BACKGROUND: HIV infection is prevalent among substance abusers. The effects of specific illicit drugs on HIV disease progression have not been established. We evaluated the relationship between substances of abuse and HIV disease progression in a cohort of HIV-1-positive active drug users. METHODS: A prospective, 30-month, longitudinal study was conducted on 222 HIV-1 seropositive drug users in Miami, FL. History of illicit drug, alcohol, and medication use, CD4+ cell count, and viral load were performed every 6 months. RESULTS: Crack-cocaine users were 2.14 times [95% confidence interval (CI): 1.08 to 4.25, P = 0.029] more likely to present a decline of CD4 to <or=200 cells/mL, independent of antiretroviral use. Viral load over 30 months was significantly higher in crack users (beta = 0.315, P = 0.037) independent of highly active antiretroviral therapy (HAART) over time. The only multidrug combination that significantly increased the risk of disease progression was crack cocaine with marijuana (hazard ratio = 2.42; 95% CI: 1.042 to 5.617, P = 0.04). Of those on HAART, a significantly lower proportion of crack-cocaine users versus nonusers had controlled viral load (P < 0.001), suggesting lower medication adherence, whereas crack-cocaine users not on HAART showed a greater risk for HIV disease progression than nonusers (hazard ratio = 3.946; 95% CI: 1.049 to 14.85, P = 0.042). CONCLUSIONS: Crack-cocaine use facilitates HIV disease progression by reducing adherence in those on HAART and by accelerating disease progression independently of HAART.
BACKGROUND:HIV infection is prevalent among substance abusers. The effects of specific illicit drugs on HIV disease progression have not been established. We evaluated the relationship between substances of abuse and HIV disease progression in a cohort of HIV-1-positive active drug users. METHODS: A prospective, 30-month, longitudinal study was conducted on 222 HIV-1 seropositive drug users in Miami, FL. History of illicit drug, alcohol, and medication use, CD4+ cell count, and viral load were performed every 6 months. RESULTS: Crack-cocaine users were 2.14 times [95% confidence interval (CI): 1.08 to 4.25, P = 0.029] more likely to present a decline of CD4 to <or=200 cells/mL, independent of antiretroviral use. Viral load over 30 months was significantly higher in crack users (beta = 0.315, P = 0.037) independent of highly active antiretroviral therapy (HAART) over time. The only multidrug combination that significantly increased the risk of disease progression was crack cocaine with marijuana (hazard ratio = 2.42; 95% CI: 1.042 to 5.617, P = 0.04). Of those on HAART, a significantly lower proportion of crack-cocaine users versus nonusers had controlled viral load (P < 0.001), suggesting lower medication adherence, whereas crack-cocaine users not on HAART showed a greater risk for HIV disease progression than nonusers (hazard ratio = 3.946; 95% CI: 1.049 to 14.85, P = 0.042). CONCLUSIONS: Crack-cocaine use facilitates HIV disease progression by reducing adherence in those on HAART and by accelerating disease progression independently of HAART.
Authors: Chukwuemeka N Okafor; Zhi Zhou; Larry E Burrell; Natalie E Kelso; Nicole E Whitehead; Jeffery S Harman; Christa L Cook; Robert L Cook Journal: Am J Drug Alcohol Abuse Date: 2016-07-11 Impact factor: 3.829
Authors: Seonaid Nolan; Alexander Y Walley; Timothy C Heeren; Gregory J Patts; Alicia S Ventura; Meg M Sullivan; Jeffrey H Samet; Richard Saitz Journal: AIDS Care Date: 2017-05-17
Authors: Adam W Carrico; Peter W Hunt; Torsten B Neilands; Samantha E Dilworth; Jeffrey N Martin; Steven G Deeks; Elise D Riley Journal: J Acquir Immune Defic Syndr Date: 2019-01-01 Impact factor: 3.731