title: Comparison of clinical cut-points and treatment targets for urine NTX and plasma βCTX-I in osteoporosis.
abstract: OBJECTIVE
  We undertook to identify levels for plasma β isomerised carboxy-terminal telopeptides of type I collagen (p-βCTX-I) that are comparable to currently used urine amino-terminal telopeptides of type I collagen (u-NTX) cut-points and treatment targets in osteoporosis.
  
  
  METHODS
  Fasting morning samples were collected from patients attending tertiary hospitals and clinics for investigation of metabolic bone disease. Patients with Paget's disease or <20years of age were excluded. Second void spot urine for NTX and plasma (EDTA) samples were utilised. Urine was analysed routinely and plasma stored at -20C until analysis by enzyme-linked immunosorbent assay (ELISA) (Immunodiagnostic Systems plc), E170 (Roche Diagnostics) and IDS-iSYS (Immunodiagnostic Systems plc) methods. The relationship of u-NTX with each p-βCTX-I method's results was assessed by Passing and Bablok regression, and p-βCTX-I levels equivalent to u-NTX cut-points and targets were interpolated.
  
  
  RESULTS
  One hundred and forty six patients were included. Spearman correlation coefficients ranged from 0.71 to 0.75 for the three βCTX-I assays. The equivalent βCTX-I concentrations for NTX/Cr values of 21 (fracture risk reduction target following risedronate therapy), 27 (healthy pre-menopausal women's mean value), and 38 (threshold for reduction of BMD on calcium alone) nmol BCE/mmol were 230, 312 and 462ng/L for the automated Roche assay and 271, 395 and 624ng/L for the automated IDS i-SYS assay respectively.
  
  
  CONCLUSIONS
  The p-βCTX-I equivalent to the only available fracture outcome based absolute treatment threshold of 21nmol BCE/mmol established for u-NTX, is close to 250ng/L but will vary between p-βCTX-I assays.
authors.affiliation: Department of Clinical Biochemistry, PathWest Laboratory Medicine WA, Royal Perth and Fiona Stanley Hospitals, GPO Box X2213, Perth, WA 6009, Australia; School of Pathology and Laboratory Medicine, University of Western Australia, Nedlands, WA 6009, Australia; School of Medicine and Pharmacology, University of Western Australia, Nedlands, WA 6009, Australia.
authors.forename: S A Paul
authors.initials: SA
authors.lastname: Chubb
authors.affiliation: Department of Clinical Biochemistry, PathWest Laboratory Medicine WA, Royal Perth and Fiona Stanley Hospitals, GPO Box X2213, Perth, WA 6009, Australia.
authors.forename: Christine
authors.initials: C
authors.lastname: Mandelt
authors.affiliation: Department of Clinical Biochemistry, PathWest Laboratory Medicine WA, Royal Perth and Fiona Stanley Hospitals, GPO Box X2213, Perth, WA 6009, Australia; School of Pathology and Laboratory Medicine, University of Western Australia, Nedlands, WA 6009, Australia. Electronic address: samuel.vasikaran@health.wa.gov.au.
authors.forename: Samuel
authors.initials: S
authors.lastname: Vasikaran
mesh_terms: D000328:Adult; D000368:Aged; D001681:Biological Assay / Q000379:methods*; D015415:Biomarkers / Q000378:metabolism*; D024042:Collagen Type I / Q000097:blood* / Q000652:urine*; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D008297:Male; D008875:Middle Aged; D010024:Osteoporosis / Q000097:blood / Q000175:diagnosis* / Q000188:drug therapy / Q000652:urine; D010455:Peptides / Q000097:blood* / Q000652:urine*; D011379:Prognosis
chemical_list: D015415:Biomarkers; D024042:Collagen Type I; D010455:Peptides; C052929:collagen type I trimeric cross-linked peptide
keywords: Antiresorptives; Biochemical markers of bone turnover; Bone remodelling; Fracture risk assessment; Osteoporosis