Toxicity of Vitamin D

Intoxication with vitamin D causes weakness, nausea, loss of appetite, headache, abdominal pains, cramps, and diarrhea. More seriously, it also causes hypercalcemia, with plasma concentrations of calcium between 2.75 to 4.5 mmol per L, compared with the normal range of 2.2 to 2.5 mmol per L. At plasma concentrations of calcium above 3.75 mmol per L, vascular smooth muscle may contract abnormally, leading to hypertension and hypertensive encephalopathy. Hypercalciuria may also result in the precipitation of calcium phosphate in the renal tubules and hence the development of urinary calculi. Hypercalcemia can also result in calcinosis - the calcification of soft tissues, including kidneys, heart, lungs, and blood vessels. This is assumed to be the result of increased calcium uptake into tissues in response to excessive plasma concentrations of the vitamin and its metabolites.

Some children are sensitive to hypercalcemia and calcinosis as a result of vitamin D intakes as low as 45 /g per day (Chesney, 1990; Holick, 1990). There is thus a narrow margin between amounts of vitamin D adequate to ensure that rickets is prevented throughout the community and the level at which vulnerable infants will develop hypercalcemia. This became a significant problem in Britain in the 1950s. Widespread fortification of infant foods had resulted in eradication of rickets, but, by 1955, 200 cases of hypercalcemia had been reported. The amounts of vitamin D added to infant foods was reduced; as a result, rickets reappeared. The problemis to identify those children at risk of deficiency, who therefore require additional supplements, without putting those with a low threshold for intoxication at risk of hypercalcemia and calcinosis.

The U.S./Canadian report (Institute of Medicine, 1997) quotes a no adverse effect level of 60 fig per day, leading to a tolerable upper level of intake of 50 fg per day (and 25 f g per day for infants). The toxic threshold for adults has not been established, but reports of hypercalcemia in adults have involved intakes in excess of 1,000 f g per day. There is no evidence of adverse effects at plasma concentrations of calcidiol lower than 140 nmol per L, which requires an intake in excess of 250 fg per day, suggesting that the currently accepted no adverse effect level is lower than necessary (Vieth, 1999).

Hypercalcemia persists for many months after the cessation of excessive intakes of vitamin D, because of the accumulation of the vitamin in adipose tissue and its slow release into the circulation. The introduction of calcitriol and 1a-hydroxycalcidiol for the treatment of such conditions as hypoparathyroidism, renal osteodystrophy, hypophosphatemic osteomalacia, and vitamin D-dependent rickets has meant that hypercalcemia is less of a problem than when high doses of vitamin D were used in the treatment of these conditions. Because calcitriol has a short half-life in the circulation, the resultant hypercalcemia is of shorter duration than alter cholecalciferol, and adjustment of the dose is easier.

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