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HIV‐Associated Thrombotic Microangiopathy in the Era of Highly Active Antiretroviral Therapy: An Observational Study
108
Citations
22
References
2004
Year
ImmunologyHuman Immunodeficiency VirusImmunotherapyThrombosisHuman RetrovirusHematologyPrimary ImmunodeficiencyAutoimmune DiseaseNeurovirologyHiv-1 Rna LevelsActive Antiretroviral TherapyAutoimmunityObservational StudyImmunologic DiseaseChronic Viral InfectionHivThrombotic MicroangiopathyAids PathogenesisTreatment And PreventionMedicine
The prevalence and predisposing factors of thrombotic microangiopathy (TMA) in the era of highly active antiretroviral therapy (HAART) were evaluated among patients in the Collaborations in Human Immunodeficiency Virus (HIV) Outcomes Research/US cohort. Of 6022 patients, 17 (0.3%) had TMA, with unadjusted incidences per 100 person-years of 0.079 for TMA, 0.009 for thrombotic thrombocytopenic purpura, and 0.069 for hemolytic-uremic syndrome. Compared with patients without TMA, patients with TMA had lower mean CD4(+) cell counts (197 vs. 439 cells/mm(3); P=.0009) and higher mean log(10) HIV-1 RNA levels (4.6 vs. 3.3 copies/mL; P=.0001) at last follow-up and a significantly greater incidence of acquired immune deficiency syndrome (82.4% vs. 55.3%; P=.025), Mycobacterium avium complex infection (17.6% vs. 3.3%; P=.018), hepatitis C (29.4% vs. 11.3%; P=.001), and death (41.2% vs. 7.4%; P<.0001). The prevalence of herpes and use of antiherpetics were slightly higher for patients with TMA, but unadjusted distributions were not statistically significant. TMA in a cohort surveyed after the introduction of HAART was rare and was associated with advanced HIV disease.
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