Vitamin A is required for the formation of rhodopsin, a photoreceptor pigment in the retina (see table Sources, Functions, and Effects of Vitamins). Vitamin A helps maintain epithelial tissues and is important for lysosome stability and glycoprotein synthesis.
vitamin A. To use vitamin A, the body releases it into the circulation bound to prealbumin (transthyretin) and retinol-binding protein. Beta-carotene and other provitamin carotenoids, contained in green leafy and yellow vegetables, carrots, and deep- or bright-colored fruits, are converted to vitamin A. Carotenoids are absorbed better from vegetables when they are cooked or homogenized and served with some fat (eg, oils).
Retinol activity equivalents (RAE) were developed because provitamin A carotenoids have less vitamin A activity than preformed vitamin A; 1 mcg retinol = 3.33 units.
Synthetic vitamin analogs (retinoids) are being used increasingly in dermatology. The possible protective role of beta-carotene and retinoids against some epithelial cancers is under study.
When taken as a supplement, beta-carotene has been associated with increased cancer and cardiovascular risk; risk does not seem to increase when carotenoids are consumed in fruits and vegetables.
(See also Overview of Vitamins.)
Acute vitamin A toxicity in children may result from taking large doses (> 300,000 units [> 100,000 RAE]), usually accidentally. In adults, acute toxicity has occurred when arctic explorers ingested polar bear or seal livers, which contain several million units of vitamin A.
Chronic vitamin A toxicity in older children and adults usually develops after doses of >>vitamin A can cause liver toxicity.
Although carotene is converted to vitamin A in the body, excessive ingestion of carotene causes carotenemia, not vitamin A toxicity. Carotenemia is usually asymptomatic but may lead to carotenosis, in which the skin becomes yellow.
Although symptoms of vitamin A toxicity may vary, headache and rash usually develop during acute or chronic toxicity.
Acute toxicity causes increased intracranial pressure. Drowsiness, irritability, abdominal pain, nausea, and vomiting are common. Sometimes the skin subsequently peels.
Early symptoms of chronic toxicity are sparsely distributed, coarse hair; alopecia of the eyebrows; dry, rough skin; dry eyes; and cracked lips. Later, severe headache, idiopathic intracranial hypertension (pseudotumor cerebri), and generalized weakness develop. Cortical hyperostosis of bone and arthralgia may occur, especially in children. Fractures may occur easily, especially in the older people. In children, toxicity can cause pruritus, anorexia, and failure to thrive. Hepatomegaly and splenomegaly may occur.
In carotenosis, the skin (but not the sclera) becomes deep yellow, especially on the palms and soles.
Clinical evaluation
> 100 mcg/dL (> 3.49 mcmol/L), sometimes to > 2000 mcg/dL (> 69.8 mcmol/L). Hypercalcemia is common.
Key Points
Acute toxicity causes rash, abdominal pain, increased intracranial pressure, and vomiting.
Chronic toxicity causes rash, increased intracranial pressure, sparse and coarse hair, dry and rough skin, and arthralgia; risk of fractures is increased, especially in the older people.
Diagnose based on clinical findings.
