Hypervitaminosis A, Fat soluble vitamins, deficiency vs excess
Patients who have chronic liver and renal disease routinely receive supplemental fat-soluble vitamin therapy, including vitamin D. Excessive amounts of vitamin D result in signs and symptoms similar to those of idiopathic hypercalcemia, including hypotonia, anorexia, irritability, constipation or diarrhea, polydipsia, and polyuria. Hypercalcemia and hypercalcuria often are noted, as in the girl described in the vignette. Vomiting, poor growth, osteopenia, and hypertension also may develop. Prolonged ingestion of excessive vitamin D may result in renal damage due to nephrocalcinosis. Metastatic calcification of the heart, blood vessels, bronchi, and stomach also may occur.
The body's vitamin D requirements are met through its production in the skin, the photochemical reaction of sunlight upon its precursor, and dietary ingestion. The primary role of the vitamin is to stimulate absorption of calcium and phosphorus from the small intestine. Children who have dark pigmented skin or limited exposure to the sun are at risk for vitamin D deficiency. Anticonvulsant therapy may alter vitamin D metabolism, resulting in a deficiency state. Human milk is normally low in vitamin D content, placing the exclusively breastfed infant at risk if the mother's vitamin D intake is suboptimal.
The metabolism of the fat-soluble vitamins A, D, E, and K differ from that of water-soluble vitamins in several respects. First, their absorption depends on normal pancreatic and hepatobiliary function. Second, they require a transport system to become soluble in blood. Third, there is significant storage of these vitamins in the body, making primary deficiency syndromes uncommon in healthy individuals. Finally, there is a potential for toxicity if excessive fat- oluble vitamin ingestion occurs over a prolonged period of time.
Hypervitaminosis A is associated with anorexia, slow growth, hepatosplenomegaly, swelling and pain of the long bones, increased intracranial pressure, and alopecia. Although many of the symptoms resemble those seen with vitamin D toxicity, hypercalciuria and hypercalcemia do not occur. Vitamin A deficiency causes photophobia, xerophthalmia, faulty epiphyseal bone formation, retarded growth, and decreased resistance to infection.
Patients who have vitamin E deficiency develop red blood cell hemolysis, loss of neural integrity, and decreased muscle function. Vitamin K deficiency results in soft-tissue hemorrhage and defective bone collagen production.
American Academy of Pediatrics Committee on Nutrition. Vitamins and
mineral supplement needs of healthy children in the United States. In:
Barness LA, ed. Pediatric Nutrition Handbook. 3rd ed. Elk Grove
Village, Ill: American Academy of Pediatrics; 1993:34-42
Forbes GB, Cafarelli C, Manning J. Vitamin D and infantile
hypercalcemia. Pediatrics. 1968;42:203-204