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

R G Klein, S B Arnaud, J C Gallagher, H F Deluca, B L Riggs, R G Klein, S B Arnaud, J C Gallagher, H F Deluca, B L Riggs

Abstract

Pharmacologic doses of corticosteroids impair intestinal calcium absorption and contribute to negative calcium balance. However, the relationship between the impaired calcium absorption and a possible defect in the conversion of vitamin D to its physiologically active form, 1,25-dihydroxyvitamin D, is unknown. We compared fractional calcium absorption (double-isotope method, 100-mg carrier) and serum 25-hydroxyvitamin D (25-OH-D) (Haddad method) 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 four 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 D(3) (0.4 mug 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.

References

    1. Metabolism. 1962 Jul;11:716-26
    1. Proc Soc Exp Biol Med. 1961 Mar;106:664-6
    1. Am J Physiol. 1960 Aug;199:265-71
    1. Can J Biochem Physiol. 1959 Aug;37(8):911-7
    1. Ann Intern Med. 1974 Feb;80(2):161-8
    1. Proc Natl Acad Sci U S A. 1974 Aug;71(8):2996-3000
    1. Kidney Int. 1973 Apr;3(4):264-72
    1. Clin Endocrinol Metab. 1973 Jul;2(2):355-68
    1. J Clin Endocrinol Metab. 1974 Dec;39(6):981-5
    1. Pharmacol Rev. 1967 Sep;19(3):317-66
    1. Ann Intern Med. 1974 Oct;81(4):505-12
    1. Am J Med. 1974 Jul;57(1):57-62
    1. J Lipid Res. 1971 Jul;12(4):460-5
    1. Clin Orthop Relat Res. 1974 Jan-Feb;(98):258-87
    1. J Clin Invest. 1972 Apr;51(4):741-8
    1. J Clin Endocrinol Metab. 1971 Dec;33(6):992-5
    1. Br Med J. 1972 Oct 7;4(5831):9-12
    1. Endocrinology. 1973 Sep;93(3):718-22
    1. J Clin Endocrinol Metab. 1968 Sep;28(9):1341-6
    1. J Clin Invest. 1971 Jun;50(6):1309-21
    1. N Engl J Med. 1976 Mar 11;294(11):589-95
    1. Pediatr Res. 1975 Jul;9(7):586-93
    1. J Lab Clin Med. 1976 Jan;87(1):7-26
    1. Pediatrics. 1976 Feb;57(2):221-5
    1. J Clin Invest. 1973 Jul;52(7):1680-5
    1. J Clin Invest. 1973 Jun;52(6):1328-35
    1. J Lab Clin Med. 1972 Apr;79(4):570-8
    1. N Engl J Med. 1969 Jun 19;280(25):1396-405
    1. Acta Endocrinol (Copenh). 1969 May;61(1):173-92
    1. Indian J Pediatr. 1975 Jan;42(324):1-9
    1. Proc Soc Exp Biol Med. 1975 Jun;149(2):570-2
    1. J Clin Invest. 1969 Sep;48(9):1705-13

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