A Look at Platelet Count in Chronic Hepatitis C Infection

*Romeo-Gabriel Mihăilă

Faculty of Medicine, “Lucian Blaga” University of Sibiu; Hematology Department, Emergency County Clinical Hospital Sibiu, Sibiu, Romania
*Correspondence to romeomihaila@yahoo.com

Disclosure: The author has declared no conflicts of interest.
Received: 15.02.17 Accepted: 19.04.17
Citation: EMJ Hepatol. 2017;5[1]:97-103.

Abstract

A complete blood count performed in chronic hepatitis C virus (HCV) infected patients can identify thrombocytopenia or an increased number of platelets, the cause of which must be established. Most of these patients are predisposed to develop thrombocytopenia as the disease progresses due to a lower thrombopoietin production, increased platelet pooling in the spleen, viral bone marrow suppression, or interferon-based therapy. However, a severe thrombocytopenia can have an autoimmune aetiology, which is very probable at values <15×103/mm3. Thrombopoietin analogues are useful both in patients with primary immune thrombocytopenia and in those who will begin the treatment with pegylated interferon and ribavirin before surgery. The common causes of an increased number of platelets in chronic HCV infected patients are splenectomy, ribavirin treatment, liver transplantation, and hepatocellular carcinoma. However, thrombocytosis can also be hereditary, reactive, or malignant, especially in essential thrombocythaemia or other myeloproliferative diseases that can be associated. A hepatic blood flow obstruction present in chronic HCV infected patients must draw attention to a possible associated myeloproliferative disorder (which frequently manifests in thrombocytosis) that represents its aetiology in two-thirds of cases and which can evolve with a constant or an intermittent increase in platelet count. The role of the JAK-STAT signalling mechanism is presented in both chronic hepatitis C patients and in those with essential thrombocythaemia. It was suggested that STAT3 could have a role in HCV RNA replication. In addition, the HCV core protein is involved in the modulation of fibrogenetic gene expression in hepatic stellate cells through a JAK2-STAT3 dependent pathway. Ruxolitinib (a JAK1/JAK2 inhibitor) can have beneficial effects in essential thrombocythaemia and is a subject of research in chronic hepatitis C. The discovery of the aetiology of thrombocytopenia or an increased number of platelets can contribute to a more complete diagnosis and appropriate treatment. The identification of associated disorders in chronic HCV infected patients is of vital importance for them.

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