Saturday, October 14, 2017

Introduction to Hypervitaminosis A



Chronic hypervitaminosis A
results from excessive ingestion of vitamin A for several weeks or months.

Toxicity can be induced in adults and children with chronic daily intakes of 15,000 g and 6,000 g, respectively. Symptoms subside rapidly on withdrawal of the vitamin.

Signs of subacute or chronic toxicity may include headache; vomiting; anorexia; dry, itchy desquamating skin; seborrheic cutaneous lesions; fissuring at the corners of the mouth; alopecia and/or coarsening of the hair; bone abnormalities; swelling of the bones; enlargement of the liver and spleen; diplopia; increased intracranial pressure; irritability; stupor; limited motion; and dryness of the mucous membranes. In addition, desquamation of the palms and the soles of the feet is common.

Radiographs show hyperostosis affecting several long bones, especially in the middle of the shafts . Serum levels of vitamin A are elevated. Hypercalcemia and/or liver cirrhosis may be present. Hypervitaminosis A is distinct from cortical hyperostosis.
In young children, toxicity is associated with vomiting and bulging fontanelles. An affected child has anorexia, pruritus, and a lack of weight gain. Acute hypervitaminosis A toxicity has occurred in infants in developing countries after ingestion of very high amounts of vitamin A during vaccine administration. Symptoms include nausea, vomiting, and drowsiness; less common symptoms include diplopia, papilledema, cranial nerve palsies, and other symptoms suggestive ofpseudotumor cerebri. Severe congenital malformations occur in infants of mothers who consumed therapeutic doses (0.5–1.5 mg/kg) of oral 13-cis-retinoic acid during the 1st trimester of pregnancy for treatment of acne or cancer. This results in a high incidence (>20%) of spontaneous abortions and birth defects.

Excessive intake of carotenoids is not associated with toxicity, but may cause yellow coloration of the skin that disappears when intake is reduced; this disorder (carotenemia) is especially likely to occur in children with liver disease, diabetes mellitus, or hypothyroidism, and in those who do not have enzymes that metabolize carotenoids.

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