Vitamin A deficiency can result from inadequate intake, fat malabsorption, or liver disorders. Deficiency impairs immunity and hematopoiesis and causes skin rashes and typical ocular effects (eg, xerophthalmia, night blindness). Diagnosis is based on typical ocular findings and low vitamin A levels. Treatment consists of vitamin A given orally or, if symptoms are severe or malabsorption is the cause, parenterally.
Primary vitamin A deficiency is usually caused by prolonged dietary deprivation. It is endemic in areas such as southern and eastern Asia, where rice, devoid of β-carotene, is the staple food. Xerophthalmia due to primary deficiency is a common cause of blindness among young children in developing countries.
Secondary vitamin A deficiency may be due to decreased bioavailability of provitamin A carotenoids or to interference with absorption, storage, or transport of vitamin A. Interference with absorption or storage is likely in sprue, cystic fibrosis, pancreatic insufficiency, duodenal bypass, chronic diarrhea, bile duct obstruction, giardiasis, and cirrhosis. Vitamin A deficiency is common in prolonged protein-energy malnutrition not only because the diet is deficient but also because vitamin A storage and transport is defective. In children with complicated measles, vitamin A can shorten the duration of the disorder and reduce the severity of symptoms and risk of death.
Symptoms and Signs
Impaired dark adaptation of the eyes, which can lead to night blindness, is an early symptom. Xerophthalmia (which is nearly pathognomonic) results from keratinization of the eyes. It involves drying (xerosis) and thickening of the conjunctivae and corneas. Superficial foamy patches composed of epithelial debris and secretions on the exposed bulbar conjunctiva (Bitot's spots) develop. In advanced deficiency, the cornea becomes hazy and can develop erosions, which can lead to its destruction (keratomalacia).
Keratinization of the skin and of the mucous membranes in the respiratory, GI, and urinary tracts can occur. Drying, scaling, and follicular thickening of the skin and respiratory infections can result. Immunity is generally impaired.
The younger the patient, the more severe are the effects of vitamin A deficiency. Growth retardation and infections are common among children. Mortality rate can exceed 50% in children with severe vitamin A deficiency.
Vitamin A toxicity can be acute (usually due to accidental ingestion by children) or chronic. Both types usually cause headache and increased intracranial pressure. Acute toxicity also causes nausea and vomiting. Chronic toxicity also causes changes in skin, hair, and nails; abnormal liver test results; and, in a fetus, birth defects. Diagnosis is usually clinical. Unless birth defects are present, adjusting the dose almost always leads to complete recovery.
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 carotenodermia, in which the skin becomes yellow. When taken as a supplement, β-carotene has been associated with increased cancer risk; risk does not appear to increase when carotenoids are consumed in fruits and vegetables.
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