title: Skeletal turnover, bone mineral density, and fractures in male chronic abusers of alcohol.
abstract: BACKGROUND
  Chronic alcohol abuse is a risk factor for osteoporosis and fractures, whose pathogenesis is still unclear. We investigated the influence of alcoholism and other risk factors on calcium and skeletal metabolism, bone mineral density (BMD), and fractures.
  
  
  METHODS
  In 51 chronic male alcoholics without liver failure and 31 healthy controls, serum total and ionised calcium, phosphate, creatinine, 25-hydroxy vitamin D (25OHD), PTH, total (ALP) and bone-specific (BALP) alkaline phosphatase, osteocalcin (BGP), carboxy-terminal telopeptide of type I collagen (beta-CTx), osteoprotegerin (OPG) and receptor activator of nuclear factor kappa B ligand (RANKL) were assessed. In patients only, we also measured serum testosterone, 17-beta estradiol, LH, and IGF-I. BMD was measured by dual energy x-ray absorptiometry at lumbar spine (LS-) and femur [neck (FN-) and total hip (TF-)]. Vertebral fractures were identified by a semiquantitative method on thoraco-lumbar spine x-ray, non-vertebral fractures (as life-style factors) by history.
  
  
  RESULTS
  Alcoholics were leaner, had significantly higher ALP and BALP, and lower BGP and 25OHD levels than controls. No significant difference in other calcium and bone metabolism parameters was found. OPG/RANKL ratio was significantly higher in alcoholics. Beta-CTx negatively correlated with abuse duration. OPG positively correlated with daily alcohol assumption and with indexes of liver cytolysis. Though LS-, FN- and TF-BMD of alcoholics and controls did not significantly differ, patients had a much higher prevalence of vertebral fractures. The same was found considering both vertebral and non-vertebral fractures.
  
  
  CONCLUSIONS
  Ethanol-induced skeletal damage seems mainly dependent on negative effects on bone formation. Lifestyle factors and traumas likely contribute to the high fracture incidence of alcohol abusers, independently of BMD.
authors.affiliation: Department of Clinical Sciences, University of Rome La Sapienza, 00161 Rome, Italy.
authors.forename: C
authors.initials: C
authors.lastname: Santori
authors.forename: M
authors.initials: M
authors.lastname: Ceccanti
authors.forename: D
authors.initials: D
authors.lastname: Diacinti
authors.forename: M L
authors.initials: ML
authors.lastname: Attilia
authors.forename: L
authors.initials: L
authors.lastname: Toppo
authors.forename: E
authors.initials: E
authors.lastname: D'Erasmo
authors.forename: E
authors.initials: E
authors.lastname: Romagnoli
authors.forename: M L
authors.initials: ML
authors.lastname: Mascia
authors.forename: C
authors.initials: C
authors.lastname: Cipriani
authors.forename: A
authors.initials: A
authors.lastname: Prastaro
authors.forename: V
authors.initials: V
authors.lastname: Carnevale
authors.forename: S
authors.initials: S
authors.lastname: Minisola
mesh_terms: D000328:Adult; D000437:Alcoholism / Q000097:blood* / Q000150:complications*; D015519:Bone Density / Q000502:physiology*; D016723:Bone Remodeling / Q000502:physiology*; D050723:Fractures, Bone / Q000097:blood* / Q000209:etiology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D010024:Osteoporosis / Q000097:blood / Q000209:etiology; D012307:Risk Factors