INTACT PARATHYROID-HORMONE LEVELS ARE NOT ELEVATED IN GLUCOCORTICOID-TREATED SUBJECTS

To assess whether chronic glucocorticoid therapy results in a compensa tory increase in parathyroid hormone (PTH), we measured intact PTH lev els and other indices of mineral metabolism in 13 postmenopausal gluco corticoid-treated women and 16 normal age-matched controls. The glucoc orticoid-treated women received a mean prednisone dose of 15.8 +/- 3.1 mg/day for 12.9 +/- 3.1 years. A linear regression analysis between i ntact PTH levels and a,vide range of prednisone doses in these 13 gluc ocorticoid-treated women and 26 additional male and female subjects re ceiving chronic glucocorticoid therapy for a variety of rheumatic and pulmonary disorders (n = 39) was also performed. Intact PTH levels usi ng the sensitive immunoradiometric assay (IRMA, Nichols Institute, San Juan Capistrano, CA) were comparable in the glucocorticoid-treated an d normal control women (35.3 +/- 4.4 vs 31.3 +/- 3.2 ng/l, respectivel y) as were the total calcium concentrations (9.67 +/- 0.12 vs 9.52 a 0 .11 mg/dl). In the glucocorticoid-treated women, the 25-hydroxyvitamin D levels, measured by competitive protein assay were similar to those of the control subjects (29.2 a 2.8 vs 29.1 +/- 2.3 ng/ml), and no pa tient was treated with vitamin D in excess of 400 IU daily. In the com bined 39 male and female patients, there were also no significant regr ession relationships between daily prednisone dose and intact PTH leve ls. Thus, secondary hyperparathyroidism does not accompany chronic ora l glucocorticoid therapy in women on low to moderate doses of oral glu cocorticoids. The lack of an elevation in intact PTH levels in the pre sence of chronic glucocorticoid therapy may represent an increased sen sitivity of bone to PTH, or an alteration in the relationship between calcium and PTH, or both.