HIV-positive persons who use stimulants such as methamphetamine experience difficulties navigating the HIV care continuum that undermine the benefits of antiretroviral therapy (ART). However, few studies have examined the association of stimulant use with viral suppression in the era of universal ART.
Zuckerberg San Francisco General Hospital.
HIV-positive persons participating in a clinical cohort study and taking ART completed assessments every 4–6 months. The exposure was the cumulative, time-varying proportion of assessments with any self-reported stimulant use. The time-varying outcome, HIV viral suppression (ie, <200 copies/mL), was measured at assessments or extracted from the clinical record.
In total, 1635 HIV-positive participants on ART contributed 17,610 person-visits over a median of 2.3 [interquartile range (IQR) = 1.0–5.3] years of follow-up. Participants were middle-aged (median = 45.0; IQR = 38.0–52.0), predominantly white (57%), sexual minority men (78%), with a median CD4+ T-cell count of 409 (IQR = 225–640) cells/mm3 at enrollment. Significant increases in odds of viral suppression over time were less pronounced among stimulant users compared with nonusers, particularly before the advent of universal ART. Increasing odds of viral suppression were paralleled by declining stimulant use over time. In the universal ART era, increasing odds of viral suppression were observed at lower levels of stimulant use, but not when participants reported using stimulants at every visit.
Although ART benefits are still not achieved as rapidly in stimulant users, this disparity is not as large in the era of universal ART.
*Department of Public Health Sciences, University of Miami School of Medicine, Miami, FL; and
†Department of Medicine, University of California, San Francisco School of Medicine, San Francisco, CA.
Correspondence to: Adam W. Carrico, PhD, Department of Public Health Sciences, University of Miami, 1120 NW 14th Street, Office 1005, Miami, FL 33136 (e-mail: email@example.com).
The SCOPE cohort is supported the UCSF/Gladstone Institute of Virology and Immunology CFAR (P30 AI027763) and the CFAR Network of Integrated Systems (R24 AI067039). Additional support was provided by the Delaney AIDS Research Enterprise (DARE; U19 AI096109, UM1 AI126611) and the amfAR Institute for HIV Cure Research (amfAR 109301).
The authors have no funding or conflicts of interest to disclose.
A.W.C., E.D.R., and P.W.H. developed study hypotheses. Analyses were conducted by T.B.N. and S.E.D. with substantial feedback from A.W.C., E.D.R., and P.W.H. A.W.C. and E.D.R. drafted the manuscript incorporating feedback from all authors.
Received February 27, 2018
Accepted August 29, 2018