THE SYNDROME of carotenemia, which was first described by von Noorden in 1907,1 has been observed in a variety of metabolic disorders, including diabetes mellitus, chronic glomerulonephritis, myxedema, acute hepatic disease, xanthomatosis, and the ingestion of unusual quantities of vegetables rich in carotenoid pigments.
Carotene is not synthesized by man. The absorption of carotene and its biologically active form, vitamin A, from the small intestine is linked with the absorption of lipids, is enhanced by the presence of lecithin, and, in the case of carotene, is dependent on the presence of bile salts. About 30 to 50% of the ingested carotene is converted to vitamin A,2 and in man both conversion and storage take place in the liver.3 Mattson and associates have demonstrated that conversion in rats takes place chiefly in the intestinal mucosa.4 Because carotenemia usually occurs in association with diseases
SHAW WM, MASON EH, KALZ FG. HYPOTHYROIDISM, LIVER DAMAGE, AND VITAMIN A DEFICIENCY AS FACTORS IN HYPERKERATOSIS. AMA Arch Derm Syphilol. 1952;66(2):197–203. doi:10.1001/archderm.1952.01530270055007
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