title: Age, initial dose and dose increase are independent risk factors for symptomatic vertebral fractures in glucocorticoid-treated male patients.
abstract: OBJECTIVE
  The incidence and risk factors for symptomatic vertebral fracture were analyzed in glucocorticoid-treated male patients.
  
  
  METHODS
  This was an observational cohort study at Shimoshizu National Hospital in Japan. Analyzed were 161 male patients newly treated with high-dose glucocorticoid (≥20 mg/day prednisolone equivalent) (initial age: 53.5±16.9, initial glucocorticoid dose: 38.9±12.9 mg/day (0.66±0.23 mg/kg/day), follow-up time: 70.4±52.5 months) and 33 male patients with no glucocorticoid (initial age: 52.7±13.0, follow-up time: 76.4±62.7 months). The vertebral fracture was determined by x-rays.
  
  
  RESULTS
  Symptomatic vertebral fractures occurred more frequently in the high-dose glucocorticoid group (21.1%) than in the no glucocorticoid group (3.0%). Using Cox model, the adjusted hazard ratio (HR) for the high-dose glucocorticoid group was 8.16 (95% confidence interval: 1.09-60.86) relative to the no glucocorticoid control group. In the high-dose glucocorticoid group, Kaplan-Meier analyses demonstrated that the incidence of fractures in the patients with glucocorticoid dose increase was significantly higher in comparison with those with no glucocorticoid dose increase. Cox model demonstrated that the risk was independently higher in every 10-year increment of initial age with HR 1.58 (1.18-2.13), in every 10 mg increment of initial dose of prednisolone with HR 2.03 (1.43-2.88), in every dose increase of glucocorticoid increase with HR 3.63 (2.04-6.46), and with each 1-gram decrease of cumulative dose of glucocorticoid with HR 0.88 (0.84-0.93).
  
  
  CONCLUSIONS
  In male patients, high-dose glucocorticoid causes a significantly high prevalence of symptomatic vertebral fractures, and the independent risk factors are age, initial glucocorticoid dose, glucocorticoid dose increase, and decrease of cumulative glucocorticoid dose.
authors.affiliation: Department of Rheumatology, National Hospital Organization Shimoshizu National Hospital, Japan.
authors.forename: Takao
authors.initials: T
authors.lastname: Sugiyama
authors.forename: Sawako
authors.initials: S
authors.lastname: Suzuki
authors.forename: Tomohiko
authors.initials: T
authors.lastname: Yoshida
authors.forename: Takafumi
authors.initials: T
authors.lastname: Mayama
authors.forename: Naoko
authors.initials: N
authors.lastname: Hashimoto
authors.forename: Keiko
authors.initials: K
authors.lastname: Suyama
authors.forename: Tomoaki
authors.initials: T
authors.lastname: Tanaka
authors.forename: Makoto
authors.initials: M
authors.lastname: Sueishi
authors.forename: Ichiro
authors.initials: I
authors.lastname: Tatsuno
mesh_terms: D000328:Adult; D000367:Age Factors; D000368:Aged; D001327:Autoimmune Diseases / Q000188:drug therapy; D016022:Case-Control Studies; D015331:Cohort Studies; D004305:Dose-Response Relationship, Drug; D005500:Follow-Up Studies; D005938:Glucocorticoids / Q000008:administration & dosage* / Q000009:adverse effects*; D006801:Humans; D015994:Incidence; D053208:Kaplan-Meier Estimate; D008297:Male; D008875:Middle Aged; D011239:Prednisolone / Q000008:administration & dosage / Q000009:adverse effects; D016016:Proportional Hazards Models; D012216:Rheumatic Diseases / Q000188:drug therapy; D012307:Risk Factors; D016103:Spinal Fractures / Q000139:chemically induced* / Q000453:epidemiology / Q000209:etiology*
chemical_list: D005938:Glucocorticoids; D011239:Prednisolone