title: Short-term effects of atorvastatin on bone turnover in male patients with hypercholesterolemia.
abstract: No consensus has been reached on whether the 3-hydroxy 3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors, known as statins, have beneficial effects on bone health. The purpose of our study was to evaluate the effects of atorvastatin on bone metabolism by means of measuring bone turnover markers in male patients with hypercholesterolemia both at diagnosis and prospectively after 3 months of treatment. Twenty-two Japanese male patients (mean age 62.36 +/- 10.1 years) with untreated hypercholesterolaemeia were selected for this study. After 3-months treatment of atorvastatin, total cholesterol and low density lipoprotein cholesterol significantly decreased as expected (p<0.001 for both parameters). Bone-specific alkaline phosphatase (BAP) did not change significantly (p = 0.444). However, serum N-terminal telopeptide of type I collagen (NTx) significantly decreased by -19.86 +/- 26.4% (p = 0.020). In addition, delta NTx during the course of this study was negatively correlated with NTx at baseline (r = -0.645, p = 0.0008). Although there was a tendency of positive correlations of delta NTx with delta total cholesterol, delta triglycerides, and delta low density lipoprotein cholesterol, and of negative correlations of delta NTx and delta BAP with delta high density lipoprotein cholesterol, none of them reached statistical significance. Our findings suggest that atorvastatin may have potentially beneficial effects on bone metabolism in patients with hypercholesterolemia mostly by reducing bone resorption rather than by stimulating bone formation. Further studies with more patients and longer duration are warranted to evaluate its effects, if any, on prevention of osteoporosis and subsequent fractures.
authors.affiliation: Department of Endocrinology and Metabolism, Rakuwakai Otowa Hospital, Kyoto, Japan.
authors.forename: Takafumi
authors.initials: T
authors.lastname: Majima
authors.forename: Yasato
authors.initials: Y
authors.lastname: Komatsu
authors.forename: Atsushi
authors.initials: A
authors.lastname: Fukao
authors.forename: Kiyoshi
authors.initials: K
authors.lastname: Ninomiya
authors.forename: Tadashi
authors.initials: T
authors.lastname: Matsumura
authors.forename: Kazuwa
authors.initials: K
authors.lastname: Nakao
mesh_terms: D000368:Aged; D000469:Alkaline Phosphatase / Q000097:blood / Q000652:urine; D000924:Anticholesteremic Agents / Q000494:pharmacology / Q000627:therapeutic use; D000069059:Atorvastatin; D015415:Biomarkers / Q000097:blood / Q000652:urine; D016723:Bone Remodeling / Q000187:drug effects*; D024042:Collagen Type I / Q000097:blood; D006538:Heptanoic Acids / Q000494:pharmacology* / Q000627:therapeutic use*; D006801:Humans; D006937:Hypercholesterolemia / Q000097:blood / Q000188:drug therapy* / Q000652:urine; D008297:Male; D008875:Middle Aged; D010455:Peptides / Q000097:blood; D011758:Pyrroles / Q000494:pharmacology* / Q000627:therapeutic use*; D013997:Time Factors
chemical_list: D000924:Anticholesteremic Agents; D015415:Biomarkers; D024042:Collagen Type I; D006538:Heptanoic Acids; D010455:Peptides; D011758:Pyrroles; C052929:collagen type I trimeric cross-linked peptide; D000069059:Atorvastatin; D000469:Alkaline Phosphatase