Human T-lymphotropic virus type I infection and idiopathic thrombocytopnic purpura

Human T-lymphotropic virus type I (HTLV-I) is the causative agent in adult T-cell leukemia and HTLV-I associated myelopathy. Some other diseases such as uveitis, chronic thyroiditis, Sjögren syndrome, arthritis, acute myeloid leukemia and myelodysplastic syndrome may be also associated with HTLV-I. Several case reports have suggested the possible combination of idiopathic thrombocytopenic purpura (ITP) and HTLV-I infection. In these studies and from our current report, we found 17 patients (22.1%) with HTLV-I infection among 77 ITP patients. The prevalence of HTLV-I infection among ITP patients was higher than that of healthy volunteers (5 approximately 10%). The ITP patients with HTLV-I infection were older than the patients without HTLV-I infection, and the ITP patients with HTLV-I infection had poor response to prednisolone therapy. Among 17 ITP patients with HTLV-I infection, 9 patients received prednisolone therapy. Although most patients had transient increase of platelet counts, only two of them had partial responses (PR) at the last observation date. Five patients underwent splenectomy, and four of them had complete responses (CR) and the remaining patient had a (PR). Four patients received eradication of Helicobactor pylori (H. pylori) infection, and all patients had CRs. Therefore, the ITP patients with HTLV-I infection should receive eradication therapy in the case of H. pylori infection as the first step of therapy and the splenectomy should be considered, if there is no response to conventional therapy. Human immunodeficiency virus (HIV) causes thrombocytopenia in 10% of patients with active HIV disease. The etiologies of HIV thrombocytopenia are considered as follows, the escalated destruction of platelets by the immune system, damage to megakaryocytes by HIV infection and the inhibition of thrombopoiesis by some anti-viral drugs. In the case of ITP patients with HTLV-I infection, the main etiology may be the increased destruction of platelets by immune system. The proviral load and the integration pattern of HTLV-I should be examined to clarify the stage of HTLV-I infection. The possibility of infection of the megakaryocytes by HTLV-I should be also examined for etiological approach.