Late onset of severe thrombocytopenia during interferon treatment for chronic hepatitis C infection: Case report

• Main Authors: Hajder Jelena, Stanisavljević Nataša, Marković Olivera, Marisavljević Dragomir
• Format: Article
• Language: English
• Published: Serbian Medical Society 2010-01-01
• Series: Srpski Arhiv za Celokupno Lekarstvo
• Subjects: immunologic thrombocytopenia; hepatitis C infection; PEG-interferon; treatment
• Online Access: http://www.doiserbia.nb.rs/img/doi/0370-8179/2010/0370-81791004240H.pdf

Introduction. Thrombocytopenia is a common finding in chronic liver diseases and it is caused by different pathophysiological mechanisms. Immunologic thrombocytopenic purpura (ITP) in hepatitis C infection is a distinct clinical entity. Possible reasons for ITP in this case could be capabillity of HCV to induce autoimmune phenomena but also immunomodulatory effects of interferon that is used for HCV infection treatment. The specific laboratory parameters for ITP diagnosis during HCV infection have not been defined yet. Case Outline. A 37-year-old patient diagnosed with HCV infection was treated with PEG-interferon and Ribavirin during 24 weeks. The partial response was achieved after the therapy with reduction of viral replications. One month after therapy completion, the patient was hospitalized due to skin haemorrhagic syndrome and a serious degree of thrombocytopenia (2×109/l). The number and megakaryocyte morphology in bone marrow aspirate were normal. An assay of thrombocyte kinetics by radioactive marker (Indium 111) showed rapid thrombocyte destruction and their early seljuestration in the spleen. Conclusion. Results of assays about thrombocyte kinetics during HCV infection show enchanced thrombocyte destruction in the liver. Accordingly, the most important parameter for ITP diagnosis in HCV infection, in this case, was rapid thrombocyte destruction and their early sequestration in the spleen approved by Indium kinetics. Also, in support of ITP is the increment of thrombocyte number during therapy with intravenous immunoglobulins. Thrombocytopenia was developing during antiviral therapy and on indirect conclusion is that viral replication is not the reason for it.