Intestinal calcium absorption in exogenous hypercortisonism. Role of 25 hydroxyvitamin D and corticosteroid dose

Abstract

Pharmacologic doses of corticosteroids impair intestinal calcium absorption and contribute to negative calcium balance. However, the relation between the impaired calcium absorption and a possible defect in the conversion of vitamin D to its physiologically active form, 1,25-dihydrovitamin D, is unknown. The fractional calcium absorption (double-isotope method, 100-mg carrier) and the serum 25-hydroxyvitamin D (25-OH-D) (Haddad method) level were compared in 27 patients receiving pharmacologic doses of prednisone with 27 age-, sex-, and season-matched normal subjects. In patients receiving high daily doses of prednisone (15-100 mg/day), calcium absorption (P<0.02) and serum 25-OH-D (P<0.001) were decreased. However, in patients receiving low doses (8-10 mg/day) or high doses (30-100 mg) of prednisone on an alternate-day schedule, both of these parameters were normal. Calcium absorption in the patients treated with daily prednisone correlated inversely with the dose of corticosteroids (r = -0.52, P<0.025) and, in all steroid-treated patients, correlated directly with serum 25-OH-D (r = 0.58, P<0.01). In 4 patients who received high-dose corticosteroid therapy for an average of 4 wk, serum 25-OH-D decreased by 35.5% from pretreatment values. Administration of a physiologic or near-physiologic dose of synthetic 1,25 dihydroxyvitamin D3 (0.4 μg daily for 7 days) to patients receiving high-dose corticosteroids led to an increase in calcium absorption in all patients. These results suggest that calcium malabsorption in the corticosteroid-treated patients is due to a dose-related abnormality of vitamin D metabolism and not to a direct effect of corticosteroids on depressing transmucosal intestinal absorption of calcium.