title: Glucocorticoid-induced osteoporosis in patients with sarcoidosis.
abstract: BACKGROUND
  Patients with sarcoidosis are at risk for osteoporosis caused by glucocorticoid therapy. However, because of potential hypercalciuria and hypercalcemia, the usual conservative treatment for low bone mass, calcium and vitamin D supplements, may not be well tolerated.
  
  
  METHODS
  Patients with sarcoidosis referred to a metabolic bone clinic were compared with other sarcoidosis patients studied prospectively and patients with chronic obstructive pulmonary disease (COPD) or asthma. The subjects underwent bone mineral density (BMD) testing, and the sarcoidosis patients underwent mobility testing and measurements of serum and urine chemistries, vitamin D levels, bone turnover markers, and sex hormone levels.
  
  
  RESULTS
  The subjects were mostly male African Americans in the 6th decade of life. Many took chronic oral glucocorticoid therapy and often used home oxygen therapy. Low hip BMD was common among the referred group, comparable with patients with COPD. Surprisingly, hypercalciuria and hypercalcemia were uncommon, and serum testosterone levels were frequently low. The use of calcium supplements, multivitamins containing vitamin D, and glucocorticoids had no impact on serum or urine calcium levels. From univariate analysis, potential risk factors for low hip BMD were low weight, low body mass index (BMI), advanced age, and current use of glucocorticoids. However, in stepwise multiple regression analysis, only low BMI predicted about 40% of hip BMD.
  
  
  CONCLUSIONS
  Despite calcium and vitamin D supplements, this group of patients with sarcoidosis had low BMD but relatively infrequent hypercalciuria and hypercalcemia. No prediction model of BMD was adequate. Therefore, we conclude that each patient needs to be assessed individually, including measurement of BMD, serum and urine calcium, and sex steroid status.
authors.affiliation: Endocrinology and Metabolism Section, McGuire Veterans Affairs Medical Center, Richmond, Virginia 23249, USA. robert.adler@med.va.gov
authors.forename: Robert A
authors.initials: RA
authors.lastname: Adler
authors.forename: Holly L
authors.initials: HL
authors.lastname: Funkhouser
authors.forename: Valentina I
authors.initials: VI
authors.lastname: Petkov
authors.forename: Meredith M
authors.initials: MM
authors.lastname: Berger
mesh_terms: D015502:Absorptiometry, Photon; D000328:Adult; D000368:Aged; D001249:Asthma / Q000503:physiopathology; D015992:Body Mass Index; D015519:Bone Density; D002112:Calcifediol / Q000097:blood; D002117:Calcitriol / Q000097:blood; D002118:Calcium / Q000008:administration & dosage / Q000097:blood / Q000652:urine; D019587:Dietary Supplements; D005260:Female; D005265:Femoral Neck Fractures; D005938:Glucocorticoids / Q000009:adverse effects*; D006801:Humans; D008297:Male; D008875:Middle Aged; D010024:Osteoporosis / Q000139:chemically induced*; D011446:Prospective Studies; D029424:Pulmonary Disease, Chronic Obstructive / Q000503:physiopathology; D012044:Regression Analysis; D012189:Retrospective Studies; D012507:Sarcoidosis / Q000188:drug therapy* / Q000503:physiopathology; D013131:Spine; D013739:Testosterone / Q000097:blood; D014807:Vitamin D / Q000008:administration & dosage
chemical_list: D005938:Glucocorticoids; D014807:Vitamin D; D013739:Testosterone; D002117:Calcitriol; D002112:Calcifediol; D002118:Calcium