Thrombocytopenia in chronic hepatitis C

Abstract

Background and aims: Thrombocytopenia in patients with chronic hepatitis C may be the result of several factors: bone marrow inhibition, the decrease of liver thrombopoietin production and an autoimmune mechanism. Clinical variables such as age, gender, severity of liver disease and degree of viremia could influence the severity of platelet reduction. The goal of this study is to determine the prevalent mechanism of thrombocytopenia in patients with chronic hepatitis C and the clinical predictors of its severity.

Methods: Eighty-one patients with chronic hepatitis C and thrombocytopenia were included. The viral inhibition on the bone marrow (central mechanism) was studied by performing bone marrow biopsy from the iliac crest. The presence of antiplatelet antibodies by ELISA assessed the peripheral mechanism. The clinical predictors included in the analysis were: age, gender, ALT level, liver fibrosis stage and HCV RNA.

Results: Coexistence of a central and peripheral mechanism was found in the vast majority (93.3%) of patients with severe thrombocytopenia (< 100,000/microL) and in most patients (61.53%) with moderate thrombocytopenia (100,000- 125,000/microL). In patients with less severe thrombocytopenia (126,000-149,000/microL), autoimmune destruction was the sole mechanism (85%). Thrombocytopenia was significantly associated with ALT values, viral load and stage of fibrosis.

Conclusions: Our data demonstrates that chronic hepatitis C is associated with a variable degree of thrombocytopenia. As the disease advances, the platelet count decreases and, in most cases, both mechanisms are involved. The stage of fibrosis is one of the major determinants of thrombocytopenia.