of concern.
10. Monitoring framework for the Goals.21
DISCUSSION
The provision of Universal Health Coverage22 is an aspiration that has been reflected in both the Alma-Ata Declaration and the Millennium Declaration. While the Health For All by 2000 AD campaign galvanized countries to action, the lack of a coherent strategy ensured that the campaign did not translate into global success. The Millennium Development Goals (MDGs) sought to correct the mistakes of the preceding campaign, and continue the progress towards achieving Universal Health Coverage. In itself, the MDG campaign sought to achieve significant improvements in eight key areas within 15 years- a laudable but improbable goal, considering the HFA-2000 campaign gave itself 20 years. With the commercial and political interests of major players at stake, little progress has been made towards achieving Goal 8: Develop a Global Partnership for development. Financing the Goals has also been a matter of concern- some countries have reduced public spending on health. In view of the global economic downturn, the SDGs will likely face greater challenges in funding and implementation.
CONCLUSION
The Sustainable Development Goals form a major commitment to the eradication of poverty in all its forms. At present, the SDGs face many challenges. However, many (if not all) challenges may be resolved before the United Nations Summit to adopt the Post-2015 Development Agenda from 25- 27 September 2015, in New York. The SDGs present a shift in thinking and approach from the MDGs. Whether this will translate into better outcomes and achievements remains to be seen.
ACKNOWLEDGEMENT
The authors acknowledge the immense help received from the scholars whose articles are cited and included in references of this manuscript. The authors are also grateful to authors/ editors/ publishers of all those articles, journals and books from where the literature for this article has been reviewed and discussed.
Englishhttp://ijcrr.com/abstract.php?article_id=488http://ijcrr.com/article_html.php?did=4881. United Nations. United Nations Web site. [Online].; 2000 [cited 2015 May 14. Available from: http://www.un.org/events/pastevents/millennium_summit.shtml.
2. United Nations Millennium Project. United Nations Millennium Project Web site. [Online].; 2006 [cited 2015 May 14. Available from: http://www.unmillenniumproject.org/goals/.
3. United Nations Millennium Project. United Nations Millennium Project Web site. [Online].; 2006 [cited 2015 May 14. Available from: http://www.unmillenniumproject.org/goals.gti.htm.
4. United Nations. United Nations Web site. [Online].; 2013 [cited 2015 May 14. Available from: www.un.org/millenniumgoals/ pdf/Goal_1_fs.pdf.
5. United Nations. The Millennium Development Goals Report 2014. New York:, Department of Economic and Social Affairs; 2014.
6. United Nations. United Nations Web site. [Online].; 2013 [cited 2015 May 14. Available from: www.un.org/millenniumgoals/ pdf/Goal_2_fs.pdf.
7. United Nations. United Nations web site. [Online].; 2013 [cited 2015 May 14. Available from: www.un.org/millenniumgoals/ pdf/Goal_3_fs.pdf
8. United Nations. United Nations Web site. [Online].; 2013 [cited 2015 May 14. Available from: www.un.org/millenniumgoals/ pdf/Goal_4_fs.pdf.
9. United Nations. United Nations Web site. [Online].; 2013 [cited 2015 May 14. Available from: www.un.org/millenniumgoals/ pdf/Goal_5_fs.pdf.
10. United Nations. United Nations Web site. [Online].; 2013 [cited 2015 May 14. Available from: www.un.org/millenniumgoals/ pdf/Goal_6_fs.pdf.
11. United Nations. United Nations Web site. [Online].; 2013 [cited 2015 May 14. Available from: www.un.org/millenniumgoals/ pdf/Goal_7_fs.pdf.
12. United Nations. United Nations Web site. [Online].; 2013 [cited 2015 May 14. Available from: www.un.org/millenniumgoals/ pdf/Goal_8_fs.pdf.
13. Bakshi SK, Kumar I. India and Sustainable Development Goals (SDGs). The Policy Brief. 2013 November: p. 1-10.
14. Cutter A, Fenn I, Seath F. Advocacy Toolkit: Influencing the Post-2015 Development Agenda. 2015. A partnership programme between CIVICUS and Stakeholder Forum in collaboration with UNDESA.
15. International Institute for Sustainable Development. International Institute for Sustainable Development Web site. [Online].; 2013 [cited 2015 May 15. Available from: https://www.iisd.org/ sd/.
16. Drexhage J, Murphy D. Sustainable Development: From Brundtland to Rio 2012. 2010 September. Background Paper prepared for consideration by the High Level Panel on Global Sustainability at its first meeting, 19 September 2010.
17. United Nations. Outcome of the Conference: The Future we want. 2012 June. Outcome Document of Rio+20.
18. United Nations. Report of the United Nations Conference on Sustainable Development, Rio de Janeiro, Brazil 20-22 June 2012. 2012.
19. United Nations. United Nations Web site. [Online].; 2015 [cited 2015 May 14. Available from: https://sustainabledevelopment. un.org/sdgsproposal.
20. Open Working Group of the General Assembly on Sustainable Development Goals. Open Working Group proposal for Sustainable Development Goals..
21. United Nations Sustainable Development Solutions Network. United Nations Sustainable Development Solutions Network Web site. [Online].; 2015 [cited 2015 May 13. Available from: http://unsdsn.org/news/2015/01/21/three-challenges-to-addressto-make-the-sdgs-work/.
22. World Health Organization. World Health Organization Web site. [Online].; 2014 [cited 2015 July 13. Available from: http:// www.who.int/features/qa/universal_health_coverage/en/
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241715EnglishN2015August11HealthcarePROFILE OF PATIENTS OF VENOUS THROMBOSIS IN MEDICAL WARDSAN OBSERVATIONAL STUDY
English6873Cheena GargEnglish Arjun AgarwalEnglish Dhruva ChaudhryEnglishIntroduction: Venous thrombosis is not an uncommon entity in medicine wards. Clinically, in majority of patients of venous thrombosis one or the other risk factor can be identified. Radiological investigations like-Duplex sonography, Coronary Transhepatic Pulmonary Angiography(CTPA) and Magnetic Resonance Imaging (MRI) venography have revolutionized the diagnosis of these disorders. There is an urgent need and scope to identify factors contributing to thrombophilia.
Method: A prospective observational study over a period of 7 months including all the patients admitted in one unit of medicine.
Results: Overall prevalence of venous thrombosis was 4.18% (26 out of 622 patients). The mean age of patients was 40.7 ± 16.2 years. Patients were divided into two groups. Group 1 (19 patients) consisting of patients with venous thrombosis (11 patients) and pulmonary thromboembolism (8 patients). Whereas group 2 (7 patients) had patients with cortical venous thrombosis (CVT). CVT and Deep Vein Thrombosis (DVT) were predominantly seen in females while pulmonary embolism was common in males. While in Group 1, Dyspnoea and pedal oedema were the commonest features. In group 2, headache followed by focal neurological deficit was common. All the cases were confirmed by necessary radiological investigations. All patients received enoxaparin. Thrombololysis
was additionally given to 5 patients of group 1.11 (42%) patients had one or more risk factors. Overall mortality was 26%.
Conclusion: Significant number of patients of venous thrombosis had one or the other risk factors. In this highly selective group wherever the tests were done, they demonstrated presence of thrombophilic state. It reinforces the belief that thrombophilias are prevalent in our population.
EnglishVenous thrombosis, Pulmonary embolism, Cortical vein thrombosis, ThrombophiliasINTRODUCTION
Venous thrombosis is the formation of a clot or thrombus inside the veins, obstructing the flow of blood through the circulatory system caused as a consequence of Virchow’s triad. Venous thrombosis of the extremities is the commonest, followed by lungs (Pulmonary Thromboembolism) and brain. Venous Thromboembolic (VTE) disease is a common and potentially life threatening complication that incorporates signs and symptoms of 2 interrelated but distinct clinical conditions, Deep venous thrombosis(DVT) and Pulmonary embolism(PE). Signs and symptoms of VTE are non-specific like- swelling and pain in limbs, breathlessness, chest pain, cough and hemoptysis. Thus, making diagnosis difficult. Several risk factors have been advocated includingmalignancy, major orthopaedic surgery, spinal cord trauma, advanced age, obesity, immobilization, previous history of thrombosis, Ischaemic Heart Disease, smoking, atrial fibrillation, inherited causes- FactorV Leiden, hyperhomocysteinemia, deficiencies of Antithrombin III, Protein C and S.1,2 Cortical venous thrombosis(CVT), is also a challenging condition because of its myriad presentation. It is not so rare, but an alarming disease usually beginning with severe headache and may lead to seizures, neurological deficits and even death. It has been reported to cause 10-20% young strokes in India.3,4 A multitude of risk factors have been associated with CVT, including- all the prothrombotic states mentioned earlier, pregnancy, puerperium, infection and some other causes still remaining unknown(20-25%).5.
MATERIALS AND METHODS
Ours was a prospective observational clinical study carried out over a period of seven months in a medicine unit. Inclusion criteria-All confirmed cases of venous thrombosis in the medicine unit were eligible for the study. Venous thrombosis was defined to include- Deep Vein thrombosis of legs, Cortical vein thrombosis, Venothromboembolic diseases, Axillary vein thrombosis, Mesentric vein thrombosis.
RESULTS
Out of total 622 patients admitted in the hospital unit, 26 (4.18%) suffered from venous thrombosis. For the study, they were further divided into two groups: Group I – Patients having venous thromboembolic (VTE) disease (19 patients) (73.1%) including deep venous thrombosis (DVT, 11 patients i.e. 58% ) and pulmonary thromboembolism (PTE, 8 patients i.e. 42% ). Group II – patients with cortical venous thrombosis (CVT) (7 Patients i.e. 26.9%). There was a variable distribution of age with a very wide range from 20-75 years with mean age of 40.7±16.2 years. Nearly 3/4th of the patients were in the range of 20-50 years (73.1%). In group I 14 patients and in group II 6 patients were in the said range, respectively. There was almost equal no. of males and females in group I. However, there were more females (7 out of 11) in the DVT subgroup and more males (6 out of 8) in the PTE subgroup. In group II all the patients were females except one. In group I, the mean age of presentation was 43.42±16.1 years. Majority of patients had breathlessness and swelling feet. While others had distended abdomen, ascites, chest pain, cough and pain in legs. There was only 1 patient with hemoptysis. Majority of patients had pallor on general physical examination (12 patients) (63.15%), followed by pedal edema, facial puffiness and cyanosis. 4 patients (21.05%) had raised Jugular Venous Pressure. Clubbing was present in only 1 patient who had carcinoma lung. All patients were hemodynamically stable, however most patients were tachypnoeic.3 patients (15.78%) had systolic murmurs (one had ejection systolic murmer in Pulmonary area, other in both Pulmonary area and Tricuspid area and third one had Pan Systolic Murmer in Mitral area and Tricuspid area). 6 patients (31.57%) had basal crepts, 4 patients (21.05%) had reduced air entry and 2 had (10.52%) spasm on inspiration. Collaterals on abdomen with flow below upwards were seen in 2 patients (10.52%) of IVC thrombus. One of them had Budd chiari syndrome and other one had ovarian carcinoma. Around 60% of the patients had one or the other clinical risk factor for VTE. (Table 1)
In group II, the mean age of presentation was 33.29±15.12 years. Majority of patients presented with headache followed by weakness of limbs and abnormal mentation. All patients were hemodynamically stable. There was no tachypnea.4 patients (57.14%) had abnormal higher mental function. Almost all patients had plantar silent or extensor. Hemiparesis incidently all left sided was observed in 3 patients. 2 had (28.57%) signs of meningeal irritation. Fundus examination showed papilloedema in one patient.
Risk factors were found clinically in all except one. (Table 2)
Baseline routine investigations were carried out in all the patients in both the groups and were insignificant statistically. Specific investigations in group I were as follows: (Table 3a, 3b)
Laboratory evaluation of risk factor was done wherever possible to further investigate the cause of venous thrombosis.(Table 5)
The following treatment was given to the patients: Thrombolysis- 5 patients of VTE were thrombolysed, which included 4 patients of PTE and 1 of DVT. 4 patients were given Urokinase 1 patient had been previously thrombolysed with streptokinase was then thrombolysed with Tissue plasminogen activator (tPA Alteplase). Anticoagulant therapy20 (76.92%) patients were treated with low molecular weight heparin and 6 (23.07%) received heparin. All patients were given coumarin derivatives after thrombolysis and heparin or Low molecular weight Heparin therapy. Antiplatelet therapy-Clopidogrel was given in 8 patients (30.76%). Out of 26 patients, 19 (73.1%) patients were discharged after treatment while 7 (26.9%) patients expired
DISCUSSION
Thromboembolic events in India are still an under reported entity .In our study, the prevalence of venous thrombosis was 4.18% in the population studied (out of which 3.05% patients were diagnosed as VTE and 1.13% patients as CVT). According to a study, a prevelance rate of 10-20% of DVT has been reported amongst the medical patients. 6 The overall incidence of venous thromboembolism was reported as 1.83 per thousand per year (1.69 to 1.98) in the western population. 7 Whereas pulmonary embolism has an average annual incidence of 1 case per 1000 in the western population.8 Studies in India are too meagre in this respect and prevelance of VTE in our population is not known. Epidemiological data though is available on CVT from India, its exact incidence is debatable. During the last 40 years, there have been clinical series from India suggesting higher incidence of CVT in the subcontinent than the western world.9.10 In group I which included VTE patients ,the mean age of presentation was 43.42±16.1 years against 39±12.1 years in a study of pulmonary embolism patients from north India.11 Many other studies also reported increased risk of VTE in patients >40 years age.12,13,14 Thus, our study supports the fact that VTE is more common around 40 years. The same study of PE from north India showed that 17 males and 7 female patients were affected i.e. males were twice more predisposed to develop PTE than females. In our study also, nearly 3/4th patients of PTE (6 out of 8 patients of PE) were males However, DVT was commoner in females( 7 out of 11) as compared to males (4 out of 11)in the present study. Breathlessness and swelling foot were the commonest complaints in contrast to the previously mentioned study11, which demonstrated dyspnoea and cough as the main presenting symptoms. This could probably be because the above referred study was done purely on patients of PE while our study included both PE and DVT, thus, more patients with swelling foot. In the present study majority (57.8%) of the patients had at least one risk factor known to predispose to VTE. However, they showed scattered distribution among the local population with no difference from literature. The risk factors observed were IHD, previous history of VTE, underlying renal glomerular disease , carcinoma ,intake of Oral Contraceptives and immobilization. Hypercoagulability in cancer patients may indicate an aggressive change in the tumor and is associated with tumor progression.15 VTE incidence is around 40-100 cases per 1000 person-years in lung carcinoma patients.16 Gastrointestinal and gynaecological malignancies have also been found to be associated with hypercoagulation more frequently.17 Interestingly, 3 patients who had venous thrombosis associated with malignancy, one patient each had lung, ovarian and esophageal carcinoma. Many studies published in the last decade, reported that the incidence of venous thromboembolism (VTE) was higher in women who used oral contraceptives (OCs).18, in more so with third generation , as was seen in one of our subjects. In group II , the mean age of presentation was 33.29±15.12 years which was similar to a previous study from India on CVT (had mean age as 33.27 years).19 It had 41% female patients whereas in our study nearly all patients (85.7%) were females. All the patients had some or the other risk factor predisposing to CVT. Most of the females were in their pospartal periods. Puerperium has a strong relationship with CVT probably due to increased levels of clotting factors during pregnancy and hormonal changes. 10It is further complicated by local customs of not hydrating the mother adequately. Therefore, it was not a surprise to observe young females mostly in their postpartal periods with CVT. On laboratory tests, positive APLA and hypertriglyceridemia were revealed in a patient each. Several researches all over the world indicate that APLA20,21,22 hypertriglyceridemia 23,24 are proven prothrombotic states .In patient of CSOM with mastoiditis, direct extension of infection to the ipsilateral transverse sinus is supposed to be the cause of venous thrombosis. Headache was the commonest presenting symptom in 71.42% of the cases. It was primarily due to raised intracranial tension secondary to impaired drainage of CSF and venous sinuses. Headache has been constantly found to be the commonest complaint 2,19,10 However, the incidence of seizures was lower(28.57%) in our study than Pillai et al (42%)19.This was due to more common involvement of Superior Saggital sinus in their study, while most of our patients had transverse sinus involvement(6 out of 7). Hemiparesis was also a common presentation in our study owing to the same reason.MRI venography due to ready availability was the main modality for diagnosis of CVT in our institution. MR venography not only seems to offer an important advantage as a non-invasive tool in diagnostic procedures but also seems useful as a follow-up instrument for documentation of thrombus regression, recanalisation and venous collateralisation.25 In group I, echocardiography showed PAH in 60% patients and dilated right ventricle and atrium in 80% patients, primarily suspected to have VTE as compared to 83.3% and 62.5% , respectively in the PGIMER study.11 .73.68% patients had evidence of DVT on Duplex ultrasonography in the present study. Lower limb DVT was more common as with many other studies .The sensitivity and specificity of duplex for proximal vein thrombosis is 98%. Further, it helps to differentiate venous thrombosis from hematoma, Baker’s cyst, abscess, other causes of leg pain and edema.6 7 out of 8patients of PTE were confirmed on CT pulmonary angiography. The use of spiral CT pulmonary angiography(CTPA) is a major advancement in the diagnosis of PE with sensitivity and specificity greater than 90%.26. Therefore, the present study confirms the utility of CTPA in the diagnosis of PE. In our hospital thrombolysis was carried out in 5 patients, of which 3 had right ventricular dysfunction and one had IVC thrombus. Thrombolysis is being used more commonly now a days, not only for treating massive PE with shock but also in patients with echocardiographic evidence of right ventricular dysfunction.27,28,29 Such therapy has been shown to preserve the pulmonary microcirculation after pulmonary embolism and to decrease the incidence of the post-thrombotic syndrome following deep venous thrombosis27 Certain specific investigations like-factor V leiden, APLA,ATIII levels, Protein C and S levels, etc. were carried out in some cases .These tests though promising, but due to their non-availability in the hospital and for economic considerations were not carried out in every case on presentation. Moreover, majority of the investigations like- Protein C and S are more relevant when done after 6 months of anticoagulation therapy as their levels may be initially falsely low due to consumption of clotting factors.
CONCLUSION
Our study has demonstrated that venous thrombosis is not an uncommon entity in medicine wards. It affects predominantly when people are economically most productive. Clinically, in majority of patients of venous thrombosis have one or the other risk factor can be identified. Radiological investigations like-Duplex sonography, CTPA and MRI venography have revolutionized the diagnosis of these disorders. They should be used at first instance wherever clinical probability is high. There is an urgent need and scope to identify factors contributing to thrombophilia.
ACKNOWLEDGEMENT
Authors acknowledge the immense help received from the scholars whose articles are cited and included in references of this manuscript. The authors are also grateful to authors / editors / publishers of all those articles, journals and books from where the literature for this article has been reviewed and discussed.
Englishhttp://ijcrr.com/abstract.php?article_id=489http://ijcrr.com/article_html.php?did=4891. Clagett GP, Anderson FA, Jr, Heit J, et al. Prevention of venous thromboembolism. Chest 1995;108 (Suppl 1):31234.
2. Bick RL, Haas S. Thromboprophylaxis and thrombosis in medical, surgical, trauma, and obstetric/gynecologic patients. Hematol Oncol Clin North Am 2003;17:21758.
3. Srinivasan K. Ischemic cerebrovasular disease in the young: Two common causes in India. Stroke 1984;15;733-5.
4. Nagaraja D, Sarma GR. Treatment of cerebral sinus/venous thrombosis. Neurol India 2002;50;2:114-6.
5. Deschiens M. Coagulation studies, factor V leiden, and anticadiolipin antibodies in 40 cases of cerebral venous thrombosis. Stroke 1996;27;1724-30.
6. Parakh R, Somaya A, Todi SK, Iyengar SK. Consensus Development Recommendations for the Role of LMWHs in Prophylaxis of Venous Thromboembolism : An Indian Perspective. SUPPLEMENT OF JAPI _ JANUARY 2007 _ VOL. 55.
7. Incidence of venous thromboembolism: a community-based study in Western France. Thromb Haemost. 2000 May ;83 (5):657-60 10823257.
8. Wells PS, Rodger M. Diagnosis of pulmonary embolism: when is imaging needed? Clin Chest Med2003:24:13-28.
9. Padmavati S, Gupta S, Singh B.A clinical study of 44 cases of hemiplegia in adult women. Neurol India 1957;5:59-65.
10. Srinivasan K.Cerebral venous and arterial thrombosis in pregnancy and puerperium:a study of 135 patients. Angiology 1983;34:731-46.
11. Agarwal R, Gulati M, Mittal BR, Jindal SK.Clinical profile, diagnosis and management of patients with symptomatic PE, PGIMER Chandigarh. Original article. Indian J Chest Dis Allied Sci 2006;48:111-114.
12. Nicolaides AN, Irving D. Clinical factors and the risk of deep venous thrombosis. In: Nicolaides A, editor. Thromboembolism Etiology. Advances in Prevention and Management. Baltimore, MD: University Park Press; 1975: 193–204.
13. Gillum RF. Pulmonary embolism and thrombophlebitis in the United States, 1970–1985. Am Heart J. 1987; 114: 1262–1264
14. Gjores JE. The incidence of venous thrombosis and its sequelae in certain districts in Sweden. Acta Chir Scand. 1993; 111 (Suppl 206): 16–24.
15. Ten Cate-Hoek AJ, Prins MH. Low molecular weight heparins in cancer Management and prevention of venous thromboembolism in patients with malignancies. [Epub ahead of print] Thromb Res. 2007 Nov 7.
16. Margot Tesselaar, ET, Susanne Osanto, Department of Clinical Oncology, Leiden University Medical Center, The Netherlands .Current Opinion in Pulmonary Medicine. 13(5):362-367, September 2007.
17. TAHRI A, El Hattaoui M,Charei N, El Belghiti M, Mahmal L, Tahiri F, Bouras N. Journal of Clinical Oncology, 2007 ASCO Annual Meeting Proceedings Part I. Vol 25, No. 18S (June 20 Supplement), 2007: 19672.
18. Farmer RD, Lawrenson RA, Thompson CR, Kennedy JG, Hambleton IR. Population-based study of risk of venous thromboembolism associated with various oral contraceptives. Department of Public Health and Primary Care, Charing Cross and Westminster Medical School, University of London, Chelesa, UK.Lancet,1997 Jan 11;349(9045):83-88.
19. Pillai Lalitha V, Ambike Dhananjay P, Nirhale Satish, Husainy S M K, Pataskar Satish. Cerebral venous thrombosis: An experience with anticoagulation with low molecular weight heparin. Critical Care Department, Lokmanya Hospital, Chinchwad, Pune, India. IJCCM 2005;9:14-18.
20. Petri, M. Epidemiology of the antiphospholipid antibody syndrome. J Autoimmun. 2000; 15: 145–151.
21. Schved JF, Dupuy-Fons C, Biron C, et al. A prospective epidemiological study on the occurrence of antiphospholipid antibody: the Montpellier Antiphospholipid (MAP) Study. Haemostasis. 1994; 24: 175–182.
22. Bick RL. Hypercoagulability and thrombosis. Med Clin North Am. 1994; 78: 635–665.
23. Carine J.M. Doggen; Nicholas L. Smith; Rozenn N. Lemaitre; Susan R. Heckbert; Frits R. Rosendaal; Bruce M. Psaty. Serum Lipid Levels and the Risk of Venous Thrombosis. Arteriosclerosis, Thrombosis, and Vascular Biology:Volume24(10)October 2004pp 1970-1975.
24. Larsen LF; Bladbjerg EM; Jespersen J; Marckmann P. Effects of dietary fat quality and quantity on postprandial activation of blood coagulation factor VII. Arterioscler Thromb Vasc Biol (United States) Nov 1997, 17 (11) p2904-9.
25. Dormont D, Axionnat R et al. MRI in cerebral venous thrombosis. J Neuroradiology 1994; 21 (2): 81-99.
26. Padley SPG.Lung scintigraphy vs spiral CT in the assessment of pulmonary emboli.Br J Radiol 2002:75:5-8.
27. Linn BJ, Mazza JJ, Friedenberg WR. Treatment of venous thrombotic disease. Postgrd. Med. 1988 79(6): 171-80.
28. South path S.A. thrombolytic therapy for venous thrombosis and pulmonary embolism. Baillieres clin hematol 1998. 11(3): 663-73.
29. Fattahi O.H. Thrombolytic Therapy for Deep Vein Thrombosis and Pulmonary Embolism. Shiraz E-Medical Journal. October 2001, Vol. 2, No. 4.
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241715EnglishN-0001November30HealthcareIMPACT OF GENDER AND HEAD SIZE ON VISUAL EVOKED POTENTIALS
English7476Rubiya ShaikhEnglish Rupali K. ParlewarEnglishThe aim of the study is to compare head circumference in Gender and then to correlate head circumference with P100 latency, N75-P100 and P100-N145 amplitude. Visual evoked potentials are electrical potential differences recorded from scalp in response to visual stimuli. Numbers of factors that influence VEP waveforms include Age, Sex, Drugs, Head circumference. In the present study head circumference, P100 latency, N75- P100amplitude and P100 -N 145amplitude were recorded in 30 healthy males and 30 healthy females in the age group of 18-25 yrs. It is observed that head circumference is more in males. Also P100 latency is more in males as compared to females which is attributed to longer visual pathway. And amplitudes are larger in females as compared to males which is attributed to genetically determined sex differences in neuro-endocrinological systems. Present study also shows positive correlation between head circumference and latency and negative correlation between head circumference and amplitude. When the latency and amplitude of both males and females of same head circumference (53-55cm) were compared it was found that latency does not show significant results. But amplitude is more in female which is attributed to genetically determined sex
differences in neuro-endocrinological systems.
EnglishVisual evoked potential, Head circumference, P100 latency, N75-P100 amplitude, P100-N145 amplitudeINTRODUCTION
Visual evoked potentials are electrical potential differences recorded from scalp in response to visual stimuli (1).Visual evoked potentials (VEPs) are used to interrogate the visual pathway from the retina up through high-level visual cortices(2).
Numbers of factors that influence VEP waveforms include Age, Sex, Drugs, Head circumference (1). Gender is presumed to be one of the factors causing inter-individual variability in the brain’s electrophysiological parameter (2).the P100 latency is longer in adult males as compared to females. This has been attributed to larger head size and lower core body temperature in males (3). The mean P100 amplitude is greater in females compared to males (1).
Not many studies carried out showing how significantly these parameters affect VEP. Hence an attempt has been made, to correlate how gender has impact on VEPs, So that these factors will be considered clinically while recording VEP. The aim of the study is to compare head circumference in Gender and then to correlate head circumference with P100 latency, N75-P100 and P100-N145 amplitude.
MATERIALS AND METHODS
The study was conducted in a Grant Govt Medical College and J J Hospitals in Mumbai with the prior permission of the Dean of the institute and the ethical committee. 60 Healthy subjects males (n=30), females (n=30).Within in the age group of 18-25 years were subjected to a series of tests exercising utmost care in conduction so as to achieve the maximum possible accuracy with the available setup. A brief explanation to subjects regarding the procedure was given and voluntary informed consent of the subjects was taken.
The subjects selected were having no, medical, neurological and ophthalmic problems. The subjects were not on any medication likely to affect or influence VEPs or drugs affecting moods (antidepressant, tranquilizers). Prior to the study all subjects completed a healthy history questionnaire and a medical examination.
Visual function tests were done. Head circumference was measured in cm. Pattern reversal VEP was done on NeuroMEP machine. The low cut filters (LF) are set at 2 Hz and high cut filters (HF) are set at 100 Hz. Electrode impedance set at < 5kΩ. Active electrode applied at midline 4cm above inion (Oz). Reference electrode applied at 12 cm above nasion (Fpz) and ground electrode at vertex (Cz).P100 latency and N75- P100 amplitude and P100 - N145 amplitude were recorded. Pearson’s Correlation Coefficient (r) was used for Correlation of Head circumference with VEP. Student’s t test –was used for analysis of VEP in Gender.
DISCUSSION
It is observed that head circumference in males is significantly more than female. Also the P100 latency and N75- P100 amplitude and P100- N 145amplitude show significant values. There is positive correlation between head circumference and latency. Increase in head circumference also increases latency. And negative correlation between head circumference and amplitude. Increase head circumference decreases amplitude.
Significant positive correlation between Head circumference and Latency is suggestive of larger the head circumference, larger is brain size and longer conduction pathway and thus prolonging VEP latencies; as per Kothari et al (4).
Also as per Schmidt Neilsen K, the assumption that the anatomic variation is isometric, differences in all dimensions will be proportional and any pathway in brain will vary in length as cube root of brain volume (5)
If we take the VEP in males and females of having same range of head circumference (53-55) it is observed that latency does not show significant changes but amplitude show significant changes
Yasuhiro Kaneda et al (3)had concluded that, the large VEP amplitude, and the tendency for increased α power % and at LP verified in their study were considered to indicate that the VEP amplitude at LP reflects the effect of estrogen more than progesterone, and that the VEP latency and EEG changes at LP reflect the effect of progesterone more than estrogen. We believe that VEP analysis is a useful tool for the study of the actions of gonadal hormones on CNS, not only in animals but also in humans. And therefore Sex differences in VEPs (more Amplitude in females) may be attributed to genetically determined sex differences in neuro-endocrinological systems
CONCLUSION
Head circumference is significantly larger in males. P100 Latency in male is more than female; this is attributed to longer visual pathway. Also larger amplitude in females, is attributed to genetically determined sex differences in neuroendocrinological systems.
Head circumference has significant Positive correlation with latency and negative correlation with amplitude. Males and Females having same range of head circumference have no significant difference in Latency.
ACKNOWLEDGEMENT
Authors acknowledge the immense help received from the scholars whose articles are cited and included in the references of this manuscript. Authors are also grateful to authors /editors /publishers of all those articles, journals and books from where the literature for this article has been reviewed and discussed.
Englishhttp://ijcrr.com/abstract.php?article_id=490http://ijcrr.com/article_html.php?did=4901. Misra UK, Kalita J. Visual Evoked Potentials, Clinical Neurophysiology. Churchill Livingstone, New Delhi 2011; 309-327.
2. J. Langrová1, J. Kremlá?ek1, M. Kuba1, Z. Kubová1, J. Szanyi1. Gender Impact on Electrophysiological Activity of the Brain Physiol. Res. 61 (Suppl. 2): S119-S127, 2012
3. Stockard JJ. Hughes JR. Sharvough FW. Visually evoked potentials to electronic pattern reversal :latency variation with gender, age and technical factors.Am J EEG Technol 1979: 19:171
4. Kothari R, Singh R, Singh S, Bokariya P. Effect of head circumference on parameters of Pattern reversal visual evoked potentials in healthy adults of central India. Nepal MedColl J 2012; 14 (2) : 75-79.
5. Schmidt Neilsen K. scaling in biology: the consequence of size. J Exp Zool 1975;194: 284-307
6. YasuhiroKaneda Y, Nakayama H, Kagawa K, Furuta N, Ikuta T: Sex differences invisual evoked potential and electroencephalogram of healthy adults. Tokushima J The J of medical investigations 1996; 43 (3-4) : 143-157.
7. B. K. Mahajan. Methods in Biostatistics. 7th Edition.