Nutrition Research
Volume 24, Issue 3 , Pages 223-227, March 2004

Increased retinol requirement in acute measles infection in children: an hypothesis on role of hypercortisolemia

  • Cyril O. Enwonwu

      Affiliations

    • Department of Biochemistry and Molecular Biology, School of Medicine, University of Maryland, 666 West Baltimore Street, Baltimore, Maryland 21201, USA
    • Department of Biomedical Sciences, School of Dentistry, University of Maryland, 666 West Baltimore Street, Baltimore, Maryland 21201, USA
    • Corresponding Author InformationCorresponding author. Tel.: (410) 706-7186; Fax: (301) 317-1117.
    • ,
  • Reshma S. Phillips

      Affiliations

    • Department of Biochemistry and Molecular Biology, School of Medicine, University of Maryland, 666 West Baltimore Street, Baltimore, Maryland 21201, USA

Received 5 May 2003; received in revised form 20 October 2003; accepted 26 October 2003.

Abstract 

Measles is a major killer of children worldwide, particularly in impoverished sub-Saharan malnourished African communities. Perhaps more than any other acute infections in children, measles elicits hyporetinemia and severe hypercortisolemia, with abolition of the normal cortisol rhythm. Hypercortisolemia promotes a shift in cytokine profile from TH1 to TH2, and influences hepatic acute phase protein response through enhancement of the activity of interleukin-6. Increased cortisol availability not only promotes depletion of hepatic retinol store directly, but also antagonizes effects of retinoids at the cellular and transcriptional levels. Glucocorticoids decrease the expression of receptors for retinoic acid, a transcriptionally active retinol metabolite considered to function as a signal of the body's retinol needs. We therefore hypothesize that increased tissue burden of cortisol offers a plausible explanation for the well documented therapeutic benefits of retinol supplementation in acute infections, particularly measles in malnourished children.

Keywords: Retinol, Glucocorticoids, Measles, Acute inflammation, Hypercortisolemia

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PII: S0271-5317(03)00251-3

doi:10.1016/j.nutres.2003.10.004

Nutrition Research
Volume 24, Issue 3 , Pages 223-227, March 2004

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