Thrombotic thrombocytopenic purpura (TTP) is a severe, occlusive, thrombotic microangiopathy characterized by a systemic platelet aggregation, organ ischemia, profound thrombocytopenia and erythrocyte fragmentation. However, in spite of the recent progresses in the pathophysiology of TTP, many aspects of this disease remain still controversial. Recently Helicobacter pylori, has been implicated in the pathogenesis of idiopathic thrombocytopenic purpura (ITP) as a triggering factor in TTP by inducing platelet aggregation through an interaction with von-Willebrand factor (VWF). In this study, an alternative pathogenic mechanism for TTP involving Helicobacter pylori infection is proposed. Ninety four patients undergoing transplantation were enrolled in them H pylori infection was recognized by UBT and stool antigen detection and the levels of two cytokines of IL-12 and IL-8 were determined by ELIZA methods. Eight patients developed TTP and 86 did not (controls). A significant higher -positive rate for H. pylori infection was shown in the TTP group (p < 0.05). However, the levels of interleukin-12 and interleukin-8 increased significantly at the onset of TTP ((p< 0.05) in compared with their levels in the control group. In conclusion, H. pylori may play a role in the pathogenesis of TTP in BMT patients, with involving IL-8 and IL-12.