title: Bone turnover is adequately suppressed in osteoporotic patients treated with bisphosphonates in daily practice.
abstract: BACKGROUND
  Monitoring osteoporosis therapy by measurement of bone turnover markers (BTMs) might detect non-compliance in an earlier stage of anti-osteoporosis treatment and improve persistence.
  
  
  METHODS
  BTMs were measured in two groups. The first group consisted of patients newly diagnosed with osteoporosis and starting treatment. We observed which proportion of patients had a decrease of serum levels of procollagen type 1 N-terminal propeptide (P1NP) and C-terminal crosslinking telopeptide (CTX) greater than the least significant change (LSC) after 3 months of treatment. Secondly, we determined which proportion of patients who were treated with bisphosphonates for ≥ 3 months reached the biological goal of therapy, BTMs in the lower half of the normal premenopausal range. P1NP and CTX were also measured in a reference population of 34 healthy premenopausal women.
  
  
  RESULTS
  In the first group 31 patients were included, in 25 patients (81%) levels of both markers decreased with ≥ LSC, in the other patients a possible explanation was found.In the second group 95 patients were included, in 95% the serum P1NP levels and CTX levels were in the lower half of the premenopausal range. In 6 of the 7 patients with a level above the premenopausal range a possible explanation was found.
  
  
  CONCLUSIONS
  A decrease in bone turnover ≥ LSC can be observed in the majority of newly treated patients. In chronically treated patients, 95% have a bone turnover in the premenopausal range. In most patients with inadequate suppression of BTMs during bisphosphonate treatment, an explanation was found. Monitoring treatment effect with BTMs in daily practice is feasible, and might be an additive tool in improving therapy compliance.
authors.affiliation: Department of Rheumatology, VU University Medical Center, Amsterdam Netherlands. d.eekman@vumc.nl
authors.forename: Danielle A
authors.initials: DA
authors.lastname: Eekman
authors.forename: Irene E M
authors.initials: IE
authors.lastname: Bultink
authors.forename: Annemieke C
authors.initials: AC
authors.lastname: Heijboer
authors.forename: Ben A C
authors.initials: BA
authors.lastname: Dijkmans
authors.forename: Willem F
authors.initials: WF
authors.lastname: Lems
mesh_terms: D000368:Aged; D015519:Bone Density / Q000187:drug effects* / Q000502:physiology; D050071:Bone Density Conservation Agents / Q000008:administration & dosage*; D024042:Collagen Type I / Q000097:blood; D004164:Diphosphonates / Q000008:administration & dosage*; D004334:Drug Administration Schedule; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D015663:Osteoporosis, Postmenopausal / Q000097:blood* / Q000188:drug therapy* / Q000503:physiopathology; D010446:Peptide Fragments / Q000097:blood; D010455:Peptides / Q000097:blood; D011347:Procollagen / Q000097:blood
chemical_list: D050071:Bone Density Conservation Agents; D024042:Collagen Type I; D004164:Diphosphonates; D010446:Peptide Fragments; D010455:Peptides; D011347:Procollagen; C052929:collagen type I trimeric cross-linked peptide; C047202:procollagen Type I N-terminal peptide