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Wallis Robert S.; Kalayjian, Robert; Jacobson, Jeffrey M.; Fox, Lawrence; Purdue, Lynette; Shikuma, Cecilia M.; Arakaki, Richard; Snyder, Stuart; Coombs, Robert W.; Bosch, Ronald J.; Spritzler, John; Chernoff, Miriam; Aga, Evgenia; Myers, Laurie; Schock, Barbara; Lederman, Michael M.
JAIDS Journal of Acquired Immune Deficiency Syndromes: March 1st, 2003
CLINICAL SCIENCE: PDF Only
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Summary:Adult Clinical Trials Group Study 349 examined the immunology, virology, and safety of 40 mg/d prednisone as an adjunct to antiretroviral therapy in 24 HIV-infected subjects with >200 CD4+ T cells/mm3 in a randomized placebocontrolled trial. After 8 weeks, median lymphocyte and CD4+ cell numbers increased >40% above baseline values (p = .08). No effect was observed on markers of cell activation or apoptosis, although the proportion of CD28+ CD8+ T cells increased (p = .006). Prednisone inhibited monocyte TNFα production without affecting T-cell responses to antigens or mitogens. Two subjects assigned to prednisone were subsequently found to have asymptomatic osteonecrosis of the hip. Many questions remain regarding the role of activation-induced sequestration and apoptosis as causes of progressive CD4+ T-cell loss in AIDS. The potential role of corticosteroids as tools to examine this question will be limited by concerns regarding their toxicity; however, further studies of other agents to limit cellular activation in AIDS are warranted.

Funding for this study was provided by NIH grants AI 25879, Al 38858, AI 38855, AI 26879, AI 36219, AI 27664, AI 30731, and MO1 RR00080.

Address correspondence and reprint requests to Robert S. Wallis, Department of Medicine, UMDNJ-New Jersey Medical School, 185 South Orange Avenue, MSB I-503, Newark, NJ 07103, U.S.A; e-mail: r.wallis@umdnj.edu

Manuscript received October 9, 2002; accepted December 17, 2002.

© 2003 Lippincott Williams & Wilkins, Inc.