期刊
JAIDS-JOURNAL OF ACQUIRED IMMUNE DEFICIENCY SYNDROMES
卷 32, 期 3, 页码 281-286出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/00126334-200303010-00006
关键词
activation; AIDS pathogenesis; clinical trial; corticosteroids; apoptosis
资金
- NCRR NIH HHS [M01 RR00080] Funding Source: Medline
- NIAID NIH HHS [AI 36219, AI 38855, AI 25879, AI 30731, AI 27664, AI 38858] Funding Source: Medline
- PHS HHS [A1 26879] Funding Source: Medline
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/mm(3) in a randomized placebo-controlled 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 TNFalpha 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.
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