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© Research
Publication : Scandinavian journal of immunology

Human immunodeficiency virus-associated thrombotic microangiopathies: clinical characteristics and outcome according to ADAMTS13 activity

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in Scandinavian journal of immunology - 01 Sep 2008

Malak S, Wolf M, Millot GA, Mariotte E, Veyradier A, Meynard JL, Korach JM, Malot S, Bussel A, Azoulay E, Boulanger E, Galicier L, Devaux E, Eschwège V, Gallien S, Adrie C, Schlemmer B, Rondeau E, Coppo P,

Link to Pubmed [PMID] – 18782260

Scand. J. Immunol. 2008 Sep;68(3):337-44

Human immunodeficiency virus (HIV) infection is a risk factor for thrombotic microangiopathy (TMA). We sought whether a severe deficiency in ADAMTS13, the enzyme specifically involved in the cleavage of von Willebrand factor, was associated with specific presenting features and outcome in HIV-associated TMA. In this prospective, multicentre, case-control study, 29 patients of 236 in the French Network on TMA had an HIV-associated TMA. Seventeen patients with severe ADAMTS13 deficiency (ADAMTS13 or=5% HIV(+) group). HIV(+) patients were also compared to 62 patients with idiopathic TMA, either with (45 patients, ADAMTS13 or=5% idiopathic group) severe ADAMTS13 deficiency. ADAMTS13 or=5% HIV(+) patients (23.5% versus 91.6%, respectively, P = 0.0005) and their median CD4(+) T cell count was higher (P = 0.05). TMA-associated death rate was higher in ADAMTS13 >or=5% HIV(+) patients than in ADAMTS13 <5% HIV(+) patients (50% versus 11.7%, respectively, P = 0.04). In ADAMTS13 or=5% HIV(+) patients was higher than in idiopathic patients (11.7% in idiopathic patients, P = 0.04). In conclusion, HIV-associated TMA with severe ADAMTS13 deficiency have less AIDS-related complications and a higher CD4(+) T cell count. TMA prognosis is better and comparable to this of idiopathic forms.