Hepatitis C virus‐related adult chronic idiopathic thrombocytopenic purpura: experience from a single Chinese center

To the Editor: Chronic idiopathic thrombocytopenic purpura (ITP) is characterised by increased platelet destruction caused by antiplatelet autoantibodies that result in platelet phagocytosis by the reticuloendothelial system (RES) (1). Several reports, including one in the first issue of this journal, have shown a high prevalence of hepatitis C virus (HCV) infection in patients with chronic ITP (2–4). We report here our experience from a single center in China. Anti-HCV antibody (HCVab) was assayed in 247 chronic ITP patients referred to our hospital between 1992 and 2001; the clinical data were retrospectively analyzed. All patients fulfill the following criteria for chronic ITP: adult patients (‡18 yr old); isolated thrombocytopenia (<100 · 10/L) that had persisted for a minimum of 6 months; a normal or increased number of bone marrow megakaryocytes; absence of myelodysplastic features on bone marrow and lack of other known causes such as Systemic Lupus Erythematosus (SLE), etc. All patients were negative for anti-human immunodeficiency virus antibodies. Treatment response was defined as follows: (a) complete remission (increase in platelet count to ‡100 · 10/L); (b) partial or no response (platelet count <100 · 10/L). Data were analyzed by SPSS 10.0 for windows. P < 0.05 was considered statistically significant. As shown in Table 1, 33 of 247 (13.4%) patients were HCVab positive. Six patients (four males and two females) had developed hepatitis before ITP was diagnosed, and two of them had liver dysfunction. None had cirrhosis and/or splenomegaly according to abdominal ultrasound examinations. Of the remaining 27 patients, HCVab was not assayed until they were seen at our hospital, so that, we cannot exclude the possibility that in some patients, HCV might have been acquired after ITP developed. Potential source of HCV transmission in these patients included intravenous immunoglobulin concentrates (2) infused prior to our HCV studies. After one course treatment with steroid, platelet counts increased to above 100 · 10/L in 37.8% of HCVab-negative patients and 31.2% of HCVabpositive patients. Those who did not respond to steroid were treated with traditional Chinese medicine, vincristine or azathioprine. Splenectomy was performed in five of 33 (15.2%) HCVab-positive patients and 60/214 (28.0%) HCVab-negative patients. Relapsed postsplenectomy occurred in two of five (40%) HCVab-positive patients and in 21 of 60 (35%) HCVab-negative patients. These relapsed patients were treated with vincristine or azathioprine. There was no difference in clinical and laboratory data between HCVab negative and positive chronic ITP patients (P > 0.05). Similar to other reports (3–5), our data confirmed the high prevalence (13.4%) of HCV infection in chronic ITP patients, and this prevalence rate is significantly higher than that (2.2%) in general Chinese population in our country (6). Some studies have shown platelets carrying HCVRNA in HCV infection patients and that free HCV could bind to normal human platelets by the putative role of human CD81 as a receptor for HCV (7). HCV-RNA in platelet could replicate actively under some conditions such as the use of immunosuppressive agents (7). Bordin et al. reported that HCV might also depress platelet production, directly causing thrombocytopenia (8). The study of Li et al. suggested that megakaryoblasts are vunerable to HCV infection and HCV can replicate in these cells, hiding in them for years (9). Treatment of HCV-associated thrombocytopenia with recombinant a2b-interferon, an inhibitor of viral replication, could lead to an increase in platelet counts in HCV-positive thrombocytopenic patients, indicating indirectly that HCV might play an important role in thrombocytopenia (9, 10). The pathophysiologic relationship of HCV and platelet or megakaryocyte in HCVassociated thrombocytopenia needs to be further studied. Eur J Haematol 2003: 70: 196–197 Printed in UK. All rights reserved Copyright Blackwell Munksgaard 2003