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Free access | 10.1172/JCI108762
Endocrinology Research and Gastroenterology Units, Department of Medicine, Mayo Clinic and Mayo Foundation, Rochester, Minnesota 55901
Department of Biochemistry, University of Wisconsin School of Agriculture, Madison, Wisconsin 53706
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Endocrinology Research and Gastroenterology Units, Department of Medicine, Mayo Clinic and Mayo Foundation, Rochester, Minnesota 55901
Department of Biochemistry, University of Wisconsin School of Agriculture, Madison, Wisconsin 53706
Find articles by Arnaud, S. in: JCI | PubMed | Google Scholar
Endocrinology Research and Gastroenterology Units, Department of Medicine, Mayo Clinic and Mayo Foundation, Rochester, Minnesota 55901
Department of Biochemistry, University of Wisconsin School of Agriculture, Madison, Wisconsin 53706
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Endocrinology Research and Gastroenterology Units, Department of Medicine, Mayo Clinic and Mayo Foundation, Rochester, Minnesota 55901
Department of Biochemistry, University of Wisconsin School of Agriculture, Madison, Wisconsin 53706
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Endocrinology Research and Gastroenterology Units, Department of Medicine, Mayo Clinic and Mayo Foundation, Rochester, Minnesota 55901
Department of Biochemistry, University of Wisconsin School of Agriculture, Madison, Wisconsin 53706
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Published July 1, 1977 - More info
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 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.