Effect of the TNFα-308 G/A Polymorphism on the Changes Produced by Atorvastatin in Bone Mineral Density in Patients with Acute Coronary Syndrome

Abstract

Aims: 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-α (TNFα)-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 (L₂–L₄), femoral neck and trochanter using an X-ray densitometer. The TNFα-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 ≤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. Conclusion: In patients with acute coronary syndrome, atorvastatin increases lumbar spine BMD solely in patients with the G/G genotype of the TNFα-308 G/A polymorphism.

Effect of atorvastatin and rosuvastatin on 25-hydroxy vitamin d levels in newly diagnosed South Indian dyslipidemic subjects

“…Peroz-Castrillon J.L et al, conducted a study and reported the similar observations showed that atorvastatin effective action was seen with plasma 25OHD concentration greater than 30nmolL. (24) Atorvastatin is metabolized by CYP3A4 to its active metabolites. 1, 25 (OH)2D is a potent enzyme inducer of CYP3A4 which accelerate the metabolism of atorvastatin and decrease the plasma concentration.…”

“…However, most of the published studies showed that either no change or increased 25OHD concentrations were reported after treatment with statins. ( 18 (23,24) The contradictory results published by the previous studies might be due to higher Vitamin-D dietary intake or Vit-D absorption are the possible explanations in patients taking statins. Descamps O.S et al, and van Himbergen T.M et al, reported that statins accelerate the cholesterol absorption which is absolute contradictory mechanism which was originally shown by statins.…”