Correlations of folic acid, vitamin B12, homocysteine, and thrombopoietin to platelet count in HCV infection

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Abstract

Introduction

The platelet count is known to decrease in proportion to the advancement of the stage of liver disease in chronic hepatitis C (CHC) viral infection. The platelet count is currently used as an index for fibrosis staging. The pathophysiology of thrombocytopenia (TCP) in patients with hepatitis C virus (HCV) infection is not completely understood.

Purpose

This work aimed to study the correlations of folic acid (FA), vitamin B12 (Vit B12), homocysteine (Hcy), and thrombopoietin to the platelet count in HCV infection.

Patients and methods

Sixty-seven patients (51 men and 16 women) with HCV infection were included in this study. All patients were sero-negative for hepatitis B viral markers. In addition, 20 healthy volunteers, matched for sex and age, were included as a control group. All patients and control individuals were subjected to the following: assessment of medical history, thorough clinical examination, and laboratory investigations including the following: complete blood cell counts, viral hepatitis markers, liver and renal function tests, HCV-RNA by quantitative PCR, serum folate, Vit B12, thrombopoietin, and plasma Hcy. Abdominal ultrasonography and ultrasound-guided liver biopsy for histopathologic examinations were carried out for the patients. Patients were divided into two groups of 36 patients with CHC and 31 patients with cirrhosis with HCV liver cirrhosis (LC).

Results

The results indicated a significant decrease in the platelet count in CHC and LC patients compared with the healthy control group. There was a highly significant decrease in the FA level in CHC and LC patients compared with the control group; also, a significant decrease in the platelet count was found in LC patients compared with CHC patients. Hcy was significantly increased in CHC and LC patients. There was a nonsignificant decrease in Vit B12 in CHC patients, whereas it was significantly increased in LC patients. There was a nonsignificant decrease in thrombopoietin in CHC patients compared with the control group, whereas in LC patients, there was a highly significant decrease. There was a highly significant positive correlation between the platelet count and FA, but an insignificant correlation between the platelet count and Hcy, Vit B12, thrombopoietin, and viral load.

Conclusion

This study concluded that TCP in HCV-related chronic liver diseases is multifactorial and decreased FA is involved in its pathogenesis as an independent risk factor. Increased Hcy may cause TCP through platelet activation and endothelial dysfunction.

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