Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241724EnglishN2015December20HealthcareA STUDY OF MORPHOLOGY OF THE PROXIMAL PART OF VENTRAL BRANCHES OF ABDOMINAL AORTA IN CADAVERS
English0105Kruti Bharatkumar TapiyawalaEnglish M. NatarajanEnglishObjective: Majority of studies in the past about ventral branches of abdominal aorta mainly focused on the branching pattern.
The cadaveric data on the vertebral level of origin of the ventral branches of abdominal aorta is less. Hence the study aimed at
the morphology of proximal part of ventral branches of abdominal aorta.
Objectives:
1. To determine the vertebral level of origin of coeliac trunk
2. To determine the vertebral level of origin of superior mesenteric artery
3. To determine the vertebral level of origin of inferior mesenteric artery
Materials and Methods: Fifty embalmed cadavers were dissected. The vertebral level of origin of ventral branches were determined
and variations were noted.
Results:
1. In 38% cases, the vertebral level of origin of coeliac trunk was found to be located at the level of intervertebral disc (IVD)
T12-L1.
2. In 24% cases, the vertebral level of origin of superior mesenteric artery was found to be located at the level of intervertebral
disc (IVD) T12-L1 and upper 1/3rd of L1.
3. In 22% cases, the vertebral level of origin of inferior mesenteric artery was found to be located at the level of intervertebral
disc (IVD) L3-L4.
Conclusion: In conclusion, the present study provides a comprehensive data about the abdominal aorta and the proximal part
of its ventral branches which will help in interpretation of radiographs and during surgery of different types of abdominal pathology
in Indian population. Awareness of these variations can prevent potential intra-operative and post- operative complications.
EnglishVentral branches, Coeliac trunk, Superior mesenteric artery, Inferior mesenteric arteryINTRODUCTION
Anatomical variations involving the visceral arteries are common. Though variations in coeliac trunk are usually asymptomatic, they may become important in patients undergoing diagnostic angiography for gastrointestinal bleeding or prior to an operative procedure. Close relation of short coeliacomesenteric trunk with median arcuate ligament and the tight tendinous ring around the aortic opening can cause compression of the trunk. This may lead to postprandial periumbilical pain. Surgical intervention in such a case may be associated with the risk of ligating the wrong vessel or severing an essential organ sustaining artery, danger of ischaemia, gangrene, leakage and bleeding from the site of repair.1 Prior knowledge of aortic variations is required to successfully accomplish aortic replacement with implantation of the coeliac trunk, mesenteric arteries and renal arteries.2 In the radiation therapy of upper gastrointestinal malignancies, treatment of lymph nodes in the region of the coeliac axis and superior mesenteric axis is often mandated.3
Evaluation of arteries branching from the abdominal aortathe level of their divergence, presence of atypical variants of a common origin of arteries plays an important role in the diagnostics of many abdominal disorders.4 Variations in morphology of the aorta and its branches are of considerable interest as vessel geometry not only determines flow dynamics, but is also crucial in the pathogenesis of vascular diseases, e.g., atherosclerosis and aneurysm formation.5 Anatomic variants of the coeliac trunk is essential to successfully accomplish surgical, oncologic, or interventional procedures including lymphadenectomy around hepato-splenomesenteric trunk, aortic replacement with reimplantation of the trunk, or chemoembolization of liver malignancies, all of which can potentially create significant morbidity because of the large visceral territory supplied by a single vessel.6
MATERIALS AND METHODS:
Fifty formalin-fixed cadavers in the department of anatomy were used for the study. This study was conducted over a period of two years. All the cadavers were ranging between the age group of 18-65 years at the time of death. None of the abdomen showed any evidence of previous surgery. After meticulous dissection satisfactory exposure of the ventral branches of abdominal aorta was done. Counting of vertebra was done from below upward, by identifying the sacral promontory first and labelling the vertebra immediately above that as fifth lumbar vertebra (L5) and so on and so forth. This counting of vertebra was also confirmed by identifying the 12th rib and tracing it to the 12th vertebra. Length of each vertebral body was measured. Each vertebra was divided into upper, middle and lower third. The study protocol was prepared in the form of a proforma. The parameters determined were:
1. To determine the vertebral level of origin of coeliac trunk
2. To determine the vertebral level of origin of superior mesenteric artery
3. To determine the vertebral level of origin of inferior mesenteric artery Any variation in the site of origin of the ventral branches were also observed.
RESULTS
VERTEBRAL LEVEL OF ORIGIN OF COELIAC TRUNK (Table-1)
The vertebral level of origin of coeliac trunk was found to be located between upper 1/3rd of T12 to IVD L1-L2. In 19 cases, it was located at the level of IVD T12-L1.
VERTEBRAL LEVEL OF ORIGIN OF SUPERIOR MESENTERIC ARTERY (Table-2)
The vertebral level of origin of superior mesenteric artery was found to be located between lower 1/3rd of T12 to upper 1/3rd of L2. In 12 cases, it was located at the level of IVD T12-L1 and upper 1/3rd of L1.
VERTEBRAL LEVEL OF ORIGIN OF INFERIOR MESENTERIC ARTERY (Table-3)
The vertebral level of origin of inferior mesenteric artery was found to be located between lower 1/3rd of L2 to middle 1/3rd of L4. In 11 cases, it was located at the level of IVD L3-L4
DISCUSSION
1. VERTEBRAL LEVEL OF ORIGIN OF COELIAC TRUNK (Table-4)
Pant P7 et al in 2013 dissected 40 cadavers and found that in maximum number of cases i.e. 76.68%, coeliac trunk originated between T12 and L1 vertebra. In 23.04% cases, it originated at the upper 1/3rd of L1 vertebra and in minimum number of cases i.e.5.12% cases, it originated at the level of lower 1/3rd of T12 vertebra. They also noticed absence of coeliac trunk in 2.5% of cases, where branches of coeliac trunk directly originated from aorta. Wadhwa A1 et al in 2011 dissected 30 adult cadavers and found that the coeliac trunk was arising at the level of IVD T12-L1 in 22 cases (73.3%) and upper 1/3rd of L1 vertebra in 8 cases (26.6%). George R8 in 1934 observed the vertebral level of origin of coeliac trunk in 97 cadavers. The author has measured the vertebral levels of origin of the unpaired visceral branches at the center of origin of the each branch. The author found that the coeliac trunk was arising at the level of upper 1/3rd of L1 in 25 cases, at the level of IVD between T12-L1 in 20 cases, at the level of lower 1/3rd of T12 in 18 cases and at the level of middle 1/3rd of L1 in 17 cases. Prakash2 et al in 2011 dissected 50 cadavers found that the coeliac trunk was located most commonly (in 64% of cadavers) at the level of T12. In 36% cases, the coeliac trunk was located at the level of L1. In the present study, the vertebral level of origin of coeliac trunk was at the level of IVD T12-L1 in 38% cases, at the level of T12 in 34% cases and at the level of L1 in 22% cases 2.
VERTEBRAL LEVEL OF ORIGIN OF SUPERIOR MESENTERIC ARTERY (Table-5)
George R8 in 1934 observed the vertebral level of origin of superior mesenteric artery in 97 cadavers. The author found that the superior mesenteric artery was arising at the level of lower 1/3rd of L1 in 29 cases, at the level of IVD between L1- L2 in 21 cases at the level of middle 1/3rd of L1 in 20 cases, at the level of upper 1/3rd of L1 in 17 cases. Prakash2 et al found the vertebral level of origin of superior mesenteric artery at the level of L1 in 76% cases, at the level of T12 in 20% cases. In the present study, the vertebral level of origin of superior mesenteric was found at the level of IVD T12-L1 in 12 cases, at the level of upper 1/3rd of L1 in 12 cases, at the level of lower 1/3rd of L1 in 10 cases, at the level of middle 1/3rd L1 in 7 cases. In 58% cases, it was located the level of L1 and in 24% cases, it was located at the level of IVD T12-L1. 3.
VERTEBRAL LEVEL OF ORIGIN OF INFERIOR MESENTERIC ARTERY (Table-6)
George R8 in 1934 observed the vertebral level of origin of inferior mesenteric artery in 97 cadavers. The author found that the inferior mesenteric artery was arising at the level of middle 1/3rd of L3 in 28 cases, at the level of lower 1/3rd of L3 in 23 cases, at the level of upper 1/3rd of L3 in 20 cases, at the level of IVD between L2-L3 in 15 cases and at the level of IVD L3-L4 in 14 cases. Prakash2 et al found that the vertebral level of origin of inferior mesenteric artery was at the level of L3 in 68% cases, at the level of L4 in 18% cases and at the level of L2 in 14% cases. In the present study, the vertebral level of origin of inferior mesenteric artery was located at the level of IVD L3-L4 in 11 cases, at the level of IVD L2-L3 in 10 cases, at the level of lower 1/3rd of L3 in 9 cases, at the level of upper 1/3rd of L3 in 8 cases and at the level of middle 1/3rdof L3 in 7 cases. In 48% cases, it was located at the level of L3 and in 22% cases, it was located at the level of IVD L3-L4. Probable embryological basis for the different vertebral levels of ventral branches: The ventral splanchnic arteries are originally paired vessels distributed to the capillary plexus in the wall of the yolk sac. After fusion of the dorsal aortae, they merge as unpaired trunks that are distributed to the increasingly defined and lengthening primitive digestive tube. Longitudinal anastomotic channels connect these branches along the dorsal and ventral aspects of the tube, forming dorsal and ventral splanchnic anastomoses. These vessels obviate the need for so many ‘subdiaphragmatic’ ventral splanchnic arteries, and these are reduced to three, the coeliac trunk and the superior and inferior mesenteric arteries. As the viscera supplied descend into the abdomen, their origins migrate caudally by differential growth: the origin of the coeliac artery is transferred from the level of the seventh cervical segment to the level of the 12th thoracic; the superior mesenteric from the second thoracic to the first lumbar; and the inferior mesenteric from the twelfth thoracic to the third lumbar.9 The yolk sac is supplied by a number of paired vessels called omphalomesenteric or vitelline arteries at the end of the fourth week of intrauterine life. The aforementioned vessels gradually fuse in the latter part of the embryonic life and in the dorsal mesentery of the gut they form arteries which in adult life are represented as the coeliac, superior mesenteric, and inferior mesenteric arteries. Defective fusion of the omphalomesenteric arteries during the embryonic stage can be important factor manifesting the variations.2
CONCLUSION
In conclusion, the present study provides a comprehensive data about the abdominal aorta and the proximal part of its ventral branches which will help in interpretation of radiographs and during surgery of different types of abdominal pathology in Indian population. Awareness of these variations can prevent potential intraoperative and post- operative complications.
ACKNOWLEDGEMENTS:
The authors wish to convey her sincere thanks to Dean, Seth G. S. Medical College and K.E.M. Hospital, Mumbai and all staff members from Department of Anatomy, Seth G. S. Medical College, Mumbai. Authors also 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=368http://ijcrr.com/article_html.php?did=3681. Wadhwa A, Soni S. A composite study of coeliac trunk in 30 adult human cadavers - its clinical implications. Global Journal of Medical research. 2011; 11(1): 34-38.
2. Prakash, Mokhasi V, Rajini T, Shashirekha M. The abdominal aorta and its branches: anatomical variations and clinical implications. Folia Morphol. 2011; 70(4):282-286.
3. Kao GD, Whittington R, Coia L. Anatomy of the coeliac axis and superior mesenteric artery and its significance in radiation therapy. Int J RadiatOncolBiol Phys. 1993; 25(1):131-134.
4. Kornafel O, Baran B, Pawlikowska I, Laszczy?ski P, Guzi?ski M, S?siadek M. Analysis of anatomical variations of the main arteries branching from the abdominal aorta, with 64-detector computed tomography. Polish Journal of Radiology. 2010; 75(2): 38-45.
5. Pennington N, Soames RW. The anterior visceral branches of the abdominal aorta and their relationship to the renal arteries. Surg and Radiol Anat. 2005; 27: 395-403.
6. Sawant S, Kolekar S, Harichandana N. Anatomical Variations in coeliac Trunk and its branches. International Journal of Recent Trends in Science And Technology. 2013; 6(3), 130-133.
7. Pant P, Mukhia R, HarithaKumari N, Mukherjee A. Variant anatomy of the coeliac trunk and its branches. Global Research Analysis. 2013; 2(6), 179-180.
8. George R. Topography of the unpaired visceral branches of the abdominal aorta. Journal of Anatomy. 1934; 69:196-205.
9. Standring S. Embryonic arteries. In Collins P, editor. Gray’s Anatomy: The Anatomical Basis of Clinical Practice. 40th ed. Edinburgh, Churchill Livingstone; 2008: 206-207.
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241724EnglishN2015December20HealthcareISOLATION AND SPECIES IDENTIFICATION OF CANDIDA ISOLATED FROM PATIENTS OF VULVOVAGINAL CANDIDIASIS IN A TERTIARY CARE HOSPITAL
English0612Twinkle GandhiEnglish Manish G. PatelEnglish Mannu JainEnglishIntroduction: An increase in the predisposing conditions in recent years has resulted in an increasing incidence of Candida infections.The accurate species identification of Candida is important for the treatment, as not all species respond to the same treatment and also because of the problem of anti-fungal resistance in certain species.Therefore, the species level identification of the Candida isolates, along with their anti-fungal susceptibility patterns can greatly influence the treatment options for the clinician. Objective: - To detect prevalence of Candida in patients with vaginal discharge. - To identify species of Candidaisolates. Methods: This study included 410 women with abnormal vaginal ischarge. Two high vaginal swabs were collected and sent immediately to the laboratory. All vaginal samples were stained with gram’s stain and oval budding yeast cells were identified as Candida. Second swab was inoculated on Sabouraud’s Dextrose agar and Candida isolates(n=122)were identified at species level by battery of various tests like GTT,Corn meal agar, Carbohydrate fermentation, Carbohydrate assimilation and CHROM agar inoculation. Results: Out of 410 samples Candida were isolated in 122 samples. Amongst the 122 Candida isolates highest was C.albicans 66.39%,followed by C.glabrata 15.65%,C.tropicalis 9.85%, C.parapsilosis 4.91%, C.krusei 2.4% and least wasC.guilliermondii 0.8%.In pregnancy and OCP users maximum isolates were of C.albicans(78.04% and 55.55%,respectively) were as in diabetic patients C.glabrata (47.05%) was predominant isolate,while in HIV positive patients all isolates wereC.albicans (100%). Conclusions: In our study the prevalence of VVC is 29.75%.Commonest species found was C.albicans 66.39%.VVC is more common in females with associated risk factors like pregnancy, diabetes, HIV and OCP users.Commonest species in pregnancy, OCP users and HIV patients wasC.albicans whileC.glabratawas more common in diabetic patient.
EnglishVulvovaginal candidiasis (VVC), Candida Spp., Germ tube test (GTT), CHROM agarINTRODUCTION
Candida albicans, the most frequent cause of candidiasis, can account for up to 75% of the yeasts recovered from clinical specimens.1 Although the frequency of isolation of nonalbicans Candida (NAC) species is increasing gradually, C. albicans is the most common cause of candidiasis.1,2 Other species of Candida such as C. glabrata, C. krusei and C. tropicalis are emerging as important opportunisticpathogens and this transition had a significant clinical impact due to decreasedsusceptibility of these non-albicans yeasts to antifungal agents.4,5Identification to the species level of yeasts cultured from various clinical specimen is increasingly necessary for clinical laboratories.6,19 Generally yeast identification procedures start with a germ tube test in clinical laboratories.3 It is a rapid method to differentiate C. albicans andC. dubliniensis from other Candida species.21 Up to 5% of the strains of C. albicans may be germ tube negative, and false positive results can occur with Candida stellatoidea (now classified as C. albicans) and other yeasts that produce germ tube like structures, e.g., pseudohyphae.25,26 When the yeast cannot be identified with this method, further tests such as culturing on cornmeal agar, carbohydrate fermentation and carbohydrate assimilation tests are performed.22Detection of growth patterns on cornmeal agar takes 24-72 hours and sugar assimilation tests may take 72 hours to twoweeks.21 These procedures are labor intensive and take longer to determine the species.1 C.albicans and related species which are pathogenic for humans, become resistant to the anti-fungal agents, in particular to the azole compounds, by the expression of the efflux pumps that reduce drug accumulation, the alteration of the structure or concentration of the anti-fungal target proteins and by the alteration of the membrane sterol composition.2,20 The clinical consequences of the anti-fungal resistance can be seen as the treatment failure in the patients and as the change in the prevalence of the Candida species which causes the infection.2 Accurate species identification is important for the treatment of the Candida infections, as the non-albicans species of Candida continue to be increasingly documented and as not all the species respond to the same treatment.4 The increase in the predisposing conditions in recent years has resulted in a concurrent increase in the numberof patients who suffer from candidiasis.15,16Hence, this study was undertaken to identify species of Candida isolated from the clinical cases of VVC.
MATERIAL AND METHODS
The present study was carried out in the Department of Microbiology, SMIMER medical college, Surat during the period of July 2010 to October 2011. Total 410 OPD patients who were attending department of Obstetrics and Gynaecology with complain of abnormal vaginal discharge were included in the study.A detailed history of patients was taken. All procedures were done under aseptic precautions and with standard protocol.
1 Collection of sample
The amount, colour, character and smell of vaginal discharge were noted. The discharge was then collected by two sterile swabs from upper part of the posterior fornix and lateral vaginal walls.
2 Processing of Specimen
First swab was used for preparation of smear for direct Gram’s staining. Second swab was inoculatedonto Sabouraud’s dextrose agar supplemented with 0.05g/L Chloramphenicol. Culture plate was incubated at 37?C for 48 hours, cultures were examined for pasty, creamy and smooth white colonies of yeasts.Colonies were confirmed by gram’s stain examination for oval budding yeast cells and further species identification done by battery of test.
3 Tests for Identification of Candida Species
A) Germ Tube Test (GTT)-
The suspected Candida colonies were inoculated into 0.5 ml human serum in a small test tube.Reading were taken after 2 -3 hrs of incubation at 37º C.A drop of suspension was examined on slide under microscope for germ tube productiontrue hyphal structure.
B) Test for Chlamydospore formation –
Pure culture of Candida species was inoculated on CornMeal agar and Dalmau plate culture was done.Inoculated plateswere incubated at 30°C for 24-48 hrs.At the end of incubation, examined microscopically through the cover slip and observe for the presence of chlamydospore.
C) Carbohydrate Assimilation testsSugar
Assimilation test was performed using following sugars. Glucose, Sucrose, Maltose, Lactose, Cellobiose, Raffinose and Trehalose.
Procedure
2-3 colonies were taken and suspension was prepared in normal saline.Lawn culture was done on Yeast Nitrogen Base (YNB, Sugar free medium).Carbohydrate discswere placed onto the surface of plateand incubated at 37°C. Results were read after 20-24 hours.In case of insufficient growth plates were further incubated till 48hours.Utilization of particular carbohydrate was determined by presence of growth around the disk.
D) Carbohydrate fermentation tests
Carbohydrate fermentation was performed for glucose, sucrose, maltose and lactose.
Procedure
1-2colonies of 1 mm diameter was inoculated into sugar fermentation tubes containing the appropriate sugars and Durham’s tubes. Inoculated tubes were incubated at 24°C for up to 1 week. Tubes were examined at 48 hours intervals for acid production (yellow colour) and gas formation (in Durham’s tubes).Production of gas indicates fermentation while only acid formation may indicate that the sugar has been assimilated. The reactions were read as A/G for each sugar separately.
E) CHROM agar Candida Differential Medium
Suspected Candida colonies from SDA agar was inoculated onto CHROMagar. The plates were incubated at 30°C for 48-72 hrs. The different Candida species shows following colours of colonies:
Results: Total 122Candida species were isolated out of 410 vaginal swab specimens. Out of 122 isolates 78were germ tube test positive while 44 isolates showed negative germ tube test. Inoculation on CHROMagar shows following results: C.albicans 81/122(66.39%), C.glabrata19/122(15.65%), C.tropicalis 12/122(9.85%), C.parapsilosis 6/122(4.91%), C.krusei 3/122(2.40%),C.guilliermondii 1/122(0.80%) (Table-1,Graph-1,Fig-1). We have considered CHROM agar as gold standard test. Inoculation on Corn meal agar had shown following results: C.albicans 81/122, C.glabrata17/122, C.tropicalis 11/122, C. parapsilosis 6/122, C.krusei 3/122, C.guilliermondii 1/122. Carbohydrate fermentation test results: C.albicans77/122, C.glabrata 17/122, C.tropicalis 10/122, C. parapsilosis 5/122, C. krusei 3/122,C.guilliermondii 0/122. Carbohydrate assimilation test had shown following results: C.albicans 78/122, C.glabrata 17/122, C.tropicalis 11/122, C. parapsilosis 5/122, C. krusei 3/122, C.guilliermondii1/122 (Table-1,Fig-2). The species isolates amongst the pregnant patients were:C.albicans 78.04% (n=32), C.glabrata 9.70% (n=4), C.tropicalis 2.4% (n=1), C.parapsilosis 2.4% (n=1), C.krusei 7.3% (n=3), C.guilliermondii 0 % (n=0) (Graph-2). The species isolates amongst the diabetic patients were:C.albicans 23.52% (n=4), C.glabrata 47.05% (n=8), C.tropicalis 17.64% (n=3), C. parapsilosis 5.88 %( n=1), C. krusei 0 % (n=0), C.guilliermondii 5.88 % (n=1) (Graph-2). The species isolates amongst the OCP users were:C.albicans 55.55% (n=10), C.glabrata 5.50% (n=1), C.tropicalis 33.33% (n=6), C. parapsilosis 5.5 %( n=1), C. krusei 0 % (n=0), C.guilliermondii 0 % (n=0) (Graph-2). The species isolated from PLWH patients were allC.albicans100 % (n=7)(Graph-2).
DISCUSSION
Despite therapeutic advances, vulvovaginal Candidiasis remains a common problem worldwide, affecting all strata of society.5 Candidial infections are more dynamic than other diseases prevailing in the community.11Their epidemiological profile varies from country to country and from one region to another within a country depending upon demographic, socio-economic and health factors.23 There is always a need of a medium whichhelps not only in the isolation but also in the identification of the agent at the species level.1 CHROMagar is a differential medium being widely used to differentiate Candida species.2 It facilitates the detection and identification of yeasts from mixed cultures and can provide results in24 to 48 hrs sooner than standard isolation and identification procedures.24It is superior to SDA in terms of suppressing the bacterial growth.A major advantage ofCHROMagar is the ability to detect mixed cultures of yeasts in clinical specimens.1,3Although CHROMagar appears to be quite accurate in identifying the most common Candida species, it is not proposed as a substitute for standard identification protocols.24 Sensitivity of GTT in our study is 96.2% which is quite comparable with J.E. Hoppe et al25(98.9%) and Arthur E. Crist et al26(94.7%). As shown in table 2 Candida albicans was the major pathogen causing VVC in various studies. Candidaalbicans produces protease, phosphates and carbohydrates which enhance its attachment to human epithelium7 .So, C. albicans is more adhesive than other non-C.albicans species (This could be considered as one of the likely reasons that this species are predominant rather than non-C. albicans species) 5 . In present study the incidence of C. albicanswas 66.39% which is quite comparable with the studies of K.kikani et al (66%)5, Vijaya et al (66%)9 ,Latha Ragunathanet al(65%),7 K Dota et al (65%)12and Emam et al8 (68.9%) (Table-2). As per Table 2 the incidence of non-albicans species is very similar to findings of Ritcher et al6 , Latha Ragunathan et al7 and Emam et al. 8 C. glabrata found second common spp. after C. albicans in most of the studies. In this study the incidence of C.glabrata is 47.1% in diabetic patientswhile it was 39%in Goswami et al13 and 61.3% in Ray et al14in diabetic patients(Table-3). Incidence of vaginal candidiasis is remarkably higher during pregnancy due to physiological changes.10Various study has reported incidence of symptomatic vaginal candidiasis high in pregnancy and increases during the course of gestation.18C.albicans was most frequently isolated also in pregnancy 78.04 % in this study. Oviasogie F.E et al10 has reported 61.5% and Dias L.B et al17 has reported 92.3% C.albicans in pregnant patients (Table-3).
CONCLUSION
In our study most common species was Candida albicans in cases of VVC. Candida glabrata was the most common species in diabetic patients and Candida albicans was the most common in HIV. In India there is an increase in prevalence of non-albicans Candida spp.due to increase in immunocompromised patients. This also specifies the need of species identification and antifungal susceptibility as a part of the laboratory diagnosis of vaginal candidiasis. CHROM agar is very good medium for species identification of Candida isolates, which give result in short time compared to other methods of species differentiation.This will ultimately help clinician to choose appropriate antifungal in cases of VVC.
Abbreviations:
VVC-Vulvovaginal Candidiasis SDA-Sabouraud’s Dextrose agar NAC-Non albicans Candida DM-Diabetes Mellitus HIV-Human Immunodeficiency Virus PLWH-Patient Living With HIV AG-acid,gas production GTT-Germ Tube Test CHROM Agar- Chromogenic agar OCP –Oral Contraceptive Pill
ACKNOWLEDGEMENT
Authors would like to thank Dean and Medical Superintendent,SMIMER Medical College and hospital for allowingus to carry out this study and for providing thefacilities and help. We are also thankful to the Head of Department Obstetrics and Gynecology, SMIMER Medical College and hospital for allowing us to collect the specimens from their patients. Weacknowledge 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=369http://ijcrr.com/article_html.php?did=3691. V. P. Baradkar, M. Mathur, S. KumarHichrom. Candida agar for identification of Candida Species.Indian Journal of Pathology and Microbiology-53(1)January-March 2010.
2. Shivanand Dharwad, Saldanha Dominic R.M.Species Identification of Candida Isolates in Various Clinical Specimens with Their Antifungal Susceptibility Patterns Journal of Clinical and Diagnostic Research. 2011 November (Suppl-1), Vol-5(6): 1177-1181.
3. Sayyada Ghufrana Nadeem, Shazia Tabassum Hakim,Shahana Urooj Kazmi.Use of CHROMagar Candida for the presumptive identification of Candida species directly from clinical specimens in resource-limited settings Libyan J Med 2010, 5: 2144 - DOI: 10.3402/ljm.v5i0.2144
4. Kelen F. D. Dota, Alessandra R. Freitas, Marcia E. L. Consolaro, Terezinha I. E. Svidzinski.A Challenge for Clinical Laboratories: Detection of Antifungal Resistance in Candida Species Causing Vulvovaginal Candidiasis. Journal of Lab medicine February 2011 Volume 42 Number 2.
5. Sandra S. Richter, Rudolph P. Galask,Shawn A.et al.Antifungal Susceptibilities of Candida Species Causing Vulvovaginitisand Epidemiology of Recurrent Cases Journal Of Clinical Microbiology, May 2005, p. 2155–2162.
6. Kikani K M. Species Distribution And Antifungal Susceptibility Pattern In The Cases Of Vaginal Candidiasis In Saurashtra Region Of Gujarat. Electronic Journal of Pharmacology and Therapy.January 1,2010.
7. Latha Ragunathan, Poongothai G.K, Annie Rofeena Sinazer et al Characterization and Antifungal Susceptibility Pattern to Fluconazole in Candida species Isolated from Vulvovaginal Candidiasis in a Tertiary Care HospitalJournal of Clinical and Diagnostic Research. 2014 May, Vol-8(5): DC01-DC04.
8. Sherin M Emam, Abeer A Abo Elazm and Ahmed Walid A.Exoenzymes Production and Antifungal Susceptibility of Candida Species Isolated from Pregnant Women with Vulvovaginitis. Journal of American Science 2012;8(12).
9. Doddaiah Vijaya, Tumkur Anjaneya Dhanalakshmi, Sunanda Kulkarni.Changing Trends of Vulvovaginal Candidiasis Journal of Laboratory Physicians / Jan-Jun 2014 / Vol-6 / Issue-1.
10. Oviasogie FE, Okungbowa FI. Candida species amongst pregnant women in Benin city, Nigeria: Effect of predisposing factors. Afr J Clin Exper Microbiol 2009;10:92-8.
11. Neerja J,Aruna A,Paramjeet G. Significance of Candida culture in women with vulvovaginal symptoms. J Obstet Gynecol India 2006;56:139-41.
12. Kelen F. D. Dota, Alessandra R. Freitas, Marcia E. L. Consolaro, Terezinha I. E. Svidzinski.A Challenge for Clinical Laboratories: Detection of Antifungal Resistance in Candida Species Causing Vulvovaginal Candidiasis. Journal of Lab medicine February 2011 Volume 42 Number 2.
13. R.Goswami,V Dadhwal,S.Tejaswi et al.Species-specific prevalence of vaginal Candidiasis among patients with Diabetes mellitus and its relation to their glycemic status Journal of infection (2000)41,162-166 .
14. Debarti Ray ,Ravinder Goswami, Uma Banerjee et al. Prevalence of Candida glabrata and Its Response to Boric Acid Vaginal Suppositories in Comparison With Oral Fluconazole in Patients With Diabetes and Vulvovaginal Candidiasis;Diabetes and vulvovaginal candidiasis;Diabetes Care, volume 30, number 2, february 2007.
15. Reza Faraji, Mehr Ali Rahimi, Fatemeh Rezvanmadani and Masoud Hashemi: Faraji et al.Prevalence of vaginal candidiasis infection in diabetic women10 January, 2012.
16. Abdullah Al-mamari, Mahmoud Mahyoob Al-buryhi and Sadeq Al-hag.Species-specific prevalence of vaginal candidiasis with type 1 and type 2 diabetes mellitus among women in Sana’a city Journal of Chemical and Pharmaceutical Research, 2013, 5(8): 217-224.
17. Luciana Basili Dias, Márcia de Souza Carvalho Melhem, Maria Walderez Szeszs et al.
18. Vulvovaginal Candidiasis In Mato Grosso, Brazil: Pregnancy Status, Causative Species And Drugs Tests. Brazilian Journal of Microbiology (2011) 42: 1300-1307.
19. Rui Fernandes Ana Viegas Fatima CerqueiraCandida Species distribution in clinical samples Revista da Faculdade de Ciencias da Saude.ISSN 1646-0480. 6 (2009) 264-271.
20. Patrick Williams Narkwa B.Sc (Hons) ;Antifungal Susceptibility Of Candida Species And Cryptococcus Neoformans Isolated From Patients At The Komfo Anokye Teaching Hospital In Kumasi;February, 2010.
21. Chander J. Candidiasis. In: A textbook of Medical Mycology, 3rd ed. Mehta Publishers, New Delhi, 2009; 266-90.
22. Fran Fisher,Norma cook,Fundamentals of diagnostic mycology,Philadelphia.W.B saunders company 1998;197-222.
23. Deepa Babin, Subbannayya Kotigadde, P.Sunil Rao et al. Clinico-mycological profile of vaginal candidiasis in a tertiary care hospital in Kerala International Journal of Research in Biological Sciences 2013; 3(1): 55-59.
24. Veena Manjunath , Vidya GS, Archana Sharma, Mridula Raj Prakash et al. Speciation of Candida by Hicrome agar and Sugar assimilation test in both HIVinfected and non infected patients. Int J Biol Med Res. 2012; 3(2):1778-1782.
25. J.E. Hoppe, P. Frey;Hoppe et al;Evaluation of Six Commercial Tests and the Germ-Tube Test for Presumptive Identification of Candida albicans ;Eur J Clin Microbiol Infect Dis (1999) 18 :188–191.
26. Arthur E. Crist, Theresa J. Dietz, And Kristin Kampschroer; Comparison of the MUREX C. albicans, Albicans-Sure, and BactiCard Candida Test Kits with the Germ Tube Test for Presumptive Identification of Candida albicans; Journal Of Clinical Microbiology, Oct. 1996, p. 2616–2618, Vol. 34, No.10
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241724EnglishN2015December20HealthcareDIAGNOSTIC ENZYMES IN PERIODONTAL DISEASE
English1317Deepti GattaniEnglish Akhilesh ShewaleEnglish Sakshi DubeyEnglish Snehal DeotaleEnglishPeriodontal disease is a Chronic inflammatory disease that affect the connective tissue attachment and supporting bone around the teeth. It is widely accepted that the initiation and the progression of periodontitis are dependent on the presence of virulent microorganisms and the host response of the individual to this pathologic infection. Host responses to the periodontal disease includes the production of different enzymes released by connective tissue, epithelial or inflammatory cells. The enzymes like acid phosphatase (ACP), alkaline phosphatase (ALP), aspartate or alanine aminotransferase(AST, ALT) and gama glutamyl transferase (GGT)are associated with cell injury and cell death. aAlterations in enzymatic activity reflects metabolic changes in the inflammatory state of the gingiva and periodontium. Hence it is important to have a knowledge about this enzymes to have an insight in the disease activity. Thus, the aim of this review is to provide a comprehensive details about various enzymes associated with periodontal disease activity .
EnglishChronic inflammatory disease, Gingival crevicular fluid, Periodontal diseaseINTRODUCTION
Prior to the 1980s, periodontitis was assumed to afflict all humans and to progress from gingivitis in a slow continuum until teeth were eventually lost .Studies since then have demonstrated these assumptions to be untrue for some individuals. For example disease activity may occur in episodes or bursts at a limited number of sites during a defined interval, with the clinical duration of activity occurring in short periods from days to months. On the other hand, there is evidence that indicates some sites in certain patients manifest periodontal breakdown that is slow but continuous in its progression. Importantly, there appears to be a small population of periodontal patients who do not respond to treatment and continue to lose attachment despite the best treatment provided. The ability to identify these various patients and diseases is poor. To avoid over treatment and to treat progressive disease appropriately, there is a need to distinguish between stable and progressive disease sites and to assess when these sites are adequately treated. Traditional diagnostic instruments, such as the periodontal probe and radiographs are inadequate in diagnosing disease activity as they indicate past tissue destruction and cannot distinguish prospectively between a progressive and a stable site. Thus ,to develop a diagnostic test, one must first define the parameters to be analyzed. For periodontics, the principal features to be established are the presence/absence of disease. Other features such as disease severity, current disease status and the possibility of future progression should also form part of the diagnostic process. A test that is easy to perform, particularly if it has chair side application and that is able to diagnose disease at a particular site will ensure periodontal treatment that is more effective and rational.
Clinical importance of enzymes
1. Enzymes are the biocatalysts, which regulate the rates at which all physiologic processes take place and it has got the central role in health and disease.
2. In liver cirrhosis, the important key enzymes, which are responsible for urea formation, are impaired. As a result, there is ammonia intoxication and ultimately hepatic coma.
3. In the impairment of enzymes, digestion of foodstuffs is stopped causing mal absorption and metabolic dis turbances. The net result is no energy production and no growth of the body.
4. Measurements of increased or decreased concentrations of certain enzymes in blood serum provide valuable diagnostic and prognostic information of the physicians.
Host response to periodontal infections includes the production of several families of enzymes that are released by stromal, epithelial or inflammatory cells(Table 1). Studies of these enzymes in Gingival crevicular fluid may lead to insights into pathogenesis and may provide a rational basis for the development of novel diagnostic tests.
Potential Disease Markers in Gingival crevicular fluid(Table 1)
I. Biochemical Mediators and products of inflammation
1. Antibodies to periodontal bacteria.(PA Murray et al, 1989)
2. Cytokines (HJ Lee et al, 1995)
3. Complement (FJ courts et al, 1977)
4. Prostaglandin (PA Heasman et al, 1998)
5. α2-macroglobulins and α 1-antitrypsin (A Gustafsson et al, 1994)
6. C-reactive protein. (E Megson et al, 2010)
7. Myeloperoxidase. (QT Smita et al, 1986; CF Cao et al, 1989)
II. Extra cellular matrix components
1. Collagen (JT Talonpoika et al, 1994)
2. Proteoglycans and Glycosaminoglycans (Smith AJ et al, 1997)
3. Osteonectin (Bowers MR et al,1989)
4. Osteocalcin (Kunimatsu K et al, 1993)
5. Fibronectin (J Talonpoika et al, 1989)
III. Host derived enzymes
1. Collagenase (T Nomura et al, 1998; R Romanelli et al, 1999)
2. Elastase (KG Palkanis et al, 1992; A Gustafsson et al, 1992)
3. Cathepsins (Kunimatsu K et al, 1990)
4. Alkaline phosphatase (Yan F et al, 1995)
5. Aryl sulfatase and β-glucuronidase. (Lamster IL et al, 1994)
6. Aspartase aminotransferase.(Persson GR et al, 1992)
Alkaline Phosphatase
It is active on a wide range of phosphate esters and is widely distributed in various mammalian tissues, but it’s exact role in metabolism is not known. It probably plays a role in calcification and its determination in serum is of practical importance in bone disease (Moss DW, 1982)1 .Analysis of Alkaline Phosphatase activity measured at pH 10 with P-nitrophenyl phosphatase as substrate, have shown that, in human gingival fluid collected from a series of patients, the concentration of Alkaline Phosphatase was found to be significantly correlated with pocket depth (Ishikawa and Cimasoni 1970)2 . ALP is known to be present in PMNS where the enzymes is found exclusively in specific or secondary granules. These cells are probably the main source of enzymes in the gingival sulcus, although it has been shown that oral bacteria, including some gram (-) ve micro organisms typical of sub gingival plaque also produce ALP (Frank RM et al 1978)3 The concentration of ALP in GCF was the best indicator of active disease.( Lamster I.B et al,1992)4 .Chapple IL et al, 1999 5 developed a chair side chemiluminescent assay for the enzyme in sub microtitre volume of GCF and serum and reported that the mean ALP concentration was 2135-IU/L for GCF and 183 IU/L for serum ( 12 fold difference).
COLLAGENASE
The presence of collagenase in GCF has been of particular interest as collagen constitutes one of major extra cellular matrix protein in the periodontium, and because significant destruction of collagen occurs during periodontal destruction. These are specialized enzymes that have evolved specifically to hydrolyze collagens because the triple helical collagen structure is resistant to more common proteinases. They belong to a family of enzymes called Matrix metallo Proteinases (MMPs) that consist of at least 13 members with closely related remain structures and discrete function. Based on their substrate specificity, MMPs are classified as Collagenases ,Geletinases ,Stromelysins ,Matrilysin. These interstetial collagenases capable of degrading native matrix collagen fibrils have be identified so far. Collagenases –I (MMP-1 or fibroblast type collagnase) is produced by a variety of human epithelial and mesenchymal cells types including keratinocytes, fibroblasts and macrophages. This enzyme can hydrolyze type I, II, III, VI, VIII and X collagens and gelatin. It hydrolyzes type III molecules faster than it does type – I. Collagenase-2 (PMN) type collagenase or MMP-8) also hydrolyzes type I and III collagen but their enzymes degrades type I faster than it does type III. Collagenase-2 is found only in the granules of PMNs. Gelatinase Group of MMPs has two prominent members, the 72 kd. (gletinase-A, MMP-2) and 92 kd. (geletainase B O2 MMP – 90 geletinases. Both these enzymes have a high affinity for gelatin, but they also degrade type IV, VII, X and XI collagens and elastin. MMP-9 is produced by eosinophils, macrophages and keratinocytes and it is stored in PMN granules. It’s synthesis is regulated by several inflammatory mediators. MMP-2 is not regulated by most mediators other than TGF-/3 and is produced by most cell types.
Stromelysins have broad specificity with the ability to degrade proteoglycans, basement membranes, laminin and fibronectin, in addition to collagens. Three stromelysein-1 (MMP-3), stromelysein-2 (MMp-10) and stromelysein-3 (MMP 11) have been described. Matrilysin (MMP-7) and metalloelatase (MMP-12) are other MMPs. JM. Korostoff 20006 substantiate the proposed role of hostderived proteases in the pathogenesis of chronic adult periodontitis. Specifically, they indicate that activated MMP-2 and a 40 kd serine protease are involved in tissue destruction associated with this form of periodontal disease. Gul Atilla et al ,20017 evaluated MMP 8 and 9 and neutrophil elastase in GCF of cyclosporin treated patients and Suggested that low GCF PMN-elastase levels can be an important factor in the pathogenesis of Cyclosporin induced gingival over growth. Sabrina Mancini et al 19998 developed and validated a novel specific, simple, rapid and reproducible assay (soluable biotinylated collagen assay; SBA) based on chemiluminescent detection of biotinylated collagen digestion products and its results indicate that active MMP-8 is detected in GCF by this assay that facilitate diagnostic discrimination between stable and progressive lesions. Sylvie Seguier, 20019 under took a study to quantify the amount of MMPs and 71TIMPs (tissue inhibitors of MMPs) in order to investigate the possible correlations between such molecules, collagen loss and inflammatory cell sub sets. The study showed an imbalance between MMPs and TIMPs associated with the pathologic breakdown of the extracellular matrix during periodontitis. This active form of MMP-9 could be marker for the clinical severity of periodontal disease.
Cathepsin D
It is a carboxyendopeptidase and one of the chief acid enzymes in lysosomes, present at high concentration in inflamed tissues, particularly abundant in human mono-nuclear leukocytes, while PMNs contain less enzymes. It’s concentrations was found to be 10 times higher in crevicular fluid than in serum and this concentration was positively correlated with periodontal destruction10.In gingival washings collected from human volunteers, the activities of both free and total cathepsin D were found to increase during a period of experimental gingivitis11. In spite of it’s unphysiological pH, the enzyme may be capable of attacking various components of the connective tissues. Sections of gingivitis cut in a cryostat and exposed to the granular fraction of human leukocytes at a pH of 3-5, which is optimum for cathepsin D activity, showed extensive destruction of both epithelium and connective tissue 12.
Cathepsin G
It Is a serine endopeptidase contained in the azurophil granules of human PMNs and also called chymotrypsin like, because it attacks a number of synthetic substrates typical for chymotrypsin and is inhibited by the same inhibitors .It has an optimum pH of 7.5 and a molecular weight of about 20,000.This Enzyme has been shown to hydrolyze hemoglobin and fibrinogen, casein and collagen13.Determination of cathepsin G was done using N-acetyl-DL-phenylaninnaphthylester, as substrate and fast garnet salt as coupling agent, and its activity could be shown in the concentrated supernatant of gingival washings.
Cathepsin B
GCF cathepsin B was investigated in a Two years longitudinal study by in which the levels of cathepsin B were found to be significantly higher in sites which want on to experience attachment loss.14
Elastase
Neutrophil elastase is a serine endopeptidase that can degrade both collagneous and non collagenous extra cellular matrix proteins. It is released at sites of inflammation.The levels of this enzyme in GCF have been noted to increased with development of gingivitis as well at sites of established periodontitis. In addition, the levels of neutrophil elastase have been found to decrease following treatment of affected periodontal sites15.Longitudinal studies have indicated that GCF levels of neutrophil elastase have some of further breakdown 16. PERIOCHECK® is a rapid chair side kit which detects neutral proteases in GCF 17. The GCF is collected on filter paper and placed in a collagen dye – labelled gel matrix, Where dye – labelled fragments are produced by the neutral collagense activity.These soluble products diffuse into the sample strip, creating a blue color which is in proportion to the neutral activity of the GCF.However the authors confirmed that this test can detect neutral proteases in GCF and reported that the highest neutral protease activity values were found in patients clinically diagnosed as having periodontal disease. However, Jepsen S et al (1996)18 tested the periocheck system in a longitudinal study of peri-implantitis lesions. They found that the neutral proteases test and bleeding on probing had high negative predictive values for future progressive peri-implantitis.
ARYL SULPHATASE AND β-GLYCURONIDASE
These lysosomal enzymes are involved in the degradation of glycosaminoglycans (GAG) and are released by activated PMNs. Following hyaluronidase action of GAGs, β-Glucuronidase may act on oligosaccharides and aryl sulphatase to catalyze the hydrolysis of sulphatase to cata- lyze the hydrolysis of sulphate esters. Lamster IL and Colleagues(1994, 2003) demonstrates that enzymes activity is related to the severity of inflammation and to pocket depth, but there appears to be a stronger relationship between absolute amounts of β-Glucuronidase and pocket depth them with the conc. of the enzymes and also In longitudinal study designs, the activity of β-glucuronidase was significantly elevated during monitoring periods that coincided with attachment loss of 2mm or more . The persistent and Long-lasting elevation of enzymes levels and the strong temporal association with clinical detection of attachment loss indicates that β-glucuronidase may exhibit some of the hall marks of a useful diagnostic test. Measurement of this enzymes may provide an assessment of PMN activity, critical element in the current concept of disease progression.
LYSOZYME
Lysozyme has bactericidal property, linked to its ability to hydrolyse β,1-4, glycosidic bonds of peptidoglycans within the bacterial cell wall. Found in a soluble and free form in fluids like saliva, nasal, gastric and intestinal secretions. Surna A et al ,200919 observed a significantly higher lysozymal activity in crevicular fluid and saliva than in serum. Also reported higher lysozymal activity in patients with severe periodontal destruction. The free enzyme may contribute to the formation of pocket by its detrimental effect upon epithelial cell stickiness and lytic activity upon the ground substance of connective tissue and can also accelerate the local release of intra cellular bacterial enzymes.
Aspartate aminotransferase (AST)
Is an enzyme released from dead cells, and many studies have demonstrated a marked elevation of AST in GCF from sites with severe gingival inflammation and in sites with a history of progressive attachment Loss20. A chair side kit has been developed for detecting GCF AST levels and is called PeriogardTM. This commercially available test kit detects AST in GCF. The GCF is collected using a paper strip which is placed in the crevice for 30S and is then placed in tromethamine hydrochloride buffer, to which a reaction mixture (L-aspartic and L-ketoglutaric acid) is added. After 10 minutes, oxalacetate and glutamate are produced if AST is present, and these react with an indicator such as fast red to produce an easily detectable colour change which is proportional to the GCF AST activity. The problem with using AST is that it has a strong relationship with gingival inflammation, which may or may not be present in site which are actively losing attachment. Persson et al (1995)20 examined the ability of PeriogardTM to distinguish between diseased and healthy sites in a before and after treatment designed longitudinal study.
Pocket watchTM.
The principle of this method is that, in the presence of pyridoxal phosphate, AST catalyzes the transfer of an amino group from cysteine sulfinic acid , by L-ketoglutaric with to yield β-sulfinyl pyruvate and glutamate. AST catalyze the formation of β-sulfinyl pyruvets. β-sulfinyl pyruvate spontaneously and rapidly decomposes and releases inorganic sulfite. The sulfite ion instantaneously reacts with malachite green (MG), simultaneously causing MG to convert from a green dye to its colourless form, thereby allowing the pinkcolored rhodamine B dye to show through. The rate of conversion of MG is directly proportional to the AST concentration.(Shimada K, et al,2000)21
Lactate dehydrogenase
It is a cytoplasmic enzyme in the anaerobic glycolytic pathway. It catalyses the reversible reduction of pyruvate to lactate. Its occurrence extra cellularly indicates cell death. Bang et al (1972)23 found GCF to contain 10-20 times more total LDH than blood. Several studies by Lamster IL et al (1985,1988,1989) have indicated a positive correlation between enzyme levels and inflammation Measurement of LDH is by a spectrophotometric assay, and like AST, it is not possible to known which dying cells are measured O2 where they are located.
CONCLUSION
From available data, it appears that PMN enzymes are not only linked casually to disease progression, but can be readily measured in GCF and will likely provide a good refection of the global host response in the periodontium. Of the enzymes discussed above, currently available evidence supports the efficacy of the MMPs, AST and elastase as the most promising enzyme markers for progressive disease.
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=370http://ijcrr.com/article_html.php?did=3701. Moss DW. Alkaline phosphatase isoenzymes Clin Chem. 1982 Oct;28(10):2007-16.
2. Ishikawa I, Cimasoni G. Alkaline phosphatase in human gingival fluid and its relation to periodontitis. Arch Oral Biol. 1970;15:1401–4.
3. Frank RM, Voegel JC. Bacterial bone resorption in advanced cases of human periodontitis. J Periodontal Res. 1978 May;13(3):251–261.
4. Lamster IB. The host response in gingival crevicular fluid: Potential applications in periodontitis clinical trials. J Periodontal. 1992;63:1117–23.
5. Chapple IL, Garner I, Saxby MS, Moscrop H, Matthews JB. Prediction and diagnosis of attachment loss by enhanced chemiluminescent assay of crevicular fluid alkaline phosphatase levels. J Clin Periodontol. 1999;26:190–8.
6. JM. Korostoff. Analysis of In Situ Protease Activity in Chronic Adult Periodontitis Patients: Expression of Activated MMP-2 and a 40 kDa Serine Protease Journal of Periodontology;March 2000,71(3),353-360.
7. Gül Atilla. Matrix Metalloproteinases (MMP-8 and -9) and Neutrophil Elastase in Gingival Crevicular Fluid of CyclosporinTreated Patients;Journal of Periodontology; March 2001, 72(3), 354-360.
8. Sabrina Mancini Raquel Romanelli Carol Laschinger Christopher M Overall Christopher A.G. McCulloch. Assessment of a Novel Screening Test for Neutrophil Collagenase Activity in the Diagnosis of Periodontal Diseases Diseases; Journal of Periodontology,1999; 70(11):1292-302.
9. Sylvie Séguier. Is Collagen Breakdown During Periodontitis Linked to Inflammatory Cells and Expression of Matrix Metalloproteinases and Tissue Inhibitors of Metalloproteinases in Human Gingival Tissue? .Oct 2001, 72(10), 1398-1406.
10. Ishikawa I, Cimasoni G. Possible role of lysosomal enzymes in the pathogenesis of periodontitis: a study on cathepsin D in human gingival fluid . Arch Oral Biol. 1972;17:111–117.
11. A. Tzamouranis, J. Matthys, I. Ishikawa, Increase of extracellular cathepsin D activity in gingival washings during experimental gingivitis in man. 1977, 22(6),375–378.
12. R, Heiniger, Cimasoni G. Lytic effect of human leukocytic proteases on gingival tissue.1980 Journal de biologie buccale 8 (1): 3-16.
13. Starkey PM, Barrett AJ. (1976) Human cathepsin G. Catalytic and immunological properties. Biochem J 155:273–278.
14. Eley BM, Cox SW. Cathepsin B- and L-like activities at local gingival sites of chronic periodontitis patients. J Clin Periodontol. 1991 Aug;18(7):499-504.
15. Meyle J, Zell S, Brecx M, Heller W. Influence of oral hygiene on elastase concentration of gingival crevicular fluid. J Periodontal Res. 1992 May;27(3):226-31.
16. Armitage GC, Jeffcoat MK, Chadwick DE, Taggart EJ, Jr, Numabe Y, Landis JR et al . Longitudinal evaluation of elastase as a marker for the progression of periodontitis.J Periodontol. 1994 Feb;65(2):120-8.
17. Bowers JE, Zahradnik RT (1989) Evaluation of a chairside gingival protease test for use in periodontal diagnosis. J Clin Dent 1: 106–109.
18. Jepsen S, Rühling A, Jepsen K, Ohlenbusch B, Albers HK Progressive peri-implantitis. Incidence and prediction of peri-implant attachment loss. Clin Oral Implants Res.1996 Jun;7(2):133-42.
19. Surna A, Kubilius R, Sakalauskiene J, Vitkauskiene A, Jonaitis J, Saferis V, et al Lysozyme and microbiota in relation to gingivitis and periodontitis. Med Sci Monit. 2009 Feb;15(2):CR66-73.
20. Persson GR, Alves ME, Chambers DA, Clark WB, Cohen R, Crawford J et al. A multicenter clinical trial of PerioGard in distinguishing between diseased and healthy periodontal sites. (I). Study design, methodology and therapeutic outcome.J Clin Periodontol. 1995 Oct;22(10):794-803.
21. Shimada K, Mizuno T, Ohshio K, Kamaga M, Murai S, Ito K Analysis of aspartate aminotransferase in gingival crevicular fluid assessed by using PocketWatch: a longitudinal study with initial therapy.J Clin Periodontol. 2000 Nov;27(11):819-82.
22. J Bang, C Rosenbush, GCimasoni.Isoenzymes of lactic dehydrogenase in human gingival fluid Helvetica odontologica acta 1972 Nov; 16(2):89-93.
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241724EnglishN2015December20HealthcareASSESMENT OF MEDICAL CERTIFICATE OF CAUSE OF DEATH (MCCD) IN VADODARA MUNICIPAL CORPORATION, GUJARAT, INDIA
English1823A.S. GanasvaEnglish B.R. BariyaEnglish K. ShringarpureEnglish J.R. DamorEnglishBackground: Death certificates are an important source of population-based mortality statistics . This information derived
from death certificates has many important uses right from development of public health programs to allocation of health care resources. There is no adequate training received by the physicians for filling up of death certificates correctly. The resulting inaccuracies in completion of this information undermines the quality of the data derived from death certificates.
Aim and Objective: To assess the completeness of Medical Certificate of Cause of Death (MCCD) and the knowledge, attitude and practices (KAP) of health personnel involved in registration system. Methods: A total of 1947 consecutive death certificates issued by community physicians were collected from 12 administrative wards of 4 zones of Vadodara Municipal Corporation (VMC) during June 2012 to November 2013. Different variables like personal action of deceased, information regarding sequence of the death event (medical part) and medico-legal portion were assessed for its completeness. Simultaneously, knowledge, attitude and practices of Registration of birth and death (RBD) staff related to filling up of the MCCD forms was assessed in different wards of VMC. Results: Out of 1947 MCCD forms only 21 (1.1%) MCCD certificates in the study were completely filled, while 1877 (97%) were notably incomplete, 4 (0.2%) slightly incomplete and 45 (2.3%) grossly incomplete. On assessing KAP of RBD staff, none of them had been imparted the training related to registration system. Almost 87% of them were dissatisfied with the completeness of MCCD-form 4A filled up by private practitioners. Majority of them (68.8%) felt that they were overburdened due to paucity of staff. Conclusion: In conclusion, the combined effort of physicians and RBD staff is required to improve the quality of diagnostic information in death certificates. Thus, more accurate cause-of-death statistics derived from death certificates will lead to better health planning.
EnglishDeath Certificate, KAP, VMCINTRODUCTION
A Death certificate is the formal document in which a physician records the time, cause and circumstances of death of an individual. Studies providing morbidity and mortality statistics are mainly based on the analysis of these certificates [1-3] Consequently, inaccuracies in the completion of death certificates may lead to biased estimation of several epidemiological parameters [4,5]. Almost every physician has to fillat least one death certificate in his/her career. However, teaching the precise wording and formulation of causes of death is not usually included either in undergraduate or in postgraduate medical education [6-9]. Myers and Farguhar examined the impact of an interactive learning method on error rates in the completion of death certificates, reporting a statistically significant decrease in errors[10].
Inaccuracies in the completion of death certificates present a problem, not onlyfrom the legal standpointbut also in collecting relevant vital statistics data from which to draw conclusions. Accordingly, every effort must be made to ensure that the completion of death certificates is performed in the most specific, accurate and complete fashion. Considering all these issues regarding the incomplete and inaccurate documentation of cause of death, the aim of the present study was to assess the MCCD certificates in 12 administrative wards Of Vadodara Municipal Corporation (VMC) in terms of their completeness and accuracy. MCCD certificates filled by clinicians as well as frequency and types of errors committed by the physicians were assessed. The results of the study may prove to be useful for VMC and for Government of Gujarat in general to plan remedial actions for improving filling up of MCCD certificates.
MATERIALS AND METHODS
Study Design:
Descriptive cross-sectional and Knowledge, Attitude and Practice study. Study period: April 2013 to September 2013. Study site:Vadodara Municipal Corporation; consistingof Four zones and twelve administrative wards in Vadodara, Gujarat. Study population: Based on available data, a total of 9710 forms (Form-4A) were filled up in the previous year 2012. A sample size consisting 20% of these forms i.e. 1942 forms were included in the study. To enable equal representation of each of the 12 wards, 231 forms per ward were taken. Therefore, 250 forms from each ward were studied for completeness. All the forms submitted between April 2013 to September 2013 were included in the study, which satisfied the sample size requirement . Out of 16 RBD staff, 4 local registrars and 12 clerks were involved in the Registration of birth and death (RBD). Informed verbal consent was taken from the participants before administering the questionnaire. Staff was interviewed for their knowledge, attitude and practice (KAP) using a pretested semi-structured study instrument.
Data Management and Analysis
Data was entered into MS Excel analysis was carried out using Epi Info (version 1.1.67, developed by WHO CDC[11]. Proportions were computed for easy interpretation of the data. To evaluate the overall completeness of MCCD certificates, a scoring system was developed. In this system a score of one was given for entry of each variable in the certificate. Thus, maximum score for completeness in MCCD certificate was 19. On the basis of total score of each form they were divided into four different categories. These categories are described in Table-1. • Each variable was categorised into one of the TWO status. These TWO categories of the variables were as follows: 1. Left blank and was correct (they were rightly left blank so they were considered as qualified for completeness) 2. Left blank but was incorrect. The columns, which were left blank in MCCD forms, were considered as incomplete.
Ethical clearance:
Ethical clearances and written permissions were obtained from concerned authority including Institutional Ethics Committee for Human Research (IECHR) prior to data collection. The process of data collection did not pose any potential risk or harm to the participants. Data safety and confidentiality was also given due consideration.
RESULTS
Total 1947 MCCD certificates filled up by private practitioners from 12 wards of Vadodara Municipal Corporation were included in the study. Different variables like personal information of deceased, information about sequence of death event (medical part) and medico-legal portion were assessed for its completeness. C
COMPLETENESS OF MCCD FORMS
Completeness in terms of filling up of name and age was 95.1% and 91.2% respectively, while gender was mentioned only in 54.3% of the forms. Date and time of death was mentioned in almost all the forms.(Percentage??) Immediate cause of death was noted in 95.9%, while the time interval between immediate cause and death was noted only in 2.6% of forms. Antecedent cause was filled in 27 % and underlying cause was filled in only 0.8%. Time interval between antecedent and underlying cause and death decreased to 1.4 % and 1.1 % respectively. Though other significant conditions were mentioned in 12.9%, time interval between other conditions and death was filled in only 2.6% of the forms. There was no form mentioning death associated with pregnancy. Manner of death was written in 88%. The forms were completed with name and signature in almost 99.5% while date of verification was present in only 34%.(Table-2) The analysis revealed that 21(1.1%) MCCDs were found completely filled. But, on lowering the criteria of completeness to a condition (slightly incomplete) where less than 15% columns were left blank; such slightly incomplete data were found in only 4 (0.2%) MCCD certificates. Most of MCCD forms were found notably incomplete (96.19%) and 45 (2.3%) MCCD forms were grossly incomplete (Table- 3, Figure-1). Out of 12 clerks, 3 were Graduates, while 9 of them had passed HSC examination. SI had completed Sanitary Inspector course after Higher Secondary Education. Majority of them (62.6%) had more than 5 years experience. Rest of them 43% (n=7) had more than 10 years experience of working in the registration system. Though no training was given to registration staff related to registration system,knowledge about rules for birth and death was satisfactory. Almost 87% of them were not satisfied with the completeness of MCCDform 4A which is filled up by private practitioners. In all ward offices, death certificates were available in computerised format. They all felt that there was lack of supervision of their work by higher authority. Majority of them (68.8%) felt that they were overburdened due to lack of sufficient staff.
DISCUSSION
Death certificate has been used as a health indicator and as a monitoring tool for public health policy. It enables us to describe disease patterns within a specified population. Moreover, the absence of reliable data on causes of death impedes the structuring of health-related activities and can thus result in misleading appraisals of research and improper decisions regarding health care. To meet this need, medical students and interns are taught about Death Certificate all over the globe [4]. However, despite repeated instructions and training workshops for clinicians, frequency of error remains more or less static . Hence this study included evaluation of death certificate, assessment incompleteness found in medical and non-medical part of certificate KAP???. Although name and age were mentioned in most cases, sex was not filled up in 106 (5.4%) cases. This may be due to ‘doctor being in a hurry’ or ‘lazy attitude of doctor’. This finding of our study is consistent with the study by G. Maudsley and EMI Williams of University of Liverpool in Journal of Public Health Medicine[13]., this picture points towards ‘attitude’ of certifier. They have further also stated that the major factors deficient in death certification is lack of ‘routinized orientation’ and Proper attitude of certifier i.e,the doctor .Apart from these causes , other errors of Non-medical part of certificate seems beyond the scope of this study [13]. Other investigators have derived similar [12]. Although there is a need to change this mindset, it cannot be done by a single individual. Strict action against erring doctor needs amendments in law. Citing an example from the Texas law, there are fines and penalties to physician for delaying death certification [13]. This study shows that only 21 out of 1947 (1.1%) MCCD certificates were completely written. EL-Nour et al found 1.8% certificates incompletely filled in a study conducted in paediatric hospitals of Khartoun state of Sudan during 2007[14].Another study by Venu states that the Overall completeness after giving score to each variable showed that, only 20(1.2%) MCCD forms were found completely filled [15]. During 1993, Hanzlick [16] reviewed 56 death certificates, and observed that 63% of certificates showed either omission or error in Cause of death This study found lower frequency of incompletely written death certificates., may be because death certificate were obtained from a teaching hospital. The accuracy of the death certificate could be audited and confirmed from a complete medical record. The best certifier should be the treating physician of the deceased who recorded all details of his/her condition on the medical record so as to put them in proper sequence in the death certificate. Most of the doctors do not refer to the corresponding diagnoses in the medical record to identify the underlying cause of death, the antecedent cause(s) and the direct cause of death . In our study 570(30.1%) certificates were not followed by proper underlying cause of death. The reason behind this may be inadequate knowledge of the certifying doctor to the illness of the deceased as the doctors are called in after death of the patient, just to fill up the Death Certificate. In this study, most of MCCD forms were found notably incomplete 1877 (96.19%) and 45 (2.3%) MCCD certificates were grossly incomplete in non-medical part of 1947 D.C. This simply suggests that doctors do not write death certificates scrupulously. This study observed that 99% have legible signature or name of doctor mentioned, but 55.7% of certificates did not have mentioned date of verification at the bottom of certificate. Pediatric hospitals of Sudan had observed 18% of certificates were not signed by doctors [14]. In Beirut, almost 50% of certificates did not contain signature of certifier [12]. ‘Omission’ in writing details of ‘Identity’ of deceased was found in 5% of certificates. 5 % and 10% of certificate did not mention sex and age of deceased respectively. B Swift and K West of Dept. of Histopathology from UK observed 10% of certificates were of very poor standard, illogical and inappropriately completed [12]. Also the RBD staff in our KAP study stated that birth certificate details are filled with caution by majority of institutions, but this is not so in case of death certificates. The reason being, that most of the births occur in hospitals wherein the medical records and date of birth are readily available, which is not the case in the occurrence of deaths. Bloor recognised that there were frequent and infrequent certifiers [12]. He described the completion of death certificates as ‘unsupervised, unreported, invisible and unconsidered’. In our KAP study,RBD staff expressed their worry about lack of enough supervision by higher authority. The staff expressed that they were not satisfied with present status of completeness in MCCD (form 4 A) and felt the need to verify death certificate. Finding reasons for incompleteness in form 4A provides scope for further research in this study.
CONCLUSION
• Only 21 (1.1%) MCCD certificates in the study were found completely filled, while 97% were notably incomplete. Forms were almost complete in terms of date and time, immediate cause and manner of death. They were incomplete in terms of antecedent cause and time interval between cause-both immediate and antecedent and death.
• The knowledge and skill of RBD staff was found to be adequate. They had a felt need of supervision of their work and training.
RECOMMENDATION
• There is a pressing need for appropriate interventions to improve and enhance the accuracy of physicians’ death certificate and completion skills.
• Emphasis on time interval between the onset of the condition and death for each condition viz. immediate cause, antecedent cause and underlying cause in future trainings and the impact of refresher trainings needs to be evaluated.
• Workload of RBD staff can be reduced by filling up the vacant posts in RBD system.
• Public private partnerships (with IMA, UNICEF, NGOs like PRIA for advocacy and training) would help to create political will and ensure speedier implementation of more universal death certification.
Englishhttp://ijcrr.com/abstract.php?article_id=371http://ijcrr.com/article_html.php?did=3711. Smith Sehdev AE, Hutchins GM. Problems with proper completion and accuracy of the cause-of-death statement.Archives of Internal Medicine 2001; 161: 277-284.
2. Kircher T, Anderson RE. Cause of death: proper completion of the death certificate. The Journal of American Medical Association 1987; 258:349–352.
3. Crowcroft N,Majeed A. Improving the certification of death and the usefulness of routine mortality statistics. Clinical Medicine 2001;1:122-125.
4. Messite J, Stellman SD.Accuracy of death certificate completion: the need for formalized physician training. The Journal of American Medical Association 1996; 275:794-796.
5. Armour A,Bharucha H.Nosological inaccuracies in death certification in Northern Ireland. The Ulster Medical Journal 1997; 66: 13-17.
6. Jordan JM, Bass MJ. Errors in death certificate completion in a teaching hospital. Clinical and Investigative Medicine 1993;16:249-255.
7. Peach HG, Brumley DJ. Death certification by doctors in non-metropolitan Victoria. Australia Family Physician 1998; 27: 178-182.
8. Lionis C, Sasarolis S, Kasotakis GI, Lapidakis GM, Stathopoulos AI. Investigation of accuracy of death certificate completion and implications on mortality statistics in Greece. European Journal of Epidemiology 2000;16:1081.
9. Slater DN. Certifying the cause of death: an audit of wording inaccuracies. Journal of Clinical Pathology 1993; 46:232-234.
10. Myers KA, Farquhar DRE. Improving the accuracy of death certification. Canadian Medical Association Journal1998; 158:1317-1323.
11. To cite Epi in publications use: Bendix Carstensen, Martyn Plummer, Esa Laara, Michael Hills (2014). Epi: A Package for Statistical Analysis in Epidemiology. R package version 1.1.67. URL http://CRAN.Rproject.org/package=Epi 1
2. Pritt BS, Hardin NJ, Richmond JA, Shapiro SL. Death certification errors at an academic institution. Archives of pathology and laboratory medicine. 2005;129(11):1476-9.
13. Maudsley G, Williams EM. Death certification by house officers and general practitioners--practice and performan
14. El-Nour AAM, Ibrahim YAH, Ali MM. Evaluation of death certificates in the pediatric hospitals in Khartoum state during 2004, Sudanese Journal of Public Health: Jan. 2007, Vol.2(1).
15. Venu r shah*1, bala d. v2 evaluation of medical certification of cause of death in one of the teaching hospitals of ahmedabad.
16. Hanzlick R: Protocol for writing cause-of-death statements for death due to natural causes. Arch Intern Med 1996;156:25–26
17. Swift B, West K. Death certification: an audit of practice entering the 21st century
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241724EnglishN2015December20HealthcareIMMUNOTHERAPEUTIC TREATMENT OF HIV-1: REVIEW OF SAFETY AND EFFICACY
English2429KariukiEnglish SMEnglish MusyokiEnglish SK and KemoiEnglish EKEnglishBackground: For over two decades, the treatment of HIV-1 patients has relied on antiretroviral (ART). These drugs have had a great deal of achievement in not only controlling the viral load but also partly reconstituting the immune system in HIV-1 infected persons. However, the misfortune is that ART is a lifelong treatment because it cannot achieve complete eradication of HIV-1 virus, yet with its side effects like many other drugs. Scientists have hence introduced immunotherapy in an effort toward complete eradication of HIV-1 in HIV/AIDS patients.
Objective: The aim of this paper was to determine the effectiveness and safety of the various immunotherapy formats used in the treatment of HIV-1 infection.
Method: We reviewed a number of peer-reviewed published articles to determine the effectiveness and safety of the different immunotherapy formats tested in randomized clinical trials and animal model experiments.
Results: Majority of immunotherapy regimens used in combination with ART to treat HIV-1 positive human or animals were found to be effective in boosting the cell-mediated immune responses in HIV-1 infection but achieved insignificant results in controlling the viral load in these experiments. Most of the immunotherapy formats were also well tolerated recording minimal to no adverse effects on HIV-1 patients.
Conclusion: Most immunotherapy agents are relatively effective and safe when used in combination with ART in modulating immune response to HIV-1. These immunotherapy agents do not significantly reduce the viral load and hence cannot eliminate HIV-1.
EnglishImmunotherapy, HIV-1, ART, HIV/AIDS, Effectiveness, Efficacy, SafetyINTRODUCTION
The traditional treatment of HIV/AIDS patients for the past two decades has been anti-retroviral drugs (ART). While these drugs have performed relatively well in dramatically keeping the viral load down and partly reconstituting the HIV-specific CD4+ T cells (1), anti-retroviral have been unable to completely clear the virus in its reservoir tissues in the body (2) and little is known about the effect of ART outside the peripheral blood circulation (3). As such these drugs are taken for life which means the patients suffer from their side effects as long as they live using them. Immunotherapy is the alternative that has emerged in the recent past years where significant amount of research is ongoing to determine its effectiveness and safety in the treatment of HIV/AIDS. Immunotherapy assists the natural immune system to control HIV infection (4). Two types of immunotherapy are being pursued by researchers i.e. “a sterilizing cure” where there is elimination of HIV-1 infected cells from the body and “functional cure” an effective human host immunity modulation which achieves a lifelong suppression of the virus replication (4). Some of the challenges that make it difficult to achieve complete control of HIV replication is the inability by the vaccines to sufficiently activate the immune system (5) and inability to eliminate the latent state of the virus (6). Several approaches have been employed to make various formats of immunotherapy. Some are non-antigenic approaches like the administration of specific cytokines which stimulate the immune system or down regulate viral replication (7). Another approach involves administration of antibodies meant to block the entry of HIV into the host cells (8). Other formats of immunotherapy against HIV virus are induction of effective CD8 T cells and harnessing dendritic cells (DC) function in order to improve the quality of T cell immune responses (4). There are a number of success stories that have been published in relation to immunotherapy in the treatment of HIV1 but the most interesting one is that of the HIV-1 patient in Berlin with acute myelogenous leukemia who received graft from a donor with polymorphism that confers resistance to HIV-1 infection. As a result, this patient remained negative for over 3 years without using anti-retroviral therapy (9). This article reviews published peer-reviewed articles on different formats of immunotherapy against HIV-1 virus to determine the effectiveness and safety of this kind of treatment. (1) says that despite some positive immunomodulation results that have been reported in animal models, there is potential for toxicity of these immunomodulators in human. Data from both randomized clinical trials (RCT) and experiments on animal models of HIV-1 will be reviewed. In the principles of immunotherapy, there are three approaches mainly used (10). These are: Non-specific enhancement of antiviral immune response by various immune stimulating cytokines including type-1 IFNs, IFN-γ, IL-12, and γ–chain signalling cytokines related to IL-2 (10). Blocking antibodies against immune suppressive receptors such as PD-1 and CTLA-4 could also provide beneficial immune stimulation (11). Antigenic formats to induce HIV-specific T cell response in order to elicit more effective CD8 T Cell-mediated immune surveillance (10). DISCUSSION FOR REVIEW a) Cytokine therapies Interferon-gamma (IFN-γ) Serum IFN-γ in the acute phase of HIV-1 infection has been shown to reduce the replication of the virus in both CD4+ and monocytes-macrophage cells (4). However, according to this article the role of IFN-γ in the chronic phase of HIV-1 is not clear since the increased activity of IFN-γ markers like β2 –microglobulin and neopterin lead to poor HIV-1 infection prognosis. Therefore IFN-γ might be helpful in the initial stages of HIV-1 infection but not in the full-blown AIDS. Of the many opportunistic infections in HIV positive patients is the cryptococcal meningitis caused by Cryptococcus neoformans. In some studies, Interferon gamma (INF-γ) monotherapy as opposed to type 1 IFNs (which have antiviral activity) is said to have no direct antiviral activity against HIV-1 as demonstrated in primary cultures, in invitro studies and ex vivo studies (12). These studies have in fact showed a possible negative role where INF-γ increases HIV-1 replication and hence their safety and efficacy cannot be guaranteed. However, the use of INF-γ in combination with the standard therapy in HIV-associated cryptococcal meningitis has been suggested in the past, to reap its benefits. In a randomized clinical trial, (13) demonstrated that treatment of HIV-positive patients with standard treatment (Amphotericin-B 1mg/kg/day plus 5-FC 100mg/kg/day for 2-weeks) in combination with 2 or 6 doses of INF-γ cleared Cryptococcus neoformans from cerebral spinal fluid (CSF) faster than the standard therapy alone (p=0.02 for 2 doses of INF-γ and p=0.006 for 6 doses of INF-γ) (Table 1). This immunotherapy treatment was well tolerated raising no additional adverse effects compared to standard therapy only.
Interleukin-2 (IL-2)
Many immunotherapy formats target to stabilize the immune system and suppress the viral load permanently, while at the same time eliminating the need to continue with the use of highly active antiretroviral drugs (HAART). Interleukin-2 (IL-2) combination with ART is known to increase CD4+ T cell responses in HIV infection and has been approved in some European Countries for use as an immunotherapy agent (14). A phase II randomized, partially blinded 2x2 factorial study found administration low dose of IL-2 to chronically infected HIV-1 patients not helpful in controlling viremia relapse after discontinuation of HAART, but induced significant levels of CD4+ T cells (10). The therapy had been administered to patients with undetectable HIV-1 RNA and CD4 T-cells count of >400 cells/µl and compared to placebo. In that study even when the low-dose of IL-2 was combined with a ALVAC vCP1452 (Canarypox) vaccine it was still found not effective in preventing replication of HIV-1 once HAART had been discontinued but was in this case found to significantly increase the concentration of circulating CD8+ T cells (Table 1). In a another study, (15) who administered a subcutaneous recombinant of human IL-2 to HIV-1 patients with low baseline CD4 count (50-299cells/mm3 ) found that IL-2 increased CD4 T cells count compared to antiretroviral therapy alone. However, a combination of antiretroviral with IL-2 therapy in this study added no value in terms of immune response. In contrast, (16) found a significant increase of CD4+ T cells count among HIV-1 patients that were treated with ART+IL-2 relative to those who received ART only, compared to the baseline CD4+ T cells count. In addition, ART + IL-2 treated patients showed an increase in CD27+CD28+CD45RA+ on naive CD4+ T cells compared to those treated with ART alone (pEnglishhttp://ijcrr.com/abstract.php?article_id=372http://ijcrr.com/article_html.php?did=3721. Haes W De, Pollard C, Vanham G, Rejman J. “ Wrapped Up ” Vaccines in the Context of HIV-1 Immunotherapy. 2012;41.
2. Poonia B. Infectious Diseases and Therapy Immunotherapy in HIV Infection. 2013;1(1):1–5.
3. Denton PW, Long JM, Wietgrefe SW, Sykes C, Spagnuolo RA, Snyder OD, et al. Targeted cytotoxic therapy kills persisting HIV infected cells during ART. PLoS pathogens [Internet]. 2014 Jan [cited 2014 Nov 2];10(1):e1003872. Available from: http:// www.pubmedcentral.nih.gov/articlerender.fcgi?artid=3887103 andtool=pmcentrezandrendertype=abstract
4. Vanham G, Van Gulck E. Can immunotherapy be useful as a “functional cure” for infection with Human Immunodeficiency Virus-1 Retrovirology [Internet]. Retrovirology; 2012 Jan [cited 2014 Nov 16];9(1):72. Available from: http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=3472319andtool=pmcent rezandrendertype=abstract
5. Luban J. Innate immune sensing of HIV-1 by dendritic cells. Cell host and microbe [Internet]. Elsevier Inc.; 2012 Oct 18 [cited 2014 Nov 16];12(4):408–18. Available from: http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=3619430andtool=pm centrezandrendertype=abstract
6. Chun T-W, Fauci AS. HIV reservoirs: pathogenesis and obstacles to viral eradication and cure. AIDS (London, England) [Internet]. 2012 Jun 19 [cited 2014 Nov 5];26(10):1261–8. Available from: http://www.ncbi.nlm.nih.gov/pubmed/22472858
7. Pett SL, Kelleher AD. Cytokine therapies in HIV-1 infection: Present and future [Internet]. Expert Review of Anti-Infective Therapy. 2003. p. 83–96. Available from: http://www.scopus.com/inward/record.url?eid=2-s2.0-2942557197andpartnerID=tZOtx3y1
8. Kwong PD, Mascola JR, Nabel GJ. Broadly neutralizing antibodies and the search for an HIV-1 vaccine: the end of the beginning. Nature Reviews Immunology [Internet]. Nature Publishing Group, a division of Macmillan Publishers Limited. All Rights Reserved.; 2013 Aug 23 [cited 2015 Sep 28];13(9):693–701. Available from: http://dx.doi.org/10.1038/nri3516
9. Nanotechnology in Diagnosis, Treatment and Prophylaxis of Infectious Diseases [Internet]. Nanotechnology in Diagnosis, Treatment and Prophylaxis of Infectious Diseases. Elsevier; 2015 [cited 2015 Sep 23]. 39-49 p. Available from: http://www. sciencedirect.com/science/article/pii/B9780128013175000037
10. Smith K a, Andjelic S, Popmihajlov Z, Kelly-Rossini L, Sass A, Lesser M, et al. Immunotherapy with canarypox vaccine and interleukin-2 for HIV-1 infection: termination of a randomized trial. PLoS clinical trials [Internet]. 2007 Jan [cited 2014 Nov 16];2(1):e5. Available from: http://www.pubmedcentral.nih. gov/articlerender.fcgi?artid=1783674andtool=pmcentrezandrender type=abstract
11. Velu V, Shetty RD, Larsson M, Shankar EM. Role of PD-1 coinhibitory pathway in HIV infection and potential therapeutic options. 2015;1–17.
12. Roff SR, Noon-Song EN, Yamamoto JK. The Significance of Interferon-γ in HIV-1 Pathogenesis, Therapy, and Prophylaxis. Frontiers in immunology [Internet]. 2014 Jan 13 [cited 2014 Nov 10];4(January):498. Available from: http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=3888948andtool=pmcent rezandrendertype=abstract
13. Jarvis JN, Meintjes G, Rebe K, Ntombomzi G, Bicanic T, Williams A, et al. Europe PMC Funders Group Adjunctive Interferon- γ Immunotherapy for the Treatment of HIV- associated Cryptococcal Meningitis : A Randomized Controlled. 2013;26(9):1105–13.
14. Ndhlovu LC, Sinclair E, Epling L, Tan QX, Ho T, Jha AR, et al. IL-2 immunotherapy to recently HIV-1 infected adults maintains the numbers of IL-17 expressing CD4+ T (T(H)17) cells in the periphery. Journal of clinical immunology [Internet]. 2010;30(5):681–92. Available from: http://www.scopus.com/inward/record.url?eid=2-s2.0- 77957571862andpartnerID=tZOtx3y1
15. Abrams D, Levy Y, Losso MH, Babiker A, Collins G, Cooper DA, et al. Interleukin-2 therapy in patients with HIV infection. N Engl J Med. 2009;361(16):1548–59.
16. Ndhlovu LC, Sinclair E, Epling L, Tan QX, Ho T, Jha AR, et al. IL-2 immunotherapy to recently HIV-1 infected adults maintains the numbers of IL-17 expressing CD4+ T (T(H)17) cells in the periphery. Journal of clinical immunology [Internet]. 2010 Sep [cited 2014 Nov 16];30(5):681–92. Available from: http://www. pubmedcentral.nih.gov/articlerender.fcgi?artid=2935971andtool= pmcentrezandrendertype=abstract
17. Connolly NC, Whiteside TL, Wilson C, Kondragunta V, Rinaldo CR, Riddler S a. Therapeutic immunization with human immunodeficiency virus type 1 (HIV-1) peptide-loaded dendritic cells is safe and induces immunogenicity in HIV-1-infected individuals. Clinical and vaccine immunology : CVI [Internet]. 2008 Feb [cited 2014 Nov 16];15(2):284–92. Available from: http://www. pubmedcentral.nih.gov/articlerender.fcgiartid=2238066andtool= pmcentrezandrendertype=abstract
18. Huang X-L, Fan Z, Borowski L, Rinaldo CR. Maturation of dendritic cells for enhanced activation of anti-HIV-1 CD8(+) T cell immunity. Journal of leukocyte biology [Internet]. 2008 Jun [cited 2014 Nov 16];83(6):1530–40. Available from: http:// www.ncbi.nlm.nih.gov/pubmed/18364435
19. Chen Y, Wang S, Lu S. DNA Immunization for HIV Vaccine Development. Vaccines [Internet]. 2014 Feb 25 [cited 2014 Nov 16];2(1):138–59. Available from: http://www.mdpi.com/2076- 393X/2/1/138/
20. Palma P, Gudmundsdotter L, Finocchi A, Eriksson L, Mora N, Santilli V, et al. Immunotherapy with an HIV-DNA Vaccine in Children and Adults. Vaccines [Internet]. 2014 Jul 17 [cited 2014 Nov 16];2(3):563–80. Available from: http://www.mdpi. com/2076-393X/2/3/563/
21. Pitisuttithum P, Gilbert P, Gurwith M, Heyward W, Martin M, van Griensven F, et al. Randomized, double-blind, placebo-controlled efficacy trial of a bivalent recombinant glycoprotein 120 HIV-1 vaccine among injection drug users in Bangkok, Thailand. The Journal of infectious diseases. 2006;194(12):1661–71.
22. Letvin NL, Walker BD. Immunopathogenesis and immunotherapy in AIDS virus infections. Nature medicine [Internet]. 2003 Jul;9(7):861–6. Available from: http://www.ncbi.nlm.nih.gov/ pubmed/12835706
23. Horwitz JA, Halper-Stromberg A, Mouquet H, Gitlin AD, Tretiakova A, Eisenreich TR, et al. HIV-1 suppression and durable control by combining single broadly neutralizing antibodies and antiretroviral drugs in humanized mice. Proceedings of the National Academy of Sciences of the United States of America [Internet]. 2013;110(41):16538–43. Available from: http://www. pubmedcentral.nih.gov/articlerender.fcgi?artid=3799352andtool= pmcentrezandrendertype=abstract
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241724EnglishN2015December20HealthcareOCCUPATIONAL HAZARDS AMONG PRACTICING DENTISTS IN CHENNAI- A SURVEY REPORT
English3038Kalpana GokulEnglish AbiramiEnglish BalaSundaramEnglishAims: This paper reports the survey results of the prevalence of occupational hazards among the practicing dentists in Chennai.
Settings and Design: A Descriptive Epidemiological study.
Methods and Material: A survey was conducted by using a self-administered questionnaire from two hundred and fifty practicing dental surgeons. Only practicing dentists were included in the study and non practitioners were excluded.
Statistical analysis used: The statistical analyses were performed with use of SPSS version 20.0 package. Results were considered significant for “p” values of ?0.05.
Results: Among all the occupational hazards experienced, lower back pain was the highest (57%), followed by neck pain (52.8%), head ache (38.4%) and frequent respiratory illness (22.4%). Among the preventive measures practiced, least employed were regular physical exercises (40.8%), engaging in sports activity (20%) and use of simple or compound loupes (20.4%). Among all the infection control protocols, least followed one was wearing protective eye goggles (67.6%).
Conclusions: There was high level of awareness of exposure to occupational hazards among the dental surgeons. However, the practical steps to prevent them were not followed and hence, needs to be reinforced. Lower back pain was the highest hazard experienced. Increased awareness must be created about complications of musculoskeletal deformities. Its prevention by regular physical exercise should be emphasized and the importance of regular monitoring of muscle health through EMG analysis could give an early insight into the muscle fatigue leading to musculoskeletal deformities.
EnglishOccupational hazards, Dentistry, Musculoskeletal deformitiesINTRODUCTION
Although dentistry is among the least hazardous of all the professions, many risks remain in dental practice which continues to challenge this status. These include per cutaneous exposure incidents; exposure to infectious diseases by bio aerosols; exposure to radiation, noise and dental materials; musculoskeletal disorders ; dermatitis ; eye injuries; vibration induced neuropathy and psychological problems.[1] BernadinoRamazzini, is referred to as the father of occupational medicine, recognized the role of occupation in the dynamics of health and diseases. [2] The practice of dentistry exposes dental professionals to a variety of work-related hazards. These include:
• Working long hours at a high level of concentration
• Working in a sedentary state
• Working with anxious patients
• Exposure to microbial aerosols
• Exposure to various chemicals used in clinical dental practice
The source of these hazards is the work environment which can include physical, chemical, biological aspects. [2]
Physical Hazards:
The sources of physical injury can include debris from the oral cavity striking the eyes, cuts from sharp instruments, or puncture wounds from needles or other sharp instruments. Such injuries can result in the transmission of serious infec tious disease to the clinician. Needle stick injuries and cuts from sharp objects and instruments (percutaneous injuries) have been reported during surgical procedures mostly associated with suturing. [3] Eye injuries may occur from projectiles such as bits of calculus during scaling procedures and splatters from body fluids (bacterial and viral aerosols) while using high-speed hand pieces. Another potential source of eye injury is the intense dental curing light. Users of dental curing lights should be advised to employ protective eye- wear during use. [4][5] The need to work in a fixed working position using a continuous repetitive motion can predispose the clinician to wrist ache, lower backache, and neck ache.[6] The most common injuries reportedly experienced by the dentists are musculoskeletal in nature.[7] Chemical Hazards: Many biomaterials and auxiliary products used in dentistry are chemically reactive. [8] Hazardous chemical agents used in clinical dentistry include mercury, powdered natural rubber latex, disinfectants, and nitrous oxide. By far the most important and most dangerous of these agents is mercury.[9] Its use in dental amalgam has the potential for continuous occupational exposure of a dental practitioner to mercurial vapour which can be absorbed via the skin and the lungs.[10] The active component in the mercurial vapour has a particular affinity for brain tissue. Mercury poisoning can be characterized by tumors of the face, arms, or legs and can also be associated with progressive, tremulous illegible handwriting and slurred speech. The exposure risks for mercury can be minimized by careful handling procedures. The continued use of powdered NRL gloves and disinfectants has predisposed clinician to hand dermatitis, contact dermatitis, contact urticaria, and allergic dermatitis.[11] The most serious potential hazard associated with the continued use of powdered NRL gloves in dental practice is latex sensitization caused by exposure to aerosolized NRL protein. This can result in dermatitis on the hands. This occurs with such frequency that it is now recognized as an occupational hazard in dentistry, and many dental offices have had to stop using latex materials such as gloves and rubber dams. [12] In recent studies, the frequency of occupational related dermatitis varied from 21% to 43% depending on the prevailing material used in the various specialties. [13] Transient irritative reactions of the eyes and air- ways have been observed mostly associated with exposure to volatiles from resin based materials, x-ray chemicals, and cleansers. These include procaine, soaps, eugenol, iodine, formalin, phenol, and other disinfectants. [8] Retrospective surveys of dental and medical personnel have linked occupational exposure to nitrous oxide with a number of health problems and reproductive derangements.[14][15] Thus, adequate pollution control mechanisms in accordance with the Federation DentaireInternationale (FDI) should be adopted.[14][15] Biological (Cross-Infection) Hazards: Dentistry is unique in that clinician is in direct contact with traumatized tissues, saliva, and blood on a daily basis. [16] There is high risk of exposure to Hepatitis B virus (HBV), HIV infection, and other types of communicable infections. [16] A study reported that the carrier rate HBV in the general population is 0.5%, while dentists have a carrier rate of approximately 1.6%. Several of the common viral agents that can cause hepatitis have been detected in body fluids including saliva and blood. The viruses most commonly implicated include hepatitis A virus (HAV), HBV, and hepatitis C. [17][18] This study was aimed at assessing the level of awareness of occupational hazards among practicing dentists in Chennai. This was done by identifying hazards and estimating their prevalence rate. Materials and Methods: The study population consisted of two hundred and fifty practicing dentists at Chennai. Data was obtained through the use of questionnaires that included questions on, awareness to occupational hazards, safety measures practiced, and experience of occupational hazard experienced in Dental practice. The questionnaire was pilot tested in a sample size of twenty subjects for validity and repeatability. Data was analyzed using frequency tables to display the responses. Where necessary, cross tabulations were carried out to determine the significant difference between variables. Chi-square test and independent sample T test was used to test the significance of difference between different variables. Results: A total of two hundred and fifty dental practitioners participated in the study (Figure-I). The mean number of practice in years among the dental practitioners was seven years. The number of practice hours per day range from one to thirteen hrs among the practitioners. Majority (57.2%) practiced around six days in a week. Table-I describes that based on the number of years in practice or number of practice hrs per day, there was no statistically significant difference in the presence of lower back pain, wrist pain or neck pain among the dentists. Figure-I show distributions of the post graduate practitioners. Figure-II shows majority (89.2%) have had previous hepatitis B vaccination and around 74% have taken insurance policy. 28.4% reported contact with amalgam, 12.8% reported sharp injury in the past six months and only 7.6% reported latex allergy.
Figure-III shows the practice of cross infection control among practitioners. Among the cross infection control mechanisms employed, wearing protective eye glasses was least employed (67.6%). Only 74.4% washed their hands before gloving. Figure-IV shows preventive measures undertaken by the practitioners in their day today practice. Least preventive measure practiced was engaging in any kind of sports activity (20%). Only 20.4% reported to use loupes during practice. Only 40.8 % dentists practiced regular physical exercises. Only 56.4% of the practitioners went on yearly vacations. 61.2% dentists used indirect vision for working on maxillary teeth. Figure-V shows the prevalence of different occupational hazards. 57% experienced lower back pain, which was the most experienced hazard. 52.8% experienced neck pain, 38.4 % reported head ache, 23.6% reported wrist pain, 22.4 % reported frequent respiratory illness and 21.6% reported vision problems. Only 5.2% reported history of hepatitis B/C. The analyses were performed with use of SPSS version 20.0 package. The data was analysed using frequency tables to suggest the responses of dentists. The significance of differences between variables was tested by the cross tabulations. Results were considered significant for “p” values of ≤0.05.
DISCUSSION
Education is one of the important strategies for the prevention of occupational injuries and diseases. The role of one’s occupation as an important factor in maintaining personal health needs to be constantly emphasized so practitioners understand any possible negative health implications of their jobs and how to minimize them. In our survey on two hundred and fifty practicing dentists, backache was observed as being highest (57%) followed by neck ache (52.8%) and head ache (38.4%). About 28.4% reported contact with amalgam. Negligence in handling amalgam has to be avoided and safety handling protocols according to the FDI/WHO guidelines will have to be followed. [9][19] Although the majority of the participants were aware they were at risk for exposure to injuries from sharps, and hepatitis B infection, not all of them were vaccinated against Hepatitis B infection. Importance of vaccination properly against Hepatitis B infection has to be emphasised because of the risk of body fluid borne infection [20][21]; this is corroborated by the fact that about 12.8% experienced an injury by a sharp object in the past six months. Awareness about the HIV policy and the post expositional prophylaxis should also be increased. [21] Only 74% had health insurance policy. Cessation of practice due to health issues will have to be anticipated and accordingly the clinician’s health has to be insured to protect them from severe financial loss. Cross infection control habits among the staff could be rated very well because most of the clinicians appeared to have followed all the protocols except the use of protective eye goggles while attending to patients.[4][5][22] The use of protective eyewear is an important means of preventing occupational injury related to the use of dental curing lights and high-speed rotary instruments. Injury from splatters and projectiles including calculus and flying debris during cavity preparation is a common cause of damage to the eyes, and the use of protective eyewear should be emphasized. [4][5][22] The most pernicious occupational hazards are not those where the effects appear immediately, as in accidents, but rather those that run an insidious course over a period of years.[23]Musculoskeletal disorders represent an important occupational health issue in dentistry that surfaces after prolonged period of practice.[23][24][25] As clinicians adapt to the work- place and routine functions over a long period of time, they are exposed to potential hazards like musculoskeletal deformities. [23][24] Clinician’s safety may be severely jeopardized if adequate safety measures are not taken. [2] 57.8% reported lower back ache which scored the highest among all the occupational hazards experienced followed by neck pain and head ache. The postures in which dentists sit require over half of the body’s muscles to work to hold the body motionless while resisting gravity. The static forces resulting from these postures have been shown to be more taxing than dynamic forces [26]. Therefore, when the supporting muscles begin to reflect fatigue, a process of pain and discomfort begins and could very well lead to musculoskeletal injury. An article by Valachi and Valachi cited a flowchart of muscle activity and pain leading to a musculoskeletal disorder: Prolonged Static Posture→ Muscle Fatigue and Muscle Imbalance→ Muscle Ischemia/Necrosis, Trigger Points and Muscle Substitution→ Pain→ Protective Muscle Contraction→ Nerve Compression, Spinal Disk Degeneration→ Musculoskeletal Disorder. Muscle imbalances could result from an awkward posture while working on patients [27]. Electromyography (EMG) is the study of muscle function through analysis of electrical signals emanated during muscular contractions [28]. These signals represent the electrical activity associated with contracting muscles and, therefore, can be affected by anatomical and physiological muscle properties. EMG analysis could give an insight into the developing muscle fatigue progressing towards more complicated nerve compression. Hence, we felt that probably preventing the development of musculoskeletal disorders is the best choice by following simple regular physical exercises, engaging in some sports activity and regular check up with EMG. If muscle fatigue, which is experienced at initial stages, can be diagnosed, appropriate treatment can be taken. This might prevent the clinician from taking painful decisions like cessation of practice or reduction of clinical practice. Conclusion: Health risks in dentistry may arise as new technologies and materials are being developed. Our effort has been to assess the prevalence of occupational hazard among the clinicians in Chennai. Musculoskeletal disorders seems to be the highest experienced according to our study. Prevention of musculoskeletal disorders is very much a possibility by simple protocols mentioned in our discussion. However, further research is needed to explore the impact of musculoskeletal disorders in this particular occupational group, especially in relation to cessation or reduction of clinical practice.
Englishhttp://ijcrr.com/abstract.php?article_id=373http://ijcrr.com/article_html.php?did=3731. Gambhir RS, Singh G, Sharma S, Brar R, Kakar H. Occupational health hazards in current dental profession – a review. Open Occup Health Saf J. 2011; 3: 57-64.
2. Asuzu MC. Occupational health: A Summary, introduction, and outline of principle. Ibadan. Afrika-Links Books, 1994: 1-11.
3. Al-Khatib IA, Ishtayeh M, Barghouty H, Akkawi B. Dentists’ perceptions of occupational hazards and preventive measuresin East Jerusalem. East Mediterr Health J 2006; 12: 153-60.
4. Eriksen P, Moscato PM, Franks JK, et. al. Optical hazard evaluation of dental curing lights. Community Dent Oral Epidemiol. 1987 Aug; 15(4):197-201.
5. Palenik CJ. Eye protection in dental laboratories. J Dent Technol. 1997 Sep; 14(7):22-6.
6. Caballero AJ, Palencia IP, Cardenas SD. Ergonomic factors that cause the presence of pain muscle in students of dentistry. Med Oral Patol Oral Cir Bucal 2010; 15: e906-11.
7. Pargali N, Jowkar N. Prevalence of musculoskeletal pain among dentists in Shiraz, Southern Iran. International J Occup Environ Med 2010; 1: 69-74.
8. Hensten-Pettersen A, Jacobsen N. The role of biomaterials as occupational hazards in dentistry. Int.Dent J. 1990 Jun; 40(3):159- 66.
9. Al-Khatib IA, Darwish R. Assessment of waste amalgam management in dental clinics in Ramallah and Al-Bireh cities in Palestine. Int J Environ Health Res. 2004; 14:179–83.
10. Kostyniak PJ. Mercury as a potential hazard for the dental practitioner. N Y State Dent J. 1998 Apr; 64(4):40-3.
11. Field EA. The use of powdered gloves in dental practice: a cause for concern? J Dent. 1997 May-Jul;25(3-4):209-14
12. Saary MJ, Kanani A, Alghadeer H, Holness DL, Tarlo SM. Changes in rates of natural rubber latex sensitivity among dental school students and staff members after changes in latex gloves. J Allergy ClinImmunol. 2002; 109:131–5.
13. Babich S, Burakott RP. Occupational hazards of dentistry. A review of literature from 1990. N Y State .Dent J. 1997 Oct; 63(8):26-31. Review.
14. Yagiela JA. Health hazards and nitrous oxide: a time for reappraisal. AnesthProg. 1991 ; 38(1):1-11.
15. Henderson KA, Matthews IP. Environmental monitoring of nitrous oxide during dental anaesthesia.Br Dent J. 2000; 188:617– 9.
16. Ayatollahi J, Sharifi MR, Sabzi F, Zare AR. Blood level antiHBS due to HB vaccine in health care personnel of ShahidSadoughi Hospital-Yazd. Iranian Journal of Obstetrics, Gyneocology and Infertility. 2004; 7:48–51.
17. Ayatollahi J. Needle-stick injuries in a general hospital: Continuing risk and under reporting. Ann Iranian Med. 2006; 3:47–50.
18. Younai FS. Health care-associated transmission of hepatitis B and C viruses in dental care (Dentistry) Clin Liver Dis. 2010; 14:93–104.
19. Szymanska J. Occupational hazards of dentistry. Ann Agric Environ Med. 1999; 6:13–9.
20. De Almeida OP, Scully C, Jorges J. Hepatitis B vaccination and infection control in Brazilian dental practice, 1990. Community Dent Oral Epidemiol. 1991 Aug; 19(4):225-7.
21. Updated U.S. Public Health Service. Updated U.S. public health service guidelines for the management of occupational exposures to HBV, HCV and HIV and recommendations for postexposure prophylaxis. MMWR Recomm Rep. 2001; 50:1–52.
22. Miller C. Make eye protection a priority to prevent contamination and injury. RDH. 1995; 15:40–2.
23. Szymanska J. Disorders of the musculoskeletal system among dentists from the aspect of ergonomics and prophylaxis. Ann Agric Environ Med. 2002; 9:169–73.
24. Hayes MJ, Cockrell D, Smith DR. A systematic review of musculoskeletal disorders among dental professionals. Int J Dent Hyg. 2009; 7:159–65.
25. Ratzon, N.Z., Yaros, T., Mizlik, A. and Kanner, T. Musculoskeletal symptoms among dentists in relation to work posture. Work; A Journal of Prevention, Assessment and Rehabilitation.2000; 15 (3), 153-158.
26. Valachi B, Valachi K. Mechanisms leading to musculoskeletal disorders in dentistry. J Am Dent Assoc.2003; 134:1344–50.
27. Sandoval, AE. “Electrodiagnostics for low back pain.” Physical medicine and rehabilitation clinics of North America. 2010; 21 (4): 767–76.
28. Leggat PA, Smith DR. Musculoskeletal disorders self-reported by dentists in Queensland, Australia. Aust Dent J. 2006; 51(4): 324-7.
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241724EnglishN2015December20HealthcareMORPHOMETRIC ANALYSIS OF EXTENSOR GROOVE OF LOWER END OF RADIUS
English3942K.C. ShanthiEnglishBackground: The tendons of Abductor pollicis longus and Extensor pollicis brevis pass through the first compartment of the extensor retinaculum. These tendons pass with their own synovial sheaths and sometimes they share a common synovial sheath which can be septate. Constant friction between these tendons in a living person results in tenosynovitis.
Aim: This study aimed to document the relationship between the tendons and the bone and variations in the tendon or the bone could produce any significant contribution to the outcome of disease. Materials and Methods: 100 radius bones of both sides were sourced for the study to measure the length, breadth and depth of the extensor groove using a Vernier caliper and the same were documented. Results: The mean length, breadth and the depth of the grooves were more on the right side than the left side. In a significant percentage, the ridge was absent. Conclusion: The morphometric data will provide an insight for corrective surgeries in tenosynovitis and for corticosteroid injections in cases of tenosynovitis.
EnglishGroove, Ridge, Tenosynovitis, Radius, Extensor retinaculum, TendonsINTRODUCTION
Pain around the wrist joint is a common complaint in elderly people. This pain can be due to various causes including trauma around the wrist. This pain can also be perennial which is accentuated by metabolic disorders also. A common cause of this pain is De Quervain’s tenosynovitis whose aetiopathology is very unclear. It is encountered in everyday clinical practice1 . This condition limits the activities of daily living in an individual. This condition is brought about by repetitive and sustained tension on the tendons of the first dorsal compartment4 . The treatment of this condition is initially by analgesics to relieve the pain and if it fails, it is followed by surgery. It is hypothesized that this condition is due to compression of tendons of Abductor Pollicis longus and Extensor Pollicis Brevis when they pass through the first compartment of the extensor retinaculum of the wrist. These tendons are covered by their own synovial sheaths when they are passing. However in rare instances, both these tendons might share the same synovial sheath6 . Constant friction between the tendons, their synovial sheaths and their opposing bone contributes to tenosynovitis. Awareness of this condition will make the treatment of De Quervain’s tenosynovitis more effective2 . Anatomically these tendons are lodged in a groove which is separated by a bony ridge, dividing the compartment into two paths (Fig-1). The depth and length of these paths of the tendons determines the rate of friction of the tendons when these muscles are put into movement. If the canals that house these tendons are deep the movement is usually smooth and if the groove is shallow the chances of compression of the tendons is all the more a possibility. In some instances the canals may not be present at all (Fig-2). Textbooks describe that the two tendons of Abductor Pollicis Longus and Extensor Pollicis Brevis pass through the first compartment of the extensor retinaculum and they may possess separate or single synovial sheaths. Sometimes there exist two separated compartments for the abductor pollicis longus and extensor pollicis brevis tendons3 Frequently the tendon of Abductor Pollicis longus may be duplicated.
Tenosynovitis of the tendons is due to palpable thickening of the synovial sheaths which also causes painful extension of the thumb. Though numerous studies have been done on the extensor retinaculum to determine the position of the tendons of Abductor Pollicis Longus and Extensor Pollicis Brevis and its accessory slips, no morphometric analysis has been done to elicit the dimensions of the first groove of the extensor retinaculum.
MATERIALS AND METHODS
This study was performed in the Department of Anatomy, VMKV Medical College, Salem. 100 radius bones were sourced for the study. Sex was not determined for the bones. Among the bones 50 bones belonged to the right side and 50 bones belonged to the left side. A hand lens was used for closer observation. A divider and measuring scale was used to morphometrically analyze the bones. The following parameters were measured 1) Presence or Absence of bony ridge 2) Length of the bony ridge 3) Length of the Lister’s tubercle 4) Length of the bony canals 5) Breadth of the bony canals
METHODOLOGY
Using a hand lens the bones were observed for presence or absence of bony ridges. Out of the 100 bones, 08 bones exhibited no ridge. The length of the Lister’s tubercle (L1) was measured from the tip of the inferior border (Point A) to the uppermost tip of the tubercle (Point B). The length of the bony ridge (L2) was measured from its lower end (Point C) to its upper end (Point D). Length of the bony canal 1(l1) was measured from the tip of the inferior border (Point E) to the tip of the uppermost end (Point F). Length of the bony canal 2 (l2) was measured from the tip of the inferior border (Point G) to the tip of the uppermost end (Point H) (Fig – 3). The breadth of the bony canals was measured as the maximum width from a midpoint of the length of each bony canal (B1, B2) (Fig – 4). The first canal is present between the listers tubercle and the bony ridge. The second canal is present between bony ridge and the palmar tubercle. Statistical Analysis The resultant measurements were statistically analyzed using SPSS software version 17.
RESULTS
Among the 100 radii examined, 08 bones did not have bony ridge with the left radius being predominantly higher than the right radius. The mean length of the bony ridge of the right side was more than the mean length of the left radii. The mean length of the listers tubercle of the right side was more than the left side. The mean length and breadth of the first bony canal on the right side was more than the left side. The mean length and breadth of the second bony canal on the right side was more than the left side. The parametric measurements of the right and left radii are given in Table -1. The resultant parameters were statistically analyzed through a paired sample’t’ test which is depicted in Table 2.
DISCUSSION
The bony ridge was absent in about 8% of the bones. This absence of bony ridge does not separate the tendons of Abductor Pollicis longus and Extensor Pollicis Brevis. It can be assumed that there may or may not be a separate synovial sheath which can contribute to the friction between the tendons. The length, breadth of the ridge as well as bony canals measurements were significantly higher on the right side than the left side. This can be due to the fact that the bones could be belonging to the right handed individuals predominantly than left handed persons. In a study conducted in the year 2012 states that specific geometrical parameters of the styloid process of the radius need to be measured and compared between different types and sides of the body5 which has been done in the present study. The deep canals on the right side may due to the usage of the limb resulting in constant wear and tear of the tendons during the movements of the wrist. In some of the bones both the canals were deeply grooved indicating that the movements of the tendons had produced them. The friction between the tendons in the absence of a groove or ridge will cause difficulty in activities of daily living in an affected person. Normal movements of the wrist will be impeded. Also movements of the tendons within their respective synovial sheaths might produce pain and multiple compartments may also predispose to De Quervain’s Tenosynovitis7 . When the synovial sheath is shared, it results in tenosynovitis.
CONCLUSION
Knowledge of the ridge and its morphometry and its variations will be useful for practicing surgeons in performing surgeries to release the tendons from their synovial sheaths in cases of entrapment. Direction of the needle within the septate tendon sheaths while giving corticosteroid injections in cases of tenosynovitis is of prime importance and variations of the ridge and the bony canal can point a right path for the drug to be injected.
ACKNOWLEDGEMENTS
The authors sincerely wish to thank the management, administrators and the Professor and Head of the department of Anatomy of Vinayaka Missions Kirupananda Variyar Medical College, Salem for their whole hearted support and permissions to utilize their resources and conduct this study. The authors acknowledge the great help received from the scholars whose articles 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.
Englishhttp://ijcrr.com/abstract.php?article_id=374http://ijcrr.com/article_html.php?did=3741. Green D. Operative Hand Surgery. 5th edition. Churchill Livingstone: Elsevier, New York; 2005: 2150.
2. Manoj M Kulkarni, A Ashok, Are Indians more prone for De Quervain’s tendinitis in Indian Journal of Basic and Applied Medical Research: June 2014: Vol.-3, Issue-3, pages 212-215.
3. Jamal Gousheh et al; Division of the First Dorsal Compartment of the Hand into Two separated canals: Rule or Exception? In Archives of Iranian Medicine, Vol-12, Number 1, 2009: 52-54.
4. Asif Iliyas et al; de quervain Tenosynovitis of the wrist In Journal of the American Academy of Orthopaedic Surgeons, Vol-15, Number 12, December 2007: 757-764.
5. Liang Xiao et al; Variations in the extensor grooves of the radial styloid process in Chinese population In Surgical and Radiologic Anatomy, Springer-Verlag 201210.1007/s00276-012-0995-y.
6. Susan Standring in Gray’s Anatomy: 40th edition: Churchill Livingstone: Elsevier, London; 2008: pages 879 – 880.
7. Soubhagya R. Nayak et al; Variations and Clinical Significance of Extensor Pollicis Brevis: A study in South Indian Cadavers; Chang Gung Med J 2009; 32: 600-4.
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241724EnglishN2015December20HealthcareCONSTRUCTION AND ANALYSIS OF MYOPATHY AND PARKINSON DISEASE PROTEIN NETWORK
English4347Sachin RahangdaleEnglish Shobha ShoucheEnglish Ravikant YadavEnglish Harshad SharmaEnglish Ankit Kumar JainEnglishNeurological Disorders are diseases of the central and peripheral nervous system. The disorders Parkinson’s disease and myopathy are the traumatic disorders of the nervous system. The myopathies are neuromuscular disorders in which the primary symptom is muscle weakness due to dysfunction of muscle fiber and Parkinson’s disease (PD) belongs to a group of conditions called motor system disorders, which are the result of the loss of dopamine-producing brain cells. Biological network is a network that applies to the biological system. These networks are widely used in many branches of biology as convenient representation of patterns of interaction between appropriate biological elements.Proteins-protein interaction (PPIs) in a cell form protein interaction networks (PINs) where proteins are nodes and their interaction are edges. In the present work we will investigate the network properties of proteins in disease protein-protein interaction network framework and identify common proteins between myopathy and Parkinson diseases.
EnglishFramework, Interaction, Network, Edges, NeuromuscularINTRODUCTION
Neurological Disorders are diseases of the central and peripheral nervous system.In other words, the brain, spinal cord, cranial nerves, peripheral nerves, nerve roots, autonomic nervous system, neuromuscular junction, and muscles are responsible for neurological disorders. These disorders include epilepsy, Alzheimer disease, myopathy and other dementias, cerebrovascular diseases including stroke, migraine and other headache disorders, multiple sclerosis, Parkinson’s disease, neuro-infections, brain tumours, traumatic disorders of the nervous system such as brain trauma, and neurological disorders as a result of malnutrition.[11] Hundreds of millions of people worldwide are affected by neurological disorders. Approximately 6.2 million people die because of stroke each year; over 80% of deaths take place in low- and middleincome countries. More than 50 million people have epilepsy worldwide. It is estimated that there are globally 35.6 million people with dementia with 7.7 million new cases every year - Alzheimer’s disease is the most common cause of dementia and may contribute to 60–70% of cases.[13] The Parkinson’s disease and myophaty on the traumatic disorders of the nervous system. The Myopathies are neuromuscular disorders in which the primary symptom is muscle weakness due to dysfunction of muscle fiber. Other symptoms of myopathy can include muscle cramps, stiffness, and spasm. Myopathies can be inherited (such as the muscular dystrophies) or acquired (such as common muscle cramps). Parkinson’s disease (PD) belongs to a group of conditions called motor system disorders, which are the result of the loss of dopamine-producing brain cells. The four primary symptoms of PD are tremor, or trembling in hands, arms, legs, jaw, and face; rigidity, or stiffness of the limbs and trunk; bradykinesia, or slowness of movement; and postural instability, or impaired balance and coordination. As these symptoms become more pronounced, patients may have difficulty in walking, talking, or completing other simple tasks. PD usually affects people over the age of 60. [12] Biological network is a network that applies to the biological system. These networks are widely used in many branches of biology as convenient representation of patterns of interaction between appropriate biological elements. [14]Proteinsprotein interaction (PPIs) in a cell form protein interaction networks (PINs) where proteins are nodes and their interaction are edges. The present study is designed to investigate the network properties of proteins in diseases, identification of common protein and their structural properties and protein-protein interaction network framework between myopathy and Parkinson diseases.
DISCUSSION
We have collected 5 miRNAs for Parkinson Disease and 31 miRNAs for Myopathy by using literature mining such as PubMed, miR2disease database. (Table-1) Using miRNA target database mirWalk, miRecords, miReg and miRTarBase. We have identified 298 targets for parkinson Disease and 1602 targets for myopathy disease. We made an interaction network using target proteins of miRs with the help of Visant. We have found the Degree of Distribution (Fig. 1, 2, 3) and Clustering- Coefficient Distribution of target proteins. (Fig 4, 5, 6) There are 131 proteins which are common between two diseases. It seems that these proteins are hotshots in these diseases, so required much more attention. We have plot a degree distribution of disease protein and the results indicate that most of the proteins are having 4 degrees. This is an interesting finding. It means that networks are obeying power law and they are scale-free in nature. The power laws are often interpreted as signatures of hierarchy and robustness.
ABCC1, ACTB, ACTG1, AKT1, ALDH1A1, APC, ARC, ARCN1, ARPP-21, ASAHL, ATP11C, BCL2, BCL2L11, BMP2, ,CBS, CBX5, CCND1, CDKN1B, CDKN1C, CEBPA, CNN3, CTGF, CXCL12, DGCR8, DICER1, DMPK, E2F1, E2F3, EGF, EGFR, EPHB2, ERBB2, ERG, ETS2, EXOSC1, FASLG, FASN, FBLIM1, FGFR1, FLT3, GALNT1, GAPDH, GRB2, HCN2, HDAC4, HELLS, HIST1, H2BB, HLA-G, HMGB1, HMOX1, HOXA9, HOXD10, HSPA1B, HSPB6, IARS, IDH1, IGF1, IGF1R, IGF2R, IL6, IMPACT, IRS1, ITGB1, ITLN1, JAG1, KLF4, KRT7, LIN28, LRRFIP1, LRRK2, MBL2, MCL1, MEF2A, MET, MLC1, MOCOS, MSI2, MYC, MYOD1, NFKB1, NFYC, NKX2- 3, NOTCH1, NPM1, NXN, PAK1, PAX3, PAX6, PAX7, PDE3A ,PIK3CA, PIWIL1, POLA2, POLR2A, POMC, PROC, PTBP1, PTBP2, PTEN,P TGS2, RAB34, RAC1, RDH10, RELB, RHOA, RHOD, RNASEN, RPE, RPL27, RUNX2, SLC11A1, SLC2A4, SLC7A1, SMAD2, SMAD5, SNCA, SOX2, SOX4, SRF, TFB1M, TGFB1, TGFBI, TGFBR2, TIAL1, TIMP2, TLR4, TLR9, TPPP, VEGFA, WT1
By doing functional annotation we found that all proteins which are common in these two diseases are reported in these following neurological pathways. (Table-2)
CONCLUSION
This study illustrates the analysis of Myopathy and Parkinson diseases. For this we have designed the protein-protein interaction analysis because each and every protein which involves in this study has their own role and importance and help to understand how Proteins are distributed in this network. We have identified about 131 common proteins which are hotshots for these two diseases and required much more attention to find out the drug target so that farther study can be designed to obtain the inhibitors of these targets.
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. The authors would also like to thank Dr. Usha Shrivastav, Principal at Govt. M.V.M Ujjain and Mr. Krishna Kant Gupta for their support.
Englishhttp://ijcrr.com/abstract.php?article_id=375http://ijcrr.com/article_html.php?did=3751. Jiang Q., Wang Y., Hao Y., Juan L., Teng M., Zhang X., Li M., Wang G., Liu Y., (2009) miR2Disease: a manually curated database for microRNA deregulation in human disease. Nucleic Acids Res 37:D98-104.
2. Hsu SD, Lin FM, Wu WY, Liang C, Huang WC, Chan WL, Tsai WT, Chen GZ, Lee CJ, Chiu CM, Chien CH, Wu MC, Huang CY, Tsou AP, Huang HD. miRTarBase: a database curates experimentally validated microRNA-target interactions. Nucleic Acids Res. 2011 Jan;39(Database issue):D163-9. Epub 2010 Nov 10.
3. Dweep H, Sticht C, Pandey P, Gretz N. miRWalk--database: prediction of possible miRNA binding sites by “walking” the genes of three genomes.J Biomed Inform. 2011 Oct;44(5):839- 47. Epub 2011 May 14.
4. Xiao F, Zuo Z, Cai G, Kang S, Gao X, Li T. miRecords: an integrated resource for microRNA-target interactions. Nucleic Acids Res. 2009 Jan;37(Database issue):D105-10. Epub 2008 Nov 7
5. Barh D, Bhat D, Viero C. miReg: a resource for microRNA regulation. J Integr Bioinform. 2010 Aug 6;7(1). doi: 10.2390/ biecoll-jib-2010-144.
6. Huang DW, Sherman BT, Lempicki RA. Systematic and integrative analysis of large gene lists using DAVID Bioinformatics Resources. Nature Protoc. 2009;4(1):44-57
7. Chen J, Bardes EE, Aronow BJ, Jegga AG. ToppGene Suite for gene list enrichment analysis and candidate gene prioritization. Nucleic Acids Res. 2009 Jul;37(Web Server issue):W305-11. Epub 2009 May 22.
8. Breitkreutz BJ, Stark C, Tyers M. Osprey: a network visualization system. Genome Biol. 2003;4(3):R22. Epub 2003 Feb 27.
9. Hu Z, Hung JH, Wang Y, Chang YC, Huang CL, Huyck M, DeLisi C. VisANT 3.5: multi-scale network visualization, analysis and inference based on the gene ontology. Nucleic Acids Res. 2009 Jul;37(Web Server issue):W115-21. Epub 2009 May 21.
10. Debmalya Barh1*, Neha Jain 1, 2, Triantafillos Liloglou3, Cedric vireo4, Kenneth Blum1,5, Vasco Azevedo6, Anil Kumar2, John K. Field3Identification of early biomarkers and molecular events in lung cancer using a novel reverse-transcriptomics approach.
11. National institute of Neurological Disorders and National Stroke, http://www.ninds.nih.gov/disorders/myopathy/myopathy.htm
12. Parkinson’s Disease Foundation,http://www.pdf.org/about_pd http://www.ucsfhealth.org/conditions/neurological_disorders
13. WHO,http://www.who.int/features/qa/55/en/
14. M. E. J. Newman, Networks: An Introduction, Oxford University Press, Oxford(2010). ISBN 0-19-920665-1
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241724EnglishN2015December20HealthcareTHE STATUS OF HEPATITIS C VIRUS SEROPOSITIVITY IN CLINICALLY ASYMPTOMATIC BLOOD DONORS IN A BLOOD BANK OF TERTIARY CARE HOSPITAL
English4850G.D. KatiyarEnglish Anjana AryaEnglishIntroduction: Hepatitis means injury to the liver with inflammation of the liver cell. Most common cause of hepatitis in world is hepatitis viruses. Particular, types B and C virus lead to chronic disease in hundreds of millions of people. Hepatitis C virus is mostly transmitted through infective blood and blood products.
Aim and Objective: This study done in order to known the status of Hepatitis C virus in clinically asymptomatic blood donors in blood bank of tertiary care hospital.
Result: A total of 11333 blood donors were screened in last three years. Out of which 3646 blood units were screened in year 2011, 7 blood units were HCV reactive. Whereas 4266 blood units were screened in 2012, 6 blood units were HCV seropositive and in year 2013 total 3421 blood units were screened, out which 16 blood units were HCV seropositive. The average prevalence of hepatitis C virus was 0.25%.
Conclusion: Blood transfusion is major route for transmission of HCV virus. This virus is greatest concern because of increasing burden of this disease and also life threatening for the recipients. This study is done to aware the public about status of HCV viral disease and prevents it mode of spread.
EnglishBlood donor, Hepatitis C virus, SeropositiveINTRODUCTION
Hepatitis means injury to the liver with inflammation of the liver cell. The word hepatitis comes from Ancient Greek word hepar meaning liver and Latin itis meaning inflammation. Hepatitis could be self-limiting or can progress to fibrosis, cirrhosis or liver cancer. Most common cause of hepatitis in world is hepatitis viruses. There are five main hepatitis viruses, types A, B, C, D and E. Particular, types B and C lead to chronic disease in hundred millions of people. The hepatitis C virus (HCV) is a spherical, enveloped, single-stranded RNA virus belonging to the Flaviviridae family. Globally prevalence of Hepatitis C virus (HCV) infection is around 3%, with 170 million persons world-wide may be infected with HCV. [1]These chronic carriers represent a reservoir for HCV to persist. Hepatitis C virus is mostly transmitted through infective blood and blood products. There is no vaccine available yet for HCV. Various author studies were suggest that despite testing of blood units, HCV infection is still a significant problem in all over India. This study was done in order to known the status of Hepatitis C virus in blood donors in blood bank of tertiary care hospital.
MATERIAL AND METHOD
This study was conducted in the Hospital based blood bank of Rohilkhand medical college and hospital, Bareilly. Three years data were collected from January 1, 2010 to December 31, 2013. For this retrospective study we collect data from blood bank records. Total numbers of 11333 units of blood were collected during this period. As a routine practice, apparently healthy donors were selected after taking proper clinical history and examination. After that every blood units were screened for transfusion transmitted infections. Screening of HCV infection was done by ELISA method.
AIM AND OBJECTIVE
This study done in order to known the status of Hepatitis C virus in clinically asymptomatic blood donors in blood bank of tertiary care hospital.
RESULT
A total of 11333 blood donors were screened in last three years. Out of 3977 are voluntary donors and 7356 were replacement donors. The number of donations approximately equal in number every year. Total 11333 blood units were screened in three year studied, out of which 3646 blood units were screened in year 2011, 7 blood units was HCV reactive. Whereas 4266 blood units were screened in 2012, 6 blood units were HCV seropositive and in year 2013, total 3421 blood units were screened, out which 16 blood units were HCV seropositive. (Table-1) Table 2 Show the comparison of studies of various authors of different regions of India. This data will help to find out the status of clinically asymptomatic Hepatitis C virus seropositive blood donors in Blood bank. The average prevalence of HCV seropositive blood donors in our study was 0.25%.
DISCUSSION
Globally prevalence of Hepatitis C virus (HCV) infection is around 3%, with 170 million persons world-wide may be infected with HCV. [1]About 20 million people are known to have HCV infection in India and a quarter of them expected to develop chronic liver disease in the next 10-15 years. [2] Hepatitis C virus (HCV) is mostly transmitted through infective blood and blood products. There is no vaccine available yet for HCV. The HCV seropositive donors are generally asymptomatic and have no symptoms that obviously relate the liver diseases and escape from routine clinical screening. Two another important short comings of Indian blood banking system responsible for increasing the prevalence of this infection in India. Inspirit of strike law against Professional blood donation it is continues to flourish and another was improper knowledge of public regarding the mode of spread of infection. The present study was conducted to evaluate the seropositivity of the Hepatitis C virus among the clinically asymptomatic blood donors in tertiary care hospital based blood bank.
In this study total of 11333 blood donors were bled in last three years. Out of which 3977 were voluntary donors and 7356 are replacement donors. Most of donors are replacement donors. Year’s wise number of donations is almost equal. In year 2011, 3646 donors were bled in blood bank, out of which 7 (0.19%) donors are HCV seropositive. Similarly in year 2012, out of 4266 blood donors, 6 (0.14%) donors are HCV seropositive. Whereas in year 2013, 3421 blood donors were bled, 16(0.4%) donors were HCV seropositive. The average prevalence of HCV seropositive in our study was 0.25%. In the study of Deshpande R.H et al, total 10, 4925 blood donors were screened in five years period at three different blood banks of Latur. The prevalence of HCV was found to be 0.22% in blood donor. [3] Similarly in our study prevalence was 0.25%. A similar studies were carried out by other authors from different state of India (between 2004- 2014) in that of following order .Nalini et al, Bagga P.K et al, M Panda et al, Arora D et al, Meena M et al, Kaur H et al, Makroo et al, Shah et al and Anuradha et al to show the prevalence of HCV infection in blood donors.
Nalini et al studied the prevalence of transfusion transmitted diseases in department of transfusion medicine, Ludhiana. The HCV seropositivity was found to be 483/44064 (1.09%). [4]Another author in 2007 studied the seroprevalence of hepatitis C virus in 5000 blood donors in Patiala. Seroprevalence of anti-HCV was 0.88%. [5] M Panda et al was conducted a retrospective study in Cuttack. 1.98% of the donors were positive for hepatitis C. [6] A study from Hisar, Haryana, reported that total 5849 blood donation, 4010 (68.6%) were replacement donors and 1839 (31.4%) were voluntary donors. Seroprevalance of HCV was 1.0%. [7] Monika et al were retrospectively studied the prevalence rates of HCV as 537(0.57%) per 94,716 donations. [8] A study done in Amritsar to analyzed the prevalence and trends of the Hepatitis C infection among voluntary and replacement donors at the blood bank. Out of 35793 healthy blood donations, 7089(19.8%) were voluntary donors and 28704 (80.1%) were replacement donors. The average prevalence was found to be 493(1.38%). [9] A similar study was conducted by Makroo et al in a hospital based blood bank in north India for a period of 11 years .Total 2, 06,022 blood donors were screened during this period. 0.39% seroreactive for anti-HCV antibodies was found in blood donors. [10] Sangita D. Shah et al was studied the increasing trend of HCV reactivity in healthy blood donors and multitransfused thalassemia patients of Gujarat State. Out of 184238 donors, 599 donors were found HCV seropositive and its seroprevalence was found to be 0.32%. [11] Another study conducted among Blood Donors in Perambalur, Tamilnadu, the seroprevalence of HCV antigen was found to be (0.47%).[12]
CONCLUSION
Blood transfusion is major route for transmission of HCV virus. This virus is greatest concern because of increasing burden of this disease and also life threatening for the recipients. These Blood donors were generally escape from routine screening in blood banks because of the long range (6-10 weeks) of window period for HCV, during which anti HCV cannot be detected in the blood, second these patients are generally asymptomatic and have no symptoms that obvi ously relate to liver disease, third these donors deny any risk factors from the exposure to viral hepatitis during the predonation questioning. Therefore in every blood banks proper donor selection, viral agents screening and strictly restricted professional donor is reduced the risk of disease transmission. This study is done to aware the public about status of this viral disease and prevents it mode of spread.
Englishhttp://ijcrr.com/abstract.php?article_id=376http://ijcrr.com/article_html.php?did=3761. Hepatitis C Articles. Global HCV. Available from: http://www. natap.org/2011/HCV/120111_01.htm. [Last accessed on 2011 -07-13].
2. Gowri V, Chandraleka C, Vanaja R. The Current Seroprevalence of Hepatitis C Virus in a Tertiary Care Centre in Vellore, Tamil Nadu. Indian J Community Med.2012; 37(2):137.
3. Deshpande Rangrao H, Waddi S.K. Seroprevalance of HCV in Blood Donors Status of blood donors seropositivity of HCV in marathwada, India.JPBMS.2012; 23(23).
4. Gupta N, Kumar V, Kaur A. Seroprevalence of HIV,HBV,HCV and Syphilis in voluntary blood donors. Indian J Med Sci 2004; 58(6):255-7.
5. Bagga P.K, Singh S.P. Seroprevalence of hepatitis C antibodies in healthy blood donors-a prospective study. Indian J Pathol Microbiol.2007; 50(2):429-32.
6. M Panda, K Kar. HIV, Hepatitis B and C infection status of the blood donors in a blood bank of a tertiary health care centre of Orissa .Indian J Public Health.2008; 52(1) : 43-44.
7. Arora D, Arora B, Khetarpal A. Seroprevalence of HIV, HBV, HCV and Syphilis in Blood Donors in Southern Haryana. Indian J Pathol Microbiol 2010; 53(2):308-9.
8. Meena M, Jindal T, Hazarika A. Prevalence of hepatitis B virus and hepatitis C virus among blood donors at a tertiary care hospital in India. Tranfusion.2011; 51(1):198-202.
9. Kaur H, Manjari M, Thaman RG, Singh G. Prevalence of Markers of Hepatitis C virus among the Blood Donors. J Clin Diagnostic Res. 2012; 6(6): 959-962.
10. Makroo RN, Walia RS, Chowdhry M, Bhatia A, Hegde V, Rosamma NL. Seroprevalence of anti-HCV antibodies among blood donors of north India. Indian J Med Res 2013; 138(1): 125-8.
11. Shah SD, Gajjar MD, Bhatnagar NM. Increasing trend of HCV reactivity in healthy blood donors and multitransfused thalassemia patients of Gujarat State. GMJ 2013; 68(2):40-5.
12. Anuradha M, Dandekar RH. Seroprevalence of TransfusionTransmissible Infections HIV, HBV and HCV among Blood Donors in Perambalur, Tamilnadu. IJHSR 2014; 4(5):76-81.
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241724EnglishN2015December20HealthcareLOWER LIMB VARICOSE VEINS AMONG NURSES: A CROSS SECTIONAL STUDY IN UDAIPUR
English5155Neeta MishraEnglish Shiv Lal SolankiEnglish Surya MishraEnglishBackground: Varicose vein is a saccular, tortuous, dilated vein of lower limb invariably associated with local valvular incompetency. They not only can cause cosmetic problems but also can cause clinical symptoms such as pain and heaviness in the lower limb. It is most often associated with occupations requiring prolong orthostasis like teachers nursing staff, shopkeepers etc. In spite of this strong relationship with occupations requiring prolonged orthostasis, epidemiological studies on working population are limited. We conducted this study to identify the occupational and demographic risk factors of lower limb varicose vein which could be interventional in improving working atmosphere and quality of life for their long term nursing career.
Method: It was a cross sectional study conducted from February 2015 to March 2015 Data was collected through a self-filled preformed questionnaire from 364 nurses working at GMCH and Associated Hospitalsin Udaipur, Rajasthan. The nurses having lower limb VV were subject to clinical examination by the experts for confirmation of the diagnosis.
Results: A total of 364 nurses participated in the survey and 88 (24.17%) had lower limb VV. The female nurses had slightly higher prevalencecompared with their male counterpart (24.50% V/S 22.58%). The occupational risk factors responsible for lower limb VV among nurses were longer work history (40.42% P- 0.001) longer working hours (>8 hrs 38.70%, p- EnglishRisk factor, Tortuous, Orthostasis, OccupationINTRODUCTION
A varicose vein is a palpable subcutaneous vein that is dilated tortuous, saccular, and generally larger than 3mm and mainly seen in lower limbs. It is invariably associated with local valvular incompetency and more common in women than men. Varicose vein are known to be more common among profession such as police men, teachers, nurses, shopkeeper& bus conductors who has to stand for longer time during their duties. Even though the exact cause of varicose vein is unknown there are some contributory factors responsible for varicose vein. Some of the major risk factors are age, gender, pregnancy, family history and prolonged standing Among these risk factors nurses have the two important risk factorsgender & prolonged standing during duty hours. They are at higher risk of developing varicose vein because of their nature of job which require prolonged standing at patient bedside& this increase their risk of getting varicose vein later in their life. With regards to the gender majority of the nurses are female nationwide & internationally. In UK male to female ratio among nurse is 1 : 10 in Canada it is 1 : 19 while in India it is around 1 : 5. The only way to avoid the varicose vein among nurses is to follow the preventive measures. Varicose vein is the most common chronic condition in north America and western Europe, less common in the Mediterranean, south America and India and even less so in the far East & Africa. According to international statistics 25 percent of women & 18 percent of men in general population are affected by varicose vein. Framingham study reported that 27 percent of the Americans had some form of varicose disease in their legs. It is estimated that 20 to 25 million Americans have varicose vein. In India 10 to 20 percent of the general population eventually develop varicose vein in due course of their life.
METHOD AND COLLECTION OF DATA
Information was collected from nurses working in GMCH and Associated Hospitals in Udaipur, through a self-filled questionnaire &the physical examination was performed by the investigator for the varicose vein (C2) based on the clinical finding using CEAP standards. (Clinical, Etiological, Anatomical & Pathophysiological classification for varicose vein)
Study Period:
February 2015 to March 2015.
Definitions:
Varicose Vein-Dilatedpalpablesubcutaneous veins of leg, generally more than 3mm in diameter (C2)
Reticular Vein- Dilated non-palpable subcutaneous veins less than 3mm in diameter. Telangiectasia- Dilated intradermal veins less than 1mm in diameter. Chronic venous insufficiency- Varicosevein with its complication (C3-C6) or symptomatic varicose vein.
Procedure & Assessment:
The collected data were entered in to the MS office including MS word, MS excel and MS access for assessment of prevalence and relationship of risk factors of varicose veins among nursing staff and further data were processed and analyzed for percentages, proportions. Appropriate statistical tests were applied to draw the inferences andsignificance and observations were presented as tables, graphs and figuresaccordingly
Ethical Clearance
Ethical clearance was obtained from Human Resource Ethical Committee of the Geetanjali Medical College and Hospital, Geetanjali University, Udaipur.
Results
A total of 364 nurses participated in the study, including 302 female nurses and 62 male nurses. The average age was 46.22 years and the male to female ratio was 1:4.8. There were88 cases of lower limb VV showing the prevalence of 24.17%. The prevalence among female nurses was slightly higher than male (24.50% V/s 22.58%) VV of lower limb were more common in older age group i.e. in the age group of 36-50 years (28.88%) and in the age group of 51-66 years (28.30%). In comparison with nurses without lower limb VV,those who had lower limb VV were more experienced having 6 or more years of experience (40.42% pEnglishhttp://ijcrr.com/abstract.php?article_id=377http://ijcrr.com/article_html.php?did=3771. Hirai M, Naiki K, Nakayama R: Prevalence and risk factors of varicose veins in Japanese women.Angiology 1990, 41:228- 232
2. Sun JM: Epidemiologic study on peripheral vascular diseases in Shanghai.ZhonghuaWaiKeZaZhi 1990, 28:480-483. 510–481
3. Ziegler S, Eckhardt G, Stoger R, Machula J, Rudiger HW. High prevalence of chronic venous disease in hospital employees. Wiener KlinischeWochenschrift 2003;115:575-579.
4. Tomei F, BaccoloTp, Tomao E, Palmi S, RosatiMv. Chronic venous disorders and occupations. American J of industrial medicine 1999;36: 653-665.
5. BN Sharif Nia H, Chan YH, Haghdoost AA, SoleimaniMA.Varicose veins of the legs among nurses: Occupational and demographic characterstics. Int. J of nursing practice Academia.edu 2014; 1-8
6. Nasiri-Foourg A, Kazemi T, Nakhaii N, Kazemi N. lower limb varicose veins and their relationship with risk factor in nurses of the Birjand University of Medical sciences hospital. J of Birjand University of Medical Sciences 2005; 12: 9-15.
7. MH Criqui, JO Denenberg, J Bergan, RD Langer, AFronek. Risk factor for chronic venous diseases : The San Diego Population Study. J of vascular surgery 2007; 46: 331-7.
8. Cornu-Thenard A, Boivin P, Baud JM, De Vincenzi I, Carpentier PH: Importance of the familial factor in varicose disease. Clinical study of 134 families.JDermatolSurgOncol 1994, 20:318- 326.
9. Stvrtinova V, Kolesar J, Wimmer G: Prevalence of varicose veins of the lower limbs in the women working at a department store.IntAngiol 1991, 10:2-5.
10. Gourgou S, Dedieu F, Sancho-Garnier H: Lower limb venous insufficiency and tobacco smoking: a case–control study.Am J Epidemiol 2002, 155:1007-1015.
11. Coughlin LB, Gandy R, Rosser S, de Cossart L. factors associated with varicose veins in pregnant women.Phlebology 2001; 16: 41-50.
12. Callam MJ. Epidemiology of varicose veins. Br J Surg 1994;81: 167-73.
13. Guberan E, Widmer LK, Rougemont A, Glaus L. Epidemiology of spider webs. Vasa 1974;3:391-5.
14. Carpentier PH, Maricq HR, Biro C, Poncot-Makinen CO, Franco A: Prevalence, risk factors, and clinical patterns of chronic venous disorders of lower limbs: a population-based study in France. J VascSurg 2004, 40:650-659.
15. Fowkes FG, Lee AJ, Evans CJ, Allan PL, Bradbury AW, Ruckley CV: Lifestyle risk factors for lower limb venous reflux in the general population: Edinburgh Vein Study. Int J Epidemiol 2001, 30:846-852.
16. Weddell JM. Varicose veins pilot study, 1966. Br J PrevSoc Med 1969;23:179-86.
17. Ahumada M, Vioque J: Prevalence and risk factors of varicose veins in adults.MedClin 2004, 123:647-651.
18. Krijnen RM, De Boer EM, Ader HJ, Bruynzeel DP. Venous insufficiency in male workers with a standing profession. Part 1:epidemiology.Dermatology 1997, 194:111-120.
19. Mekky S, Schilling RS, Walford J: Varicose veins in women cotton workers. An epidemiological study in England and Egypt.Br Med J 1969, 2:591-595.
20. Tuchsen F, Krause N, Hannerz H, Burr H, Kristensen TS: Standing at work and varicose veins.Scand J Work EnviroHealth 2000, 26:414-420.
21. Stachowiak G, Polac I, Stefanczyk L, Owczarek D, Jedrzejczyk S, Pertynski T. The impact of hormone replacement therapy applied in women with varicose veins on changes in coagulation and fibrinolysis. 2003;15(90):521-4.
Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-5241724EnglishN2015December20HealthcareVITILIGO ASSOCIATED WITH BREAST CANCER - A REPORT OF TWO CASES
English5658Balasubramanian A.English N.S. KannanEnglishAim: Aim of this study is to report two cases of generalised vitiligo (GV) who developed cancer (CA) breast.
Case Report: First case is one of CA right breast with history of GV since three years treated with right modified radical mastectomy. Other one is also a case of CA right breast with history of GV since two years treated with neoadjuvant chemotherapy and radiotherapy and followed by right modified radical mastectomy. The second patient developed fresh area of depigmentation at the site of radiotherapy.
Discussion: Even though the association of autoimmune disease (AD) and cancer is well known, there are not much of reports in the literature. The association might be incidental/coincidental or cause and effect relationship. The association might also be cancer (CA) developing in a patient of AD or development of AD in a cancer patient during or after treatment. AD may increase the risk of developing CA or reduce the risk. AD may worsen pre-existing CA or may be a sign of CA regression. Both our cases were known patients of GV who developed CA breast. One of them had developed fresh area of vitiligo after radiotherapy in the post mastectomy site.
Conclusion: Association between AD and CA is well known for a long time. But many aspects of this association with reference to incidence, exact type of association or background of such association whether genetic, environmental or post therapeutic are still not well understood. Our case reports may incite and add up for further studies on these issues..
EnglishAutoimmune diseases, Generalised vitiligo, AssociationINTRODUCTION
Even though the association of autoimmune disease (AD) and cancer is well known, there are not much of reports in the literature. The association might be incidental/coincidental or cause and effect relationship1 . The association might also be cancer (CA) developing in a patient of AD or development of AD in a cancer patient during or after treatment1-4. AD may increase the risk of developing CA or reduce the risk; AD may worsen pre-existing CA or may be a sign of CA regression5-8. We are reporting two cases of generalised vitiligo (GV) who developed CA breast.
Case details:
Case 1
A 66 years old female presented to our department with complaints of painless swelling in the right breast of 2 months duration. She had generalised vitiligo almost all over the body since three years and on examination, a 6 x 4 cm hard irregular lump was detected in the inner upper and lower quadrants of the right breast without any palpable axillary lymphadenopathy and there was no distant metastasis on evaluation. After necessary work up, right modified radical mastectotomy was done. Postoperative histopathological examination of the specimen was reported as Grade I Infiltrating Ductal Carcinoma and 1 out of 15 lymph nodes positive for metastasis (p T3 N1). The tumour was positive for estrogen and progesterone receptors and negative for Her 2 neu receptor status. There was no history of vitiligo or any cancers in her family (Figure 1).
Case 2
A 44 year old woman, a known case of generalised vitiligo for 2 years presented with locally advanced breast carcinoma on the right side. After clinical and radiologic evaluation and core biopsy confirmation of the diagnosis of infiltrating ductal carcinoma, she was treated with neoadjuvant chemotherapy and radiotherapy followed by right modified radical mastectomy. Patient developed fresh area of depigmentation at the site of radiotherapy (Figure 2). There was no history of vitiligo or any cancers in her family.
DISCUSSION
Evidence suggests that parts of the immune system may generate anticancer responses, while other parts may promote cancer1 . In a state of perpetual activation, immune mediators such as cytokines, chemokines and free radicals, may cause tissue damage leading to chronic inflammation, and subsequently increase the risk of carcinogenesis; other factors affecting immune activity, such as genetic mutations, environmental exposure, and immunomodulatory treatments, may also bolster a carcinogenic environment2-7. Vitiligo is one among the diseases generally considered as autoimmune8 . Generalized vitiligo (GV) is the most common depigmentation disorder, in which acquired multifocal patches of white skin and overlying hair result from loss of melanocytes in the involved areas9,10 1,2. Vitiligo is a chronic disorder with an estimated worldwide prevalence of 0.5–4%11. The prevalence of vitiligo in India has been speculated to vary from 0.1% to >8.8%12. Vitiligo is an acquired hypomelanotic disorder characterized by circumscribed depigmented macules in the skin that result from the loss of functional melanocytes. Vitiligo patches can appear anywhere on the skin but common sites are usually around the body orifices, the genitals, or any sun-exposed areas, such as the face and hands13. Examples of autoimmune disorders associated with development of lymphomas are rheumatoid arthritis, lupus erythematosus, Sjögren’s syndrome, Celiac disease and Hashimoto’s thyroiditis14. There have been several papers published related to cancer other than lymphomas in the ADs including rheumatic diseases, particularly inflammatory arthritis, Sjogren’s syndrome, systemic lupus erythematosus, and scleroderma/ systemic sclerosis15. Incidence of pernicious anaemia and carcinoma stomach associated with vitiligo has also been reported earlier16. The association of GV with malignant melanoma is well documented17. The association of GV with SCC and BCC has been reported earlier18-20. Besides, actinic keratosis and keratoacanthoma centrifugum marginatum have been documented in vitiligo patients21,22. Fresh depigmented lesions in the radiation portals - Koebner’s phenomenon (KP) have however been previously reported in patients with vitiligo who underwent radiation for breast cancer or other cancers23-28. Patients with estrogen receptor - negative breast cancer had a statistically significant better overall survival when they had a history of AD especially among premenopausal patients8 . Both of our patients were known case of GV and have developed cancer breast. One of them developed fresh area of vitiligo after radiotherapy in the post mastectomy site.
CONCLUSION
Association between AD and CA is well known for a long time. But many aspects of this association with reference to incidence, exact type of association or background of such association whether genetic, environmental or post therapeutic (chemotherapy, radiotherapy, hormonal or immuno therapy) are still not well understood. Our case reports may incite and add up for further studies on these issues.
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=378http://ijcrr.com/article_html.php?did=3781. Franks AL, Slansky JE. Multiple associations between a broad spectrum of autoimmune diseases, chronic inflammatory diseases and cancer. Anticancer Res. 2012;32(4):1119-36.
2. Alexandrescu DT, Riordan NH, Ichim TE, Kauffman CL, Kabigting F, Dutton CT, et al. On the missing link between inflammation and cancer. Dermatol Online J. 2011;17:10.
3. Sansone P, Bromberg J. Environment, inflammation, and cancer. Curr Opin Genet Dev. 2011;21:80–5.
4. Grivennikov SI, Greten FR, Karin M. Immunity, inflammation, and cancer. Cell. 2010;140:883–99.
5. Moss SF, Blaser MJ. Mechanisms of disease: Inflammation and the origins of cancer. Nat Clin Pract Oncol. 2005;2:90–7.
6. Goldin LR, Landgren O. Autoimmunity and lymphomagenesis. Int J Cancer. 2009;124:1497–502.
7. Martin DN, Mikhail IS, Landgren O. Autoimmunity and hematologic malignancies: associations and mechanisms. Leuk Lymphoma. 2009;50:541–50.
8. Einefors R, Kogler U, Ellberg C, Olsson H. Autoimmune diseases and hypersensitivities improve the prognosis in ER-negative breast cancer. SpringerPlus 2013;2:357.
9. Taïeb A, Picardo M. Clinical practice: vitiligo. N Engl J Med 2009;360(2):160–9.
10. Birlea SA, Spritz RA, Norris DA: Vitiligo. In Fitzpatrick’s Dermatology in General Medicine. 8th edition. Edited by Wolff K. New York: McGraw-Hill;
11. Forschner T, Buchholtz S, Stockfleth E. Current state of vitiligo therapy-evidence-based analysis of the literature. J Dtsch Dermatol Ges. 2007;5:467–75.
12. Sehgal VN, Srivastava G. Vitiligo: Compendium of clinicoepidemiological features. Indian J Dermatol Venereol Leprol. 2007;73:149–56.
13. Whitton ME, Ashcroft DM, Barrett CW, Gonzalez U. Interventions for vitiligo. Cochrane Database Syst Rev 2006;1:CD003263.
14. Tai P, Yu E, Joseph K, Miale T. A review of autoimmune diseases associated with cancer. Front Biosci (Elite Ed). 2010;2:122-6.
15. Bernatsky S, Ramsey-Goldman R, Clarke A. Malignancy and autoimmunity. Curr Opin Rheumatol. 2006;18(2):129-34.
16. Wright PD, Venables CW, Dawber RP. Vitiligo and gastric carcinoma. Br Med J. 1970;3:148.
17. Spritz RA. The genetics of generalized vitiligo: autoimmune pathways and an inverse relationship with malignant melanoma. Genome Med. 2010;2(10):78.
18. Dhawan AK, Verma P, Singal A, Sharma S. Squamous cell carcinoma complicating vitiligo in an Indian man. J Cutan Aesthet Surg. 2012;5(1):36-7.
19. Lassus A, Apajalahti A, Blomqvist K, Mustakallio M, Kiistala U. Vitiligo and neoplasms. Acta Derm Venereol. 1972;52:229–32.
20. Ortonne JP, Pelletier N, Chabanon M, Thivolet J. Vitiligo and cutaneous epitheliomas. Ann Dermatol Venereol. 1978;105:1063– 4.
21. Buckley DA, Rogers S. Multiple keratosis and squamous carcinoma after PUVA treatment of vitiligo. Clin Exp Dermatol. 1996;21:43–5.
22. Attili S, Attili VR. Keratoacanthoma centrifugum marginatum arising in vitiligo: A case report. Dermatol Online J. 2006;28:18.
23. Munshi A, Jain S, Budrukkar A, Jalali R, Sarin R. Radiotherapyinduced depigmentation in a patient with breast cancer. Indian J Cancer 2007;44:157-8.
24. Koo SW, Suh CO, Hann SK. Vitiligo following radiotherapy for carcinoma of the breast. Br J Dermatol 1996;135:852-3.
25. Levine EL, Ribeiro GG. Vitiligo and radiotherapy: The Koebner phenomenon demonstrated in patients with vitiligo undergoing radiotherapy for carcinoma of the breast. Clin Oncol (R Coll Radiol) 1994;6:133-4.
26. Weitzen R, Pfeffer R, Mandel M. Benign lesions in cancer patients: Case 3, Vitiligo after radiotherapy for breast cancer in a woman with depigmentation disorder. J Clin Oncol 2005;23:644.
27. Polat M, Yalηin B, Alli N. Vitiligo at the site of radiotherapy for nasopharyngeal carcinoma. Am J Clin Dermatol 2007;8:247-9.
28. Weiss G, Shemer A, Trau H. The Koebner phenomenon: review of the literature. J Eur Acad Dermatol Venereol 2002;16:241-8.