Deficiency and Interventions

K P West Jr, Johns Hopkins University, Baltimore,


© 2005 Elsevier Ltd. All rights reserved.

Vitamin A (VA) deficiency is the leading cause of pediatric blindness, increases risk of severe infection, and is an underlying cause of child mortality in many developing countries. Night blindness, the mildest ocular manifestation of VA deficiency, has been recognized since antiquity, with the condition depicted in bas-relief on the Egyptian pyramid in Sakura, dating to the Middle Kingdom, and Hippocrates in the fourth century BC recognizing and treating the condition with animal liver. Corneal destruction and consequent blindness, as well as milder conjunctival lesions of xerophthalmia, were linked to dietary insufficiency in the eighteenth and nineteenth centuries, with cod liver oil emerging as recommended treatment for the various conditions of night blindness, Bitot's spots, and corneal necrosis (keratomalacia) more than a century ago. Discovery in the early twentieth century of 'fat-soluble A,' an ether-soluble factor in butter and egg yolk critical for sustaining growth, health, and vision in animals, accelerated recognition and treatment of xerophthal-mia in children as well as decades of subsequent research that led to the synthesis of vitamin A and its analogues, an understanding of the vitamin's roles in the visual cycle, and discovery of the vitamin's involvement in maintaining epithelial, immune, hematopoietic, and osteoid function and multiple facets of human health.

Biochemical Depletion

Tissue depletion of vitamin A, although not a disorder per se, precedes the functional consequences of deficiency. In uncomplicated hypovitami-nosis A, plasma retinol tends to be homoeostatically controlled until body (primarily liver) stores are low, after which plasma concentration declines. Plasma retinol may also decline during states of chronic inflammation and clinically significant infection, in parallel with raised circulating concentrations of acute phase proteins, likely reflecting increased tissue delivery, reduced hepatic mobilization via retinol binding protein, and increased urinary loss of vitamin A. Plasma retinol gradually normalizes during recovery from infection if there are adequate hepatic stores of the vitamin. If not, infection can leave the host more tissue depleted and at risk. Despite nondietary influences, plasma or serum retinol measurement remains the most common biochemical index of vitamin A status. Vitamin A deficiency is generally diagnosed at a serum retinol concentration below a cutoff of 0.70 mmol/l (20 mg/dl), below which 20 to >50% of concentrations occur in a VA-deficient population compared to <3% of well-nourished societies. A serum retinol concentration of <0.35 mmol/l is indicative of severe deficiency. Decrements in serum retinol concentration below these cutoffs are associated with marked increases in risk of xerophthalmia and infection. Other indices of tissue retinol depletion include the relative dose-response, a before-after test dose difference in serum retinol that indirectly reflects hepatic retinol adequacy, breast milk retinol concentration for assessing both maternal status

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