The etiology and pathogenesis of thrombotic thrombocytopenic purpura (TTP) are complex and not well understood. Often, patients themselves have susceptibility factors such as structural defects in ADAMTS13 itself or the presence of inhibitory anti-ADAMTS13 antibodies in the circulation causing decreased ADAMTS13 activity, resulting in decreased VWF supramolecular multimer (UL-VWF) catabolism. In the presence of triggers such as infection, drugs or even pregnancy, the activation of microcirculatory endothelial cells and platelets leads to the formation of microvascular thrombosis and causes tissue necrosis and infarction. Therefore, due to the existence of susceptibility factors, TTP has a high recurrence rate, especially when it is secondary to autoimmune diseases (e.g., systemic lupus erythematosus, rheumatoid arthritis, polyarteritis, etc.) To prevent recurrence, attention should first be paid to avoid triggers such as infections, drugs, pregnancy, etc. Infections are often viral (e.g., coxsackievirus and even vaccination); drugs include antitumor drugs ( mitomycin, vincristine, cisplatin, bleomycin, cytarabine, erythromycin, cytarabine, etc.), antiplatelet drugs (ticlopidine, clopidogrel, etc.), calcium-modulating drugs (zolay phosphate, etc.). For refractory and recurrent TTP, increased frequency of plasma exchange, splenectomy and treatment with anti-CD20 monoclonal antibodies (melphalan) may be considered. For you, “pregnancy” is the main trigger, and the possibility of recurrence is reduced without further pregnancy.