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JAIDS Journal of Acquired Immune Deficiency Syndromes:
doi: 10.1097/01.QAI.0000026542.53543.A5
Articles: PDF Only

Vitamin A Deficiency and the Acute Phase Response Among HIV-1-Infected and -Uninfected Women in Kenya.

Baeten, Jared M.; McClelland, Scott R.; Richardson, Barbra A.; Bankson, Daniel D.; Lavreys, Ludo; Wener, Mark H.; Overbaugh, Julie; Mandaliya, Kishorchandra; Ndinya-Achola, Jeckoniah O.; Bwayo, Job J.; Kreiss, Joan K.

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Summary: Among HIV-1-infected individuals, vitamin A deficiency has been associated with faster disease progression and greater infectivity in observational studies, but randomized clinical trials have shown no effect of vitamin A supplementation. We conducted a cross-sectional study of 400 HIV-1-infected and 200 HIV-1-uninfected women in Mombasa, Kenya to examine the relations between vitamin A deficiency (serum retinol <30 [mu]g/dL) and HIV-1 status, HIV-1 disease stage, and the acute phase response (serum C-reactive protein >=10 mg/L and/or [alpha]1-acid glycoprotein >=1.2 g/L). Among the HIV-1-infected women, the effect of vitamin A supplementation was examined in a randomized trial. Vitamin A deficiency was independently associated with HIV-1 infection (OR = 2.7, 95% CI: 1.9-4.0) and the acute phase response (OR = 2.8, 95% CI: 1.9-4.1). Among HIV-1-infected women, vitamin A deficiency and the acute phase response were associated with each other and were both independently associated with higher HIV-1 plasma viral load and lower CD4 count. HIV-1-infected women having an acute phase response had no increase in serum vitamin A levels after supplementation. Serum levels increased significantly among women without an acute phase response, although not to normal levels among women who were deficient at baseline. Among HIV-1-infected individuals, it is likely that low serum vitamin A concentrations reflect more active infection and the acute phase response. These results provide possible explanations for the disparity between observational studies and randomized trials of vitamin A for HIV-1 infection.

(C) 2002 Lippincott Williams & Wilkins, Inc.


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