title: Serum levels of parathyroid hormone and markers of bone metabolism in patients with rheumatoid arthritis. Relationship to disease activity and glucocorticoid treatment.
abstract: OBJECTIVE
  To evaluate the influence of inflammatory activity and glucocorticoid (GC) treatment on serum parathyroid hormone (s-PTH) and bone metabolism in patients with rheumatoid arthritis (RA). Furthermore, in patients with active RA, to examine the PTH secretion and Ca2+ set point before and after treatment with GC.
  
  
  METHODS
  A range of biochemical markers of bone metabolism and calcium homeostasis were measured in 95 patients with definite RA stratified into groups according to disease activity and GC treatment. In a subgroup of 12 patients with active disease, initiating slow-acting-anti-rheumatic-drugs (SAARDs) +/- GC, the PTH secretion and calcium set point were evaluated by use of the Cica clamp technique before and after 1 month of treatment.
  
  
  RESULTS
  S-osteocalcin, s-total alkaline phosphatase (s-TAP) and s-carboxyterminal cross-linked telopeptide of type I collagen (s-ICTP) were elevated in all groups. The levels of urine pyridinoline (Pyr) and s-albumin-corrected calcium (s-AlbCorrCa2+) were elevated in patients with active disease and patients treated with GC. S-PTH and s-phosphate were within normal ranges. S-TAP, s-ICTP, Pyr and s-AlbCorrCa2+ correlated positively with indices of disease activity. In the subgroups undergoing the Cica clamp technique, no difference in PTH responsiveness of B-Ca2+ was unveiled.
  
  
  CONCLUSIONS
  Neither active disease nor GC therapy appears to induce secondary hyperparathyroidism, nor is there an alteration in PTH responsiveness of B-Ca2+ in patients with RA. The increased levels of markers of type I collagen metabolism (s-ICTP, Pyr) and s-AlbCorrCa2+ in patients with active disease and patients treated with GC may be a result of increased degradation in synovium, cartilage and bone due to the inflammatory process.
authors.affiliation: Department of Rheumatology, H:S Hvidovre Hospital, University of Copenhagen, Denmark. twj@dadlnet.dk
authors.forename: T
authors.initials: T
authors.lastname: Jensen
authors.forename: M
authors.initials: M
authors.lastname: Hansen
authors.forename: J C
authors.initials: JC
authors.lastname: Madsen
authors.forename: G
authors.initials: G
authors.lastname: Kollerup
authors.forename: M
authors.initials: M
authors.lastname: Stoltenberg
authors.forename: A
authors.initials: A
authors.lastname: Florescu
authors.forename: P
authors.initials: P
authors.lastname: Schwarz
mesh_terms: D000893:Anti-Inflammatory Agents / Q000627:therapeutic use*; D001172:Arthritis, Rheumatoid / Q000097:blood* / Q000188:drug therapy; D015415:Biomarkers / Q000097:blood*; D001842:Bone and Bones / Q000378:metabolism*; D015331:Cohort Studies; D003430:Cross-Sectional Studies; D005938:Glucocorticoids / Q000627:therapeutic use*; D006801:Humans; D010281:Parathyroid Hormone / Q000097:blood*; D013256:Steroids
chemical_list: D000893:Anti-Inflammatory Agents; D015415:Biomarkers; D005938:Glucocorticoids; D010281:Parathyroid Hormone; D013256:Steroids