title: Bone mineral density is not significantly reduced in adult patients on low-dose glucocorticoid replacement therapy.
abstract: BACKGROUND
  Patients with primary adrenal insufficiency (PAI) and patients with congenital adrenal hyperplasia (CAH) receive glucocorticoid replacement therapy, which might cause osteoporosis.
  
  
  OBJECTIVE
  Questions addressed by this study were: 1) Is bone mineral density (BMD) reduced in PAI and CAH on lower glucocorticoid doses than previously reported? 2) Is BMD in PAI influenced by the type of glucocorticoid used? and 3) Does DHEA treatment affect BMD in PAI women?
  
  
  METHODS
  We conducted a prospective, cross-sectional study including 81 PAI patients and 41 CAH patients.
  
  
  METHODS
  BMD was measured by dual-energy x-ray absorptiometry. Serum levels of bone turnover markers, minerals, vitamins, hormones, and urinary crosslinks were measured.
  
  
  RESULTS
  PAI and CAH patients received average daily hydrocortisone doses of 12.0 ± 2.7 mg/m(2) (range, 4.9-19.1) and 15.5 ± 7.8 mg/m(2) (range, 5.7-33.7), respectively. BMD varied within the normal reference range (-2 to +2) in both cohorts. However, lower Z-scores for femoral neck and Ward's region were found in CAH compared to PAI women, but not in men. Prednisolone treatment showed significant lower osteocalcin levels and lower Z-scores for lumbar spine and femoral neck compared to PAI patients on hydrocortisone. PAI women treated with DHEA had significantly lower urinary collagen crosslinks and bone alkaline phosphatase, and significantly higher Z-scores in lumbar spine and femoral Ward's region compared to non-DHEA-treated women.
  
  
  CONCLUSIONS
  Adult PAI and CAH patients on low glucocorticoid doses showed normal BMD within the normal reference range. The use of longer acting prednisolone resulted in significantly lower BMD in PAI. In addition, DHEA treatment may have a beneficial effect on bone in Addison's women.
authors: Department of Clinical Endocrinology, Charite Campus Mitte, Charite University Medicine, D-10117 Berlin, Germany.
authors: K R
authors: KR
authors: Koetz
authors: M
authors: M
authors: Ventz
authors: S
authors: S
authors: Diederich
authors: M
authors: M
authors: Quinkler
mesh_terms: D015502:Absorptiometry, Photon; D000224:Addison Disease / Q000188:drug therapy / Q000453:epidemiology / Q000378:metabolism / Q000503:physiopathology; D000312:Adrenal Hyperplasia, Congenital / Q000188:drug therapy* / Q000453:epidemiology / Q000378:metabolism / Q000503:physiopathology; D000328:Adult; D000368:Aged; D015519:Bone Density / Q000187:drug effects*; D003430:Cross-Sectional Studies; D003907:Dexamethasone / Q000008:administration & dosage / Q000009:adverse effects / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D015536:Down-Regulation / Q000187:drug effects; D005260:Female; D005272:Femur Neck / Q000187:drug effects; D005938:Glucocorticoids / Q000008:administration & dosage* / Q000009:adverse effects / Q000494:pharmacology*; D020249:Hormone Replacement Therapy / Q000009:adverse effects / Q000379:methods; D006801:Humans; D008297:Male; D008875:Middle Aged; D010024:Osteoporosis / Q000139:chemically induced / Q000175:diagnosis / Q000453:epidemiology; D011239:Prednisolone / Q000008:administration & dosage / Q000009:adverse effects / Q000494:pharmacology
chemical_list: D005938:Glucocorticoids; D003907:Dexamethasone; D011239:Prednisolone