title: Intact parathyroid hormone levels are not elevated in glucocorticoid-treated subjects.
abstract: To assess whether chronic glucocorticoid therapy results in a compensatory increase in parathyroid hormone (PTH), we measured intact PTH levels and other indices of mineral metabolism in 13 postmenopausal glucocorticoid-treated women and 16 normal age-matched controls. The glucocorticoid-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 intact PTH levels and a wide range of prednisone doses in these 13 glucocorticoid-treated women and 26 additional male and female subjects receiving chronic glucocorticoid therapy for a variety of rheumatic and pulmonary disorders (n = 39) was also performed. Intact PTH levels using the sensitive immunoradiometric assay (IRMA, Nichols Institute, San Juan Capistrano, CA) were comparable in the glucocorticoid-treated and normal control women (35.3 +/- 4.4 vs 31.3 +/- 3.2 ng/l, respectively) as wee the total calcium concentrations (9.67 +/- 0.12 vs 9.52 +/- 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 +/- 2.8 vs 29.1 +/- 2.3 mg/ml), and no patient was treated with vitamin D in excess of 400 IU daily. In the combined 39 male and female patients, there were also no significant regression relationships between daily prednisone dose and intact PTH levels. Thus, secondary hyperparathyroidism does not accompany chronic oral glucocorticoid therapy in women on low to moderate doses of oral glucocorticoids. The lack of an elevation in intact PTH levels in the presence of chronic glucocorticoid therapy may represent an increased sensitivity of bone to PTH, or an alteration in the relationship between calcium and PTH, or both.
authors.affiliation: Mount Sinai Hospital, New York, New York, USA.
authors.forename: E
authors.initials: E
authors.lastname: Paz-Pacheco
authors.forename: G E
authors.initials: GE
authors.lastname: Fuleihan
authors.forename: M S
authors.initials: MS
authors.lastname: LeBoff
mesh_terms: D000284:Administration, Oral; D000328:Adult; D000368:Aged; D015519:Bone Density / Q000187:drug effects* / Q000502:physiology; D002118:Calcium / Q000378:metabolism; D005260:Female; D005938:Glucocorticoids / Q000008:administration & dosage / Q000009:adverse effects*; D006801:Humans; D006887:Hydroxycholecalciferols / Q000378:metabolism; D006962:Hyperparathyroidism, Secondary / Q000139:chemically induced; D016014:Linear Models; D008171:Lung Diseases / Q000188:drug therapy; D008297:Male; D008875:Middle Aged; D010281:Parathyroid Hormone / Q000378:metabolism*; D017698:Postmenopause; D011241:Prednisone / Q000008:administration & dosage / Q000009:adverse effects*; D012216:Rheumatic Diseases / Q000188:drug therapy
chemical_list: D005938:Glucocorticoids; D006887:Hydroxycholecalciferols; D010281:Parathyroid Hormone; D002118:Calcium; D011241:Prednisone