title: Bone turnover and hip bone mineral density in patients with sarcoidosis.
abstract: OBJECTIVE
  Sarcoidosis is a chronic inflammatory T-cell-driven disease that can also affect bone. We evaluated bone remodelling and bone mineral density (BMD) in patients with sarcoidosis and their dependency of disease-related and treatment-related factors.
  
  
  METHODS
  In 124 patients BMD of the hip (DXA) and markers of bone resorption (ICTP) and formation (PINP) were evaluated. Furthermore a lateral DXA of the spine for morphometric assessment of vertebral deformities was performed in 87 patients. Potential predictors of bone markers, BMD and determinants of prevalent vertebral deformities were assessed using multiple and logistic regression analysis.
  
  
  RESULTS
  The population studied comprised untreated patients (n=51), patients that previously used glucocorticoids (n=31) and patients currently using glucocorticoids (n=42). In all these groups the age- and gender corrected Z-scores of the hip were normal, except in untreated patients, which revealed an increased Z-score at the trochanter (p = 0.004). In all but the patients currently on glucocorticoids the Z-scores for PINP and ICTP were increased (p < 0.05). In patients currently on glucocorticoids the Z-ICTP was also increased (p < 0.05), but the Z-PINP decreased (p < 0.01 compared to untreated patients). In 20.6% of patients one or more morphometric vertebral deformities were found.
  
  
  CONCLUSIONS
  Hip BMD is normal in patients with sarcoidosis, despite an increased bone turnover. This may imply that in sarcoidosis mechanisms are involved that compensate for the well-known effects of cytokines in inflammatory diseases on osteoclastogenesis and bone resorption. Nonetheless, vertebral deformities suggestive of fracture were found in a significant number of patients which indicates that patients with sarcoidosis still have a relevant fracture risk.
authors: Department of Internal Medicine, Division of Endocrinology, University Hospital Maastricht, The Netherlands. c.heijckmann@bernhoven.nl
authors: A Caroline
authors: AC
authors: Heijckmann
authors: Maya S P
authors: MS
authors: Huijberts
authors: Jolanda
authors: J
authors: De Vries
authors: Paul P C A
authors: PP
authors: Menheere
authors: Eveline
authors: E
authors: Van Der Veer
authors: Arie C Nieuwenhuijzen
authors: AC
authors: Kruseman
authors: Bruce H R
authors: BH
authors: Wolffenbuttel
authors: Piet
authors: P
authors: Geusens
authors: Marjolein
authors: M
authors: Drent
mesh_terms: D000328:Adult; D000368:Aged; D015519:Bone Density / Q000187:drug effects; D016723:Bone Remodeling; D001862:Bone Resorption; D024042:Collagen Type I; D005260:Female; D050723:Fractures, Bone; D005938:Glucocorticoids / Q000627:therapeutic use; D006615:Hip; D006801:Humans; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D010024:Osteoporosis / Q000209:etiology; D010446:Peptide Fragments / Q000097:blood; D010455:Peptides; D011347:Procollagen / Q000097:blood; D015375:Receptors, Interleukin-2 / Q000097:blood*; D012507:Sarcoidosis / Q000150:complications / Q000503:physiopathology*
chemical_list: D024042:Collagen Type I; D005938:Glucocorticoids; D010446:Peptide Fragments; D010455:Peptides; D011347:Procollagen; D015375:Receptors, Interleukin-2; C052929:collagen type I trimeric cross-linked peptide; C047202:procollagen Type I N-terminal peptide