title: Effect of the TNFalpha-308 G/A polymorphism on the changes produced by atorvastatin in bone mineral density in patients with acute coronary syndrome.
abstract: OBJECTIVE
  To evaluate the effect of atorvastatin on bone mass and markers of bone remodeling in patients with acute coronary syndrome depending on the tumor necrosis factor-alpha (TNFalpha)-308 G/A polymorphism.
  
  
  METHODS
  Sixty-two patients with acute coronary syndrome (35 males and 27 females), average age 60 +/- 10 years, were included. Patients were given low (10-20 mg) and high doses (40-80 mg) atorvastatin according to their baseline levels of cholesterol and triglycerides and their index of vascular risk. Patients were studied during hospital admission (baseline) and at 12 months of follow-up. Cholesterol, triglycerides, total calcium, phosphorus, magnesium, osteocalcin and urinary deoxypyridinoline were determined in all patients at baseline and at 12 months of follow-up. Densitometric studies were conducted in the lumbar spine (L(2)-L(4)), femoral neck and trochanter using an X-ray densitometer. The TNFalpha-308 G/A polymorphism was determined by the polymerase chain reaction.
  
  
  RESULTS
  Forty-five patients were homozygous for G/G (72.5%) and 17 were heterozygous for G/A (27.5%). The prevalence of osteoporosis (T score < or = 2.5 in the lumbar spine and/or hip) was 33% for the G/G genotype and 35% for the G/A genotype, with no statistically significant differences between groups. There was a statistically significant increase in bone mineral density (BMD) in the lumbar spine (1.107 +/- 0.32 vs. 1.129 +/- 0.23; p = 0.0001) in patients with the G/G genotype. No changes were observed in patients with the G/A genotype.
  
  
  CONCLUSIONS
  In patients with acute coronary syndrome, atorvastatin increases lumbar spine BMD solely in patients with the G/G genotype of the TNFalpha-308 G/A polymorphism.
authors.affiliation: Department of Internal Medicine, Rio Hortega University Hospital, Faculty of Medicine, Valladolid, Spain. castrv@terra.es
authors.forename: José Luis
authors.initials: JL
authors.lastname: Pérez-Castrillón
authors.forename: Gemma
authors.initials: G
authors.lastname: Vega
authors.forename: Laura
authors.initials: L
authors.lastname: Abad
authors.forename: Alberto
authors.initials: A
authors.lastname: Sanz-Cantalapiedra
authors.forename: Manuel
authors.initials: M
authors.lastname: Gonzalez Sagredo
authors.forename: Daniel
authors.initials: D
authors.lastname: de Luis
authors.forename: Antonio
authors.initials: A
authors.lastname: Duenas-Laita
mesh_terms: D015502:Absorptiometry, Photon / Q000379:methods; D054058:Acute Coronary Syndrome / Q000188:drug therapy; D000596:Amino Acids / Q000652:urine; D000924:Anticholesteremic Agents / Q000009:adverse effects* / Q000627:therapeutic use; D000069059:Atorvastatin; D015519:Bone Density / Q000187:drug effects*; D002118:Calcium / Q000097:blood; D002784:Cholesterol / Q000097:blood; D004305:Dose-Response Relationship, Drug; D005260:Female; D005272:Femur Neck / Q000187:drug effects / Q000378:metabolism; D005500:Follow-Up Studies; D005838:Genotype; D006538:Heptanoic Acids / Q000009:adverse effects* / Q000627:therapeutic use; D006801:Humans; D008274:Magnesium / Q000097:blood; D008297:Male; D008875:Middle Aged; D015675:Osteocalcin / Q000097:blood; D010024:Osteoporosis / Q000453:epidemiology*; D010758:Phosphorus / Q000097:blood; D016133:Polymerase Chain Reaction / Q000379:methods; D011110:Polymorphism, Genetic; D011758:Pyrroles / Q000009:adverse effects* / Q000627:therapeutic use; D012307:Risk Factors; D014280:Triglycerides / Q000097:blood; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics*
chemical_list: D000596:Amino Acids; D000924:Anticholesteremic Agents; D006538:Heptanoic Acids; D011758:Pyrroles; D014280:Triglycerides; D014409:Tumor Necrosis Factor-alpha; D015675:Osteocalcin; D010758:Phosphorus; C036020:deoxypyridinoline; D002784:Cholesterol; D000069059:Atorvastatin; D008274:Magnesium; D002118:Calcium