Published online Sep 21, 2017. doi: 10.3748/wjg.v23.i35.6540
Peer-review started: May 18, 2017
First decision: June 22, 2017
Revised: July 6, 2017
Accepted: August 8, 2017
Article in press: August 8, 2017
Published online: September 21, 2017
We report the first case of a patient with hepatitis C virus (HCV) infection and idiopathic thrombocytopenic purpura (ITP), who later developed acquired amegakaryocytic thrombocytopenia (AAMT), with autoantibodies to the thrombopoietin (TPO) receptor (c-Mpl). A 64-year-old woman, with chronic hepatitis C, developed severe thrombocytopenia and was diagnosed with ITP. She died of liver failure. Autopsy revealed cirrhosis and liver carcinoma. In the bone marrow, a marked reduction in the number of megakaryocytes was observed, while other cell lineages were preserved. Therefore, she was diagnosed with AAMT. Additionally, autoantibodies to c-Mpl were detected in her serum. Autoantibodies to c-Mpl are one of the causes of AAMT, acting through inhibition of TPO function, megakaryocytic maturation, and platelet formation. HCV infection induces several autoantibodies. HCV infection might also induce autoantibodies to c-Mpl, resulting in the development of AAMT. This mechanism may be one of the causes of thrombocytopenia in patients with HCV infection.
Core tip: Thrombocytopenia occurs frequently in patients with hepatitis C virus (HCV) infection. Acquired amegakaryocytic thrombocytopenia (AAMT) is one of the causes of severe thrombocytopenia. The exact mechanisms of AAMT have not been fully elucidated. However, patients with autoantibodies to thrombopoietin receptor (c-Mpl) develop AAMT. Similarly, autoantibodies are sometimes generated in patients with HCV infection. Here, we report the first case of a patient with HCV infection who later developed AAMT with autoantibodies to c-Mpl. AAMT with autoantibodies to c-Mpl may be one of the causes of thrombocytopenia in patients with HCV infection.