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.
References:
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