TTP is a multisystem disorder characterized by deposition of intra-vascular platelet microthrombi, causing consumption thrombocytopenia, microangiopathic hemolytic anemia, renal abnormalities, neurologic disturbances and fever. ITP is characterized by low platelet count with otherwise normal results on complete blood count and peripheral blood smear. It is an isolated thrombocytopenia with no other underlying etiology. Contrary to the two above-mentioned disorders, ET is a myeloproliferative disease characterized by sustained and unexplained proliferation of megakaryocytes leading to increased platelet count, often in excess of 1,000,000/mm3.
ITP is a disease caused by autoantibodies to platelets. The antigenic target in most patients appears to be the platelet glycoprotein IIb/IIIa complex  Platelets with antibodies on their surface are trapped in the spleen, where they are efficiently removed by splenic macrophages. The origin of these antibodies is not known. They may be directed towards the viral antigens and then cross-react with platelet antigens. Recent observations have documented that a deficiency of a Von Willebrand factor (VWF)-cleaving protease, termed ADAMTS13 ('a disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13'), that normally cleaves hyper-reactive unusually large VWF multimers into smaller and less adhesive VWF forms, may be responsible for many cases of TTP . A mutation in JAK2 kinase (V617F) was found to be associated with essential thrombocytosis . A diagnosis of ET is made when a patient has an elevated platelet count, an increased number of megakaryocytes in the bone marrow with no identifiable underlying abnormality known to cause thrombocytosis and the absence of findings suggestive of a different myeloproliferative disorder.
TTP transformation to ITP has been described previously in the literature [4, 5] as has their coexistence in a single patient with HIV , in post-partum states , and in patients with systemic lupus erythematosus (SLE) , all of which were absent in our patient.
A review performed by Baron et al. in 2001 identified 11 cases in the literature that developed both ITP and TTP concomitantly or sequentially . In the 11 described cases, two were male, nine were female, and their ages ranged from 14 to 62 years. Associated medical conditions were autoimmune disorders such as hypothyroidism, SLE, rheumatoid arthritis and Sjogren's disease. The two conditions, TTP and ITP, were noted to occur days to years apart, the longest duration being two and a half years.
None of the patients previously reported to have TTP and ITP had essential thrombocythemia as part of their clinical course.
Our patient had no evidence of HIV infection, had no associated autoimmune disease and was not pregnant. Moreover, the increased platelet count in our patient was of primary origin, was not post-splenectomy and was not reactive to drugs as suggested by the findings on bone marrow biopsy. ITP occurred seven years after the diagnosis of TTP.
The fact that both immune and thrombotic thrombocytopenic purpura occur with increased frequency among persons with systemic lupus erythematosus, HIV or pregnancy supports the hypothesis that some pathophysiologic factors are shared. These include: circulating antibodies or antigen-antibody complexes caused by the primary autoimmune disorder and inducing endothelial dysfunction ; platelet damage by TTP and production of autoantibodies ; deficiency of Von-Willebrand factor cleaving protease activity  or autoantibody against VWF cleaving protease ; molecular mimicry or redundancy of the immune system, also known as the kaleidoscope of immunity, which is the co-occurrence of various autoimmune diseases within an individual .
The association of TTP and ITP in the same patient supports the notion that TTP and ITP share similar pathogenetic mechanism; however, there is no known common factor implicated in the etiology of all three platelet disorders.