Abstract
A 76-year-old female patient who had been taking vitamin D2 100, 000U/day for more than 14 years due to hypoparathyroidism following total thyroidectomy was admitted because of protracted hypercalcemia.
On admission, the levels of serum vitamin D2 (99.8ng/ml) and 25-OHD2 (356ng/ml) were very high, and 1, 25-(OH)2D2 was low (4.0-18.7pg/ml). Serum D3, 25-OHD3 and 1, 25-(OH)2D3 were below the normal range. Despite intensive hydration with saline, intravenous hyperalimentation with phosphate-and calcium-free nutrients, and administration of glucocorticoid and calcitonin, the hypercalcemia persisted, accompanied by hypoproteinemia, edema, pleural effusion and congestive heart failure. The serum D2 and 25-OHD2 concentrations remained high and were accompanied by a gradual increase in 1, 25-(OH)2D2 (121pg/ml), which further increased after the administration of bisphosphonate (pamidronate) to 183pg/ml. Seventeen months later, serum calcium and 1, 25-(OH)2D2 were normalized but serum D2 and 25-OHD2 remained high. The serum 24, 25-(OH)2D2/25-OHD2 ratio was relatively constant throughout her clinical course, whereas the low serum 1, 25-(OH)2D2/25-OHD2 ratio at admission gradually increased during admission, suggesting that the increase in serum 1, 25-(OH)2D2 is due to increased production rather than decreased degradation. The administration of pamidronate further increased serum 1, 25-(OH)2D2.
These features of the clinical course demonstrate that the 1, 25-dihydroxyvitamin D concentration in hypercalcemic patients with protracted vitamin D intoxication may be decreased, normal or increased. Possible factors responsible for a protracted increase in serum 1, 25-(OH)2D2 are body weight loss, hypoproteinemia, and phosphate depletion. In addition, some bisphosphonates would certainly promote PTH-independent production of 1, 25-(OH)2D2.
