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American Journal of Clinical Nutrition, Vol 26, 973-981, Copyright © 1973 by The American Society for Clinical Nutrition, Inc.

Serum vitamin A, retinol-binding protein, and prealbumin concentrations in protein-calorie malnutrition

I. A functional defect in hepatic retinol release

Frank Rees Smith M.D.1, DeWitt S. Goodman M.D.1, Mona S. Zaklama M.S.1, Mamdouh K. Gabr M.D.1, Safinaz El Maraghy M.D.1, and Vinayak N. Patwardhan Ph.D.1

1 From the Department of Medicine, Columbia University, College of Physicians and Surgeons, New York, N.Y.; the United States Naval Medical Research Unit No. 3 and the Pediatric Department, Cairo University Faculty of Medicine, Cairo, Egypt; and the Division of Nutrition, Vanderbilt University, Nashville, Tennessee 37203

The components of the plasma vitamin A transport system have been examined in 33 Egyptian children with protein-calorie malnutrition and in 15 control children. Twenty-one children with classical kwashiorkor had significantly decreased concentrations of serum retinol-binding protein (RBP), pre-albumin (PA), and vitamin A as well as of carotenoids, albumin, and total protein. After treatment with calories and proteins but without supplemental vitamin A, 11 patients with kwashiorkor were clinically judged to be cured; these patients demonstrated highly significant increases in the concentrations of vitamin A, RBP, and PA by the end of the 2nd week with further progressive increases occurring by the 4th week. The concentrations of vitamin A, RBP, and PA were comparable to or above those of the control children at discharge. Six children with kwashiorkor who were considered improved showed lesser increases in the concentrations of the three components of the retinol transport system. Six children with marasmus had pretreatment concentrations of vitamin A and RBP not significantly different from controls. Over the wide concentration range observed in kwashiorkor during treatment, the serum vitamin A, RBP, and PA concentrations were highly significantly correlated with each other. These findings suggest that the low serum vitamin A levels in kwashiorkor largely reflect a functional impairment in the hepatic release of vitamin A rather than vitamin A deficiency per se. Hepatic release of vitamin A is apparently impaired because of defective hepatic production of plasma proteins, including the plasma transport proteins for retinol because of a limiting supply of substrate for protein synthesis. When substrate is provided by dietary calories and protein, the hepatic production of plasma proteins increases, plasma RBP and PA concentrations rise, and hence, plasma vitamin A concentration increases.




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