Abstract

The inflammatory effects of injection drug use (IDU) may result in an impaired immune response to antiretroviral therapy (ART). We examined CD4 response to first ART regimen among individuals in routine HIV care, stratified by IDU-related HIV acquisition. Cohort study including patients who initiated ART between 2000 and 2015 in the Johns Hopkins HIV Clinic. We followed individuals from ART initiation until death, loss to follow-up, loss of viral load suppression (<500 copies/mL), or administrative censoring. We described CD4 trajectories after ART initiation using inverse probability weighted quantile regression models with restricted cubic splines for time. Weights accounted for differences in baseline characteristics of persons comparing those with IDU-related HIV acquisition to those with other HIV acquisition risks (non-IDU) and possible nondifferential censoring due to death, loss to follow-up, or loss of viral load suppression. We also examined CD4 response by strata of CD4 at ART initiation (≤200, 201-350, >350). Of 1244 patients initiating ART, 30.4% were IDU. Absolute CD4 cell difference at the 50th percentile comparing IDU with non-IDU was -25 cells [95% confidence interval (CI): -63 to 35], -66 cells (95% CI: -141 to 16), and -91 cells (95% CI: -190 to -5) at 2, 4, and 6 years after ART initiation, respectively. Results were similar (non-IDU with slightly higher CD4 count, but not statistically significant differences) at other percentiles and stratified by baseline CD4. CD4 recovery after ART initiation was similar for IDU and non-IDU, conditional on consistent viral load suppression.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.