title: Contributors to secondary osteoporosis and metabolic bone diseases in patients presenting with a clinical fracture.
abstract: BACKGROUND
  Previously undetected contributors to secondary osteoporosis and metabolic bone diseases (SECOB) are frequently found in patients with osteoporosis, but the prevalence in patients at the time they present with a clinical fracture is unknown.
  
  
  METHODS
  All consecutive patients with a recent clinical vertebral or nonvertebral fracture, who were able and willing to be investigated (n = 626: 482 women, 144 men, age range 50-97 yr) had bone mineral density and laboratory investigations (serum calcium, inorganic phosphate, 25-hydroxyvitamin D, creatinine, intact PTH, TSH, free T(4), serum and urine protein electrophoresis, and in men also serum testosterone).
  
  
  RESULTS
  Known SECOB contributors were present in 23.0% of patients and newly diagnosed SECOB contributors in 26.5%: monoclonal proteinemia (14 of 626), renal insufficiency grade III or greater (54 of 626), primary (17 of 626) and secondary (64 of 626) hyperparathyroidism, hyperthyroidism (39 of 626), and hypogonadism in men (12 of 144). Newly diagnosed SECOBs, serum 25-hydroxyvitamin D less than 50 nmol/liter (in 63.9%), and dietary calcium intake less than 1200 mg/d (in 90.6%) were found at any age, in both sexes, after any fracture (except SECOB in men with finger and toe fractures) and at any level of bone mineral density.
  
  
  CONCLUSIONS
  At presentation with a fracture, 26.5% of patients have previously unknown contributors to SECOB, which are treatable or need follow-up, and more than 90% of patients have an inadequate vitamin D status and/or calcium intake. Systematic screening of patients with a recent fracture identifies those in whom potentially reversible contributors to SECOB and calcium and vitamin D deficiency are present.
authors.affiliation: Department of Internal Medicine, VieCuri Medisch Centrum Noord-Limburg, 5912 BL Venlo, The Netherlands. s.bours@mumc.nl
authors.forename: Sandrine P G
authors.initials: SP
authors.lastname: Bours
authors.forename: Tineke A C M
authors.initials: TA
authors.lastname: van Geel
authors.forename: Piet P M M
authors.initials: PP
authors.lastname: Geusens
authors.forename: Marcel J W
authors.initials: MJ
authors.lastname: Janssen
authors.forename: Heinrich M J
authors.initials: HM
authors.lastname: Janzing
authors.forename: Ge A
authors.initials: GA
authors.lastname: Hoffland
authors.forename: Paul C
authors.initials: PC
authors.lastname: Willems
authors.forename: Joop P W
authors.initials: JP
authors.lastname: van den Bergh
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000469:Alkaline Phosphatase / Q000097:blood; D015519:Bone Density; D001851:Bone Diseases, Metabolic / Q000209:etiology*; D002118:Calcium / Q000097:blood; D003404:Creatinine / Q000097:blood; D003430:Cross-Sectional Studies; D005260:Female; D050723:Fractures, Bone / Q000453:epidemiology*; D006801:Humans; D006887:Hydroxycholecalciferols / Q000097:blood; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D010024:Osteoporosis / Q000209:etiology*; D010281:Parathyroid Hormone / Q000097:blood; D010710:Phosphates / Q000097:blood; D011446:Prospective Studies; D011507:Proteinuria / Q000150:complications; D016103:Spinal Fractures / Q000453:epidemiology; D013739:Testosterone / Q000097:blood; D013972:Thyrotropin / Q000097:blood; D013974:Thyroxine / Q000097:blood / Q000652:urine
chemical_list: D006887:Hydroxycholecalciferols; D010281:Parathyroid Hormone; D010710:Phosphates; D013739:Testosterone; D013972:Thyrotropin; D003404:Creatinine; D000469:Alkaline Phosphatase; D013974:Thyroxine; D002118:Calcium