INTRODUCTION
Thrombotic thrombocytopenic purpura (TTP) is triad of severe thrombocytopenia (usually less than 100x109/l), macroangiopathic hemolytic anemia and varying end organ involvement (1). Also called Moschcowitz disease, this occurs following the increase in prothrombotic state with the deficiency in the disintegrin and metalloproteinase with thrombospondin motifs 13 (ADAMTS 13), the molecule that cleaves and thereby activates the von Williebrand factor (vWF) (2). Large, uncleaved multimers of vWF forms a substrate for the binding of platelets within the blood vessels with subsequent mechanical fragmentation of red blood cell, occlusion of the microcirculatory bed and organ ischemia. The more prevalent form of this disease is acquired, with the formation of autoantibodies against ADAMTS 13 however, compound heterogeneous or homogeneous mutations may also occur: Upshaw-Schulman syndrome (3, 4). TTP usually presents acutely with rapid deterioration of the patient and has a high mortality and recurrence rate in those who survive an acute episode. Neurologic (headache, seizures and coma), cardiac (ST- elevation and non-ST elevation myocardial infarction, heart failure) and renal manifestations have been documented and many patients develop multi organ failure leading to their eventual demise within weeks if not adequately managed (5, 6). The bedrock of treatment is the use of therapeutic plasma exchange with fresh frozen plasma as this reduces the autoantibodies against ADAMTS 13 and improves the levels of functional vWF.(7)