IJCRR - 8(8), April, 2016
Pages: 01-03
Date of Publication: 20-Apr-2016
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CORRELATION OF COAGULATION PROFILE IN LIVER DISEASE PATIENTS IN A TERTIARY CARE HOSPITAL
Author: G. K. Tripathi, Ankita A. Katara, Shweta V. Awasthi, Shashank V. Srivastava
Category: Healthcare
Abstract:Objective: To determine the coagulation abnormalities among liver disease patients admitted in a tertiary care hospital of Hind Institute of Medical Sciences, Barabanki, Uttar Pradesh (India) for a period of 1 year (January 2015 to December 2015). Methods: Patients were labeled as liver disease patients on the basis of Liver Function Tests (LFT) done in the hospital at the time of admission. Patients blood were collected in sodium citrate and plain vaccutainer for coagulation tests [prothrombin time (PT), activated partial thromboplastin time (aPTT)] and liver function tests respectively. The prothrombin time ratio was calculated and then used to calculate the international normalized ratio. Following parameters were included in Liver Function Test, serum bilirubin, SGOT, SGPT, ALP, Total Protein and serum albumin. Results: Total number of cases studied in a period of 1 year (January 2015 to December 2015) were 311. In 284(91.3%) cases both LFT and coagulation profile were done. In 261 (83.9%) cases (out of total 311 cases) coagulation tests were normal and in 50 (16.1%) cases coagulation tests were found to be deranged. Out of these 50 cases, PT was raised in 44(100%) cases, APTT was raised in 21(95.4%) cases and both PT and APTT were raised in 15(93.75%) cases. Conclusion: Coagulation abnormalities were profound patients with chronic liver diseases. In case of acute liver disease ,usually PT( Prothrombin Time) is increased, but aPTT (activated partial thromboplastin time)is found to be normal. aPTT (activated partial thromboplastin time)is usually increased in chronic liver diseases, but the PT(Prothrombin Time) prolongation is usually not seen in initial stages of chronic liver disease until the stage of liver fibrosis and cirrhosis is reached. Nevertheless, these parameters (PT and aPTT) were still widely used as prognostic markers in liver disease patients..
Keywords: Coagulation abnormalities, Chronic liver disease, PT, aPTT
Full Text:
INTRODUCTION Liver plays a major role in hemostasis, as most of the coagulation factors, anticoagulant proteins and components of the fibrinolytic system are synthesized here. Additionally, it acts as a reticuloendothelial system and regulates coagulation and fibrinolysis by removing these coagulation factors from the circulation. As the liver is a highly vascularized organ liver diseases can alter the abdominal blood flow and predispose patients to significant bleeding problems. Impaired haemostasis resulting from abnormal liver function has multifactorial etiology like impaired coagulation factor synthesis, synthesis of coagulation factors with altered function, increased consumption of coagulation factors and altered clearance of coagulation factors . Coagulation disorders in liver disease are usually measured by the prolongation of global screening tests such as the prothrombin time (PT) and the activated partial thromboplastin time (aPTT)8 . PT determines the time needed for the platelet-poor plasma to clot after the addition of tissue factor (thromboplastin) and calcium chloride. Whereas aPTT determines the time needed for the platelet-poor plasma to clot when mixed with a particulate or soluble activator of the contact coagulation factors (factor XII, pre-kallikrein and high-molecular-weight kininogen) and negatively charged phospholipids such as platelet substitutes9 . PT determines vitamin K dependent extrinsic factors VII, X, II, V and fibrinogen. The aPTT measures the activities of intrinsic and common pathways of coagulation cascade most sensitive to factor VIII, IX, XI, XII and those of the contact system10.
MATERIALS AND METHODS Patients were labeled as liver disease patients on the basis of Liver Function Tests( LFT) done in the hospital at the time of admission. Patients blood were collected in sodium citrate and plain vaccutainer for coagulation tests[prothrombin time (PT), activated partial thromboplastin time (aPTT)] and liver function tests respectively. The prothrombin time ratio was calculated and then used to calculate the international normalized ratio. Following parameters were included in Liver Function Test, serum bilirubin, SGOT, SGPT, ALP ,Total Protein and serum albumin.
RESULTS Total number of cases studied in a period of 1 year ( January 2015 to December 2015) were 311. In 284(91.3%) cases both LFT and coagulation profile were done (Table 1). Out of these 284 cases LFT was deranged in 83(29.2%) cases and 201(70.7%) cases LFT was found to be normal (Table 2). In 261 (83.9%) cases (out of total 311 cases) coagulation tests were normal and in 50 (16.1%) cases coagulation tests were found to be deranged (Table 3). Our study was mainly focused on these 50 (16.1%) cases of deranged coagulation tests. We did LFT in these 50 cases of deranged coagulation tests and found that out of these 50 cases LFT was found to be deranged in 44(88%) cases only. 6(12%)cases in which LFT was found normal were of anticoagulant medication.
Out of these 50 cases only PT was done in 28 (56%) cases, only APTT was done in 6 (12%) cases and in 16(32%) cases both PT and APTT was done (Table 4). Total number of cases in which PT was done were 44 and total number of cases in which APTT was done were 22 (Table 5). PT was raised in 44(100%)cases, APTT was raised in 21(95.4%) cases and both PT and APTT were raised in 15(93.75%) cases (Table 6).
DISCUSSION Liver plays a major role in hemostasis , as it is the primary site for synthesis of most of the coagulation factors and various proteins involved in fibrinolytic pathway. These include vitamin K dependent coagulation factors( factor II, VII, IX, X, Protein C and Protein S ), factor V, XIII, fibrinogen, antithrombin and plasminogen. All the Vitamin K dependent factors have glutamic residues at their amino terminal. These glutamic residues must be converted to gamma-carboxyglutamic acid residues, which then bind to calcium and lead to formation of activation complexes1 . Most of the patients with liver disease have coagulopathies1 , resulting in imbalanced hemostasis.
These changes lead to increase risk of bleeding as well as thrombosis. Coagulation tests are especially important in patients who are at bleeding and thrombotic risks such as gastrointestinal varices and vascular stasis. PT is a measure of synthetic function of liver and is involved in most of the liver disease .It is used all over the world as a major therapeutic indicator regarding liver transplantation in acute liver failure and cirrhosis, or regarding steroid therapy in alcoholic hepatitis234. Various hepatic disorders, vitamin K deficiency, warfarin toxicity, and fibrinolysis may be associated with prolongation of PT 5 . In acute liver diseases, usually PT is increased, but the aPTT is normal and, but in chronic liver disease, prolongation of PT is not seen initially until the stage of cirrhosis and the liver fibrosis reaches6 .
As the disease progresses both PT and aPTT levels are prolonged, but in compensated cirrhosis, high level of factor VIII may blunt the prolongation of aPTT7 . This finding matches with our study, as in our study PT(44)was increased in more number of patients in comparision to aPTT(21) [TABLE-5].In addition, in advanced liver disease there is a strict balance of the procoagulant.
CONCLUSION Coagulation abnormalities were profound patients with chronic liver diseases.. . In acute liver diseases, usually PT is increased,but the aPTT is normal and, but in chronic liver disease , prolongation of PT is not seen initially until the stage of cirrhosis and the liver fibrosis. Nevertheless, these parameters (PT and aPTT) were still widely used as prognostic markers in liver disease patients.
References:
1. Borowski M, Furie BC, Bauminger S et al. (1986) Prothrombin requires two sequential metal dependent conformational transitions to bind phospholipid. Conformation- specific antibodies directed against the phospholipid-binding site on prothrombin.JBiol Chem261 (32),14969-14975.
2. Caraceni P, Van Thiel DH. Acute liver failure.Lancet 1995;345:163-169.
3. Dickson ER, Grambsch PM, Fleming TR, Fischear LD, Langworthy A. Progformer. Hepatology1989;10:1-7.
4. Carithers RL, Herlong HF, Diehl AM, Shaw EW, Combes B, Fallon HJ, Maddrey WC. Methyl prednisolone therapy in patients with severe alcoholic hepatitis. Ann Intern Med 1989;110:685- 690.
5. Michal J, Carey , George M. Rodgers . Disseminated Intravascular Coagulation: Clinical and Laboratory Aspects, American Journal of hematology1998; 73: 65-73.
6. Xavier Forns ,SergiAmpurdanès, Josep M. Llovet, and et al. Identification of chronic hepatitis C patients without hepatic fibrosis by a simple predictive model. Hepatology 2003; 36 : 986 – 992.
7. TTOCO2.4 Synthetic Function. 2.4.2 The liver and coagulation, page 255-263.
8. Rverter JC. Abnormal hemostasis tests and bleeding in chronic liver disease: are they related? Yes. J Thrombheamost 2006; 4: 717-20.
9. Tripodi A. Tests of coagulation in liver disease. Clin Liver Dis 2009; 13: 55-61.
10. Thachil J. Relevance of clotting tests in liver disease. Postgrad Med J 2008; 84: 177-81.
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