Bhalli A, Mohsin S, Aslam M, Saeed T, Hussain S, Bashir N.
Antithrombin III as marker of fibrosis in chronic hepatitis C.
Biomedica Jan ;31(3):228-31.

Background and Objective: Chronic hepatitis C is one of the most common causes of liver cirrhosis. Haemostasis profile derangement including decrease in anticoagulant factors is a regular feature in liver disease but degree of decrease in anticoagulant factors and its clinical significance is currently unclear. Liver biopsy is the gold standard for the assessment of cirrhosis in chronic hepatitis. However, biopsy is invasive and costly and is associated with patient discomfort and risk of major complications. Antithrombin – III (AT) is synthesized in liver and changes in its levels are associated with the extent of cirrhosis. This study aimed to establish the role of AT as a noninvasive marker of fibrosis in chronic hepatitis C patients. Methods: Fifty chronic hepatitis patients were included in this study. They were further divided into two groups on the basis of their histological stages of fibrosis. Group A included stages 0-3 of fibrosis whereas group B included stages 4 – 7 of fibrosis. Each group comprised of 25 chronic hepatitis patients. AT, Aspartate aminotransferase (AST), Alanine aminotransferase (ALT) and platelet count were performed on all subjects. Results: Mean ± SD of AT in patients with group A (fibrosis stage 0 – 3) was 96.48 ± 12.13% whereas AT level in group B patients (fibrosis stage 4 – 6) was 58.92 ± 22.03% (p value < 0.001). Conclusion: These results showed level of AT was reduced in advanced stage of fibrosis when compared with early stage of fibrosis.

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