Background: Women who use antiretroviral therapy (ART) solely for the prevention of mother-to-child transmission of HIV discontinue postpartum. We hypothesized that women discontinuing ART by 6 weeks postpartum (“discontinuers”) would have elevated postpartum inflammatory biomarker levels relative to women remaining on ART postpartum (“continuers”).
Methods: Data from HIV-infected pregnant women enrolled in the International Maternal Pediatric Adolescent AIDS Clinical Trials Group P1025 with CD4 counts >350 cells per cubic millimeter before initiating ART or first pregnancy CD4 counts >400 cells per cubic millimeter after starting ART and with available stored plasma samples at >20 weeks of gestation, delivery, and 6 weeks postpartum were analyzed. Plasma samples were tested for highly sensitive C-reactive protein, D-dimer, and interleukin-6. We used longitudinal linear spline regression to model biomarkers over time.
Results: Data from 128 women (65 continuers and 63 discontinuers) were analyzed. All biomarkers increased from late pregnancy to delivery, then decreased postpartum (slopes different from 0, P < 0.001). Continuers had a steeper decrease in log D-dimer between delivery and 6 weeks postpartum than discontinuers (P = 0.002).
Conclusions: In contrast to results from treatment interruption studies in adults, both ART continuers and ART discontinuers had significant decreases in the levels of D-dimer, highly sensitive C-reactive protein, or interleukin-6 postpartum. Continuation was associated with a more rapid decline in D-dimer levels compared with discontinuation.
*Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA;
†Center for Biostatistics in AIDS Research, Harvard School of Public Health, Boston, MA; and
‡National Vaccine Program Office/Office of the Assistant Secretary for Health/Office of the Secretary/Department of Health and Human Services, Washington, DC.
Correspondence to: Risa M. Hoffman, MD, MPH, David Geffen School of Medicine, University of California, Los Angeles, 10833 Le Conte Avenue 37-121 CHS, Los Angeles, CA 90095 (e-mail: firstname.lastname@example.org).
Supported by the University of California, Los Angeles, Iris Cantor Center for Women’s Health Seed Grant Program and National Institutes of Health (NIH, grant AI56933; J.S.C., Principle Investigator). The content is solely the responsibility of the authors and does not necessarily represent the official views of the NIH. Overall support for the International Maternal Pediatric Adolescent AIDS Clinical Trials Group (IMPAACT) was provided by the National Institute of Allergy and Infectious Diseases (NIAID) (U01 AI068632), the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), and the National Institute of Mental Health (AI068632). This work was supported by the Statistical and Data Analysis Center at Harvard School of Public Health, under NIAID cooperative agreement #5 U01 AI41110 with the Pediatric AIDS Clinical Trials Group and #1 U01AI068616 with the IMPAACT. Support of the sites was provided by the NIAID and the NICHD International and Domestic Pediatric and Maternal HIV Clinical Trials Network funded by NICHD (contract number N01-DK-9-001/HHSN267200800001C).
Presented in part at the 19th Conference on Retroviruses and Opportunistic Infections, March 5–8, 2012, Seattle, WA. Abstract 1056.
The authors have no conflicts of interest to disclose.
Received February 01, 2013
Accepted April 29, 2013