Coagulative Disorders in HIV-Infected Patients Leading to Microvascular Risk of Thrombosis
Microthrombotic Disease in HIVPatients
Thrombotic thrombocytopenic purpura (TTP) is a microthrombotic disease of rare occurrence. The most clinically sensitive microcirculations to TTP are those of the brain, kidney, and liver, explaining the most frequent clinical manifestations of the disease.
One of the main pathogenic mechanism of TTP is a deficiency (hereditary or acquired) of an endogenous metalloprotease (ADAMS 13) which physiologically degrades the highest-molecular-weight forms of VWF into lower-molecular-weight fragments. The increased concentration of higher-molecular-weight forms of VWF triggers in vivo platelet aggregation and formation of platelet microthrombi, which plug the microcirculations of the most sensitive organs. The treatment is based on plasma exchange and infusion of fresh frozen plasma to remove the highest-molecular-weight forms of VWF, to remove the inhibitors of ADAMS 13, and to replenish ADAMS 13. From an epidemiologic point of view, TTP in HIV infection is associated with opportunistic infections (cryptosporidiosis, cytomega lovirus infection) [54], with HIV-associated malignancies, or with HIV-associated wasting syndrome. The incidence of TTP is significantly reduced after the introduction of HAART (Fig. 4) [55, 56].
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