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C-reactive protein independently predicts HIV-related outcomes among women and children in a resource-poor setting

Drain, Paul Ka,*; Kupka, Rolandb; Msamanga, Gernard Id; Urassa, Willye; Mugusi, Ferdinandf; Fawzi, Wafaie Wb,c

doi: 10.1097/QAD.0b013e32826fb6c7
Epidemiology and Social

Objective: To evaluate C-reactive protein (CRP) as a predictor of HIV-related outcomes among women and children in a resource-poor setting.

Design: We measured serum CRP concentration among 606 HIV-infected women, all of whom were not taking highly-active antiretroviral therapy, 3 to 11 months after they gave birth, and assessed relationships of CRP to HIV-related endpoints, including maternal disease progression, mother-to-child transmission of HIV, and maternal and child mortality.

Methods: We used Cox proportional hazards and regression models adjusted for age, sociodemographic characteristics, anthropometric measurements, hemoglobin, CD4 cell count, HIV viral load, and, for child outcomes, breastfeeding status.

Results: Ninety-four women had a high CRP concentration (> 10 mg/l). During the follow-up, 56 women progressed to WHO stage 4 and 188 died, and a high maternal CRP concentration was associated with a 2.26-fold [95% confidence interval (CI), 1.64–3.12] greater risk of progression to stage 4 or death. Among children, 174 acquired HIV and 116 died by age 2 years, and a high maternal CRP concentration was associated with a 3.03-fold (95% CI, 1.85–4.96) greater risk of child mortality. In multivariate analyses among adults, a high maternal CRP concentration was associated with a 1.55-fold (95% CI, 1.08–2.23) greater risk of progression to stage 4 or death. A maternal CRP concentration was not significantly associated with mother-to-child transmission of HIV.

Conclusions: A high maternal CRP concentration independently predicts HIV disease progression, maternal mortality, and child mortality in a resource-poor setting. C-reactive protein may be an important and inexpensive prognostic indicator for HIV-infected women and their children.

From the aSchool of Medicine, University of Washington, Seattle, Washington, USA

bDepartments of Nutrition, USA

cEpidemiology, Harvard School of Public Health, Boston, Massachusetts, USA

dDepartments of Community Health, Tanzania

eMicrobiology and Immunology, Tanzania

fInternal Medicine, Muhimbili University College of Health Sciences, Dar es Salaam, Tanzania.

*Current affiliation at Stanford Hospitals & Clinics, Stanford University, Palo Alto, California.

Received 9 September, 2006

Revised 16 April, 2007

Accepted 25 April, 2007

Correspondence to Dr Paul Drain, S101, Stanford University, 300 Pasteur Drive, Stanford, CA, 94305-5109, USA. E-mail: pkdrain@stanford.edu

© 2007 Lippincott Williams & Wilkins, Inc.