HIV associated thrombotic microangiopathy

Abstract

Thrombotic microangiopathy (TMA) is a known complication of HIV infection. Endothelial cell injury appears to be the primary event causing platelet activation and deposition in the microvasculature. Direct cytopathic roles of HIV as well as other factors such as malignancy, drugs, and infectious agents have been implicated in the pathogenesis of HIV-TMA. Although the the majority of patients present in a more advanced stage of HIV disease, TMA can be the initial presenting symptom of HIV infection. Clinical features are those of idiopathic TMA, and the diagnosis should be suspected in any patient with new onset thrombocytopenia and microangiopathic haemolytic anaemia. Therapy with plasma exchange or infusion appears to be efficacious. A rapid diagnosis and institution of plasmapheresis is crucial for a favourable outcome. The long term prognosis of HIV-TMA is unfavourable and may depend on the stage of HIV infection. The recent data after the use of highly active retroviral treatment, however, are unavailable and current prognosis is therefore uncertain.

ADAMTS13 activity in thrombotic thrombocytopenic purpura–hemolytic uremic syndrome: relation to presenting features and clinical outcomes in a prospective cohort of 142 patients

“…TTP-HUS was considered to be the only clinical diagnosis responsible for the presenting features in patients in categories 1 to 4 and 6. Patients in category 5 who were described as having an additional disorder also had an established diagnosis of an autoimmune disorder 26 (n ϭ 17) or HIV infection 27 (n ϭ 2) at the time the diagnosis of TTP-HUS was made. All 142 patients had diagnostic tests for HIV infection at the time of the first plasma exchange; only 2 (1%) patients had confirmed positive tests.…”

The Role of Platelets in Viral Hemorrhagic Fevers

“…Certainly a severe thrombocytopenia occurs and is implicated in poor prognosis, however, is this secondary to DHF/DSS, or is it a key player in the pathogenesis? Anti-platelet antibodies or platelet-associated antibodies have been detected in some patients [108,111,[143][144][145], and this may be due to molecular mimicry between a platelet antigen and a DENV antigen [144], and molecular mimicry is known to occur with other microorganisms [146][147][148]. However, this does not explain why a repeat infection is required for thrombocytopenia, as the platelet antigen should drive the immune response.…”

“…Endothelial cell infection can lead to activation and subsequent adhesion of platelets [110]. Thus, endothelial cell activation has been suggested to drive HIV-associated thrombocytopenia [111], and DENV-infected endothelial cells support platelet adhesion [112]. The presence of activated platelets or platelet-leucocyte aggregates has also been shown to lead to activation of the endothelium [113].…”

Thrombocytopenia

“…Морфологически ТМА опреде-ляется как уплотнение сосудистой стенки с набуханием или отделением эндотелиальных клеток от базальной мембраны и отложени-ем гиалиновых депозитов в субэндотелиаль-ном пространстве, внутрисосудистые тром-боцитарные тромбы и окклюзия сосудов [19].…”