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Vitamin A deficiency
Last reviewed: 06.07.2025
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Vitamin A deficiency is a systemic disease affecting cells and organs throughout the body. The resulting changes in the epithelium are called "keratotic metaplasia". Keratotic metaplasia of the epithelium of the respiratory and urinary tracts and related changes in the epithelium of the digestive tract develop relatively early in the disease, even before clinically evident changes in the conjunctiva of the eyes, but in most cases they are latent. Typical clinical manifestations of vitamin A deficiency include decreased dark adaptation and impaired twilight vision (hemeralopia), slow bone growth, hyperkeratosis, and dry cornea (xerophthalmia). These processes increase the risk of developing inflammatory diseases of the skin and mucous membranes (dermatitis, rhinitis, bronchitis, etc.). The physiological consequences of vitamin A deficiency, such as impaired dark adaptation or abnormal conjunctival epithelial differentiation (detected by cytological examination of conjunctival imprint smears), usually begin to develop at serum retinol concentrations below 1 μmol/L. Overt xerophthalmia usually appears at concentrations below 0.7 μmol/L and becomes more severe at values below 0.35 μmol/L (severe deficiency and depletion of liver stores). The risk of impaired iron utilization and death gradually increases as serum vitamin A concentrations decrease.
Taking drugs that lower blood cholesterol levels reduces the absorption of vitamin A in the intestine.
There are two forms of vitamin A deficiency in the body: primary (alimentary), associated with insufficient intake of retinol or carotenoids with food, and secondary, which occurs when vitamin A metabolism is disrupted, most often with diseases of the gastrointestinal tract, liver, and pancreas.
Doses of vitamin A over 100,000 IU/day in adults and 18,500 IU/day in children, taken over many months, can cause a toxic effect, manifested by decreased appetite, hair loss, insomnia, nausea, vomiting, diarrhea, yellow-red pigmentation of the skin and mucous membranes, bone pain, headache, and liver enlargement. Symptoms of intoxication occur when the content of vitamin A in the blood serum exceeds the ability of the vitamin A-binding protein to bind it. Normally, the molar ratio of vitamin A/vitamin A-binding protein is 0.8-1; in case of intoxication, it decreases. In the development of acute hypervitaminosis A, retinol esters can make up more than 30% of the total amount of vitamin A (62.82 μmol/l).
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