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TTP in HIV-positive individuals may be associated with the presence of severe ADAMTS13 deficiency and anti-ADAMTS13 antibodies. Those with severe ADAMTS13 deficiency (5%, who have an increased mortality (Malak et?al, 2008). Pregnancy can be the initiating event for approximately 5�C25% of TTP cases (Ridolfi & Bell, 1981; Vesely et?al, 2004; Scully et?al, 2008), http://en.wikipedia.org/wiki/Methisazone which are late onset adult congenital TTP or acute idiopathic TTP. Differentiating TTP from the more common pregnancy-related TMAs, such as pre-eclampsia, HELLP syndrome (haemolysis, elevated liver enzymes, low platelets) and HUS is difficult, especially if TTP presents post-partum (Table?4). Thrombosis occurs in the placenta in untreated TTP pregnancies and results in fetal growth restriction, intrauterine fetal death and pre eclampsia. There is a continued risk of relapse during subsequent pregnancies. Women with normal levels of ADAMTS13 pre-pregnancy have a lower risk of relapse (Ducloy-Bouthors et?al, 2003; Scully et?al, 2006b). Drugs appear to http://www.selleckchem.com/products/bay-57-1293.html be responsible for http://www.selleckchem.com/products/Roscovitine.html TTP associated with oestrogen-containing hormonal preparations such as the combined oral contraceptive pill (COCP) and hormone replacement therapy (Scully et?al, 2008). Some chemotherapy agents, such as gemcitabine, bleomycin and mitomycin�CC can cause HUS but not TTP. 1 Medications associated with precipitation of TTP include quinine and oestrogen-containing medications, which should be avoided to prevent relapse in patients with a previous episode of TTP (2C). 2 Women with previous TTP should be offered non-oestrogen containing contraception (1C). Transplant-associated microangiopathy (TAM) is a MAHA and thrombocytopenia that occurs after bone marrow transplantation. It may reflect endothelial toxicity associated with chemotherapy, infections, immunosuppressives, such as ciclosporin A (CSA), and graft-versus-host disease (GVHD).