BACKGROUND: The aim of our study was to evaluate whether pravastatin treatment affected biochemical markers of bone turnover. METHODS: Thirty-six hypercholesterolemic post-menopausal women, not on hormonal replacement therapy, were selected from a population study evaluating factors affecting cholesterol response to pravastatin. After a 6-week period on a 30% fat diet, participants received treatment with 20 mg/day of pravastatin during a 16-week follow-up period. Pre- and post-treatment samples were analyzed for procollagen I aminoterminal peptide (PINP) and bone alkaline phosphatase (bAP) as markers of bone formation, carboxyterminal telopeptide of collagen I (CTX) as a marker of bone resorption, and procollagen III aminoterminal propeptide (PIIINP) as a marker of fibrogenesis. RESULTS: Total cholesterol decreased from 7.26+/-0.83 to 6.1+/-0.77 mmol/l with pravastatin treatment. PINP levels significantly increased (from 33.6+/-13 to 37.4+/-16, p=0.03) without changes in bAP or CTX. Individual changes in PINP correlated with individual reduction in cholesterol levels (r=0.337, p=0.04). There was no significant change in PIIINP concentration. CONCLUSIONS: Pravastatin treatment increased PINP levels, a marker of bone formation, in hypercholesterolemic, post-menopausal women, without affecting bone resorption. PIIINP concentration, a marker of liver fibrogenesis, was not affected by the treatment.
BACKGROUND: The aim of our study was to evaluate whether pravastatin treatment affected biochemical markers of bone turnover. METHODS: Thirty-six hypercholesterolemic post-menopausal women, not on hormonal replacement therapy, were selected from a population study evaluating factors affecting cholesterol response to pravastatin. After a 6-week period on a 30% fat diet, participants received treatment with 20 mg/day of pravastatin during a 16-week follow-up period. Pre- and post-treatment samples were analyzed for procollagen I aminoterminal peptide (PINP) and bone alkaline phosphatase (bAP) as markers of bone formation, carboxyterminal telopeptide of collagen I (CTX) as a marker of bone resorption, and procollagen III aminoterminal propeptide (PIIINP) as a marker of fibrogenesis. RESULTS: Total cholesterol decreased from 7.26+/-0.83 to 6.1+/-0.77 mmol/l with pravastatin treatment. PINP levels significantly increased (from 33.6+/-13 to 37.4+/-16, p=0.03) without changes in bAP or CTX. Individual changes in PINP correlated with individual reduction in cholesterol levels (r=0.337, p=0.04). There was no significant change in PIIINP concentration. CONCLUSIONS:Pravastatin treatment increased PINP levels, a marker of bone formation, in hypercholesterolemic, post-menopausal women, without affecting bone resorption. PIIINP concentration, a marker of liver fibrogenesis, was not affected by the treatment.
Authors: Ki Hyun Baek; Won Young Lee; Ki Won Oh; Hyun Jung Tae; Jung Min Lee; En Jung Lee; Je Ho Han; Moo Il Kang; Bong Yun Cha; Kwang Woo Lee; Ho Young Son; Sung Koo Kang Journal: J Korean Med Sci Date: 2005-06 Impact factor: 2.153