High-sensitivity C-reactive protein and fracture risk in elderly women.
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Biomedical subjects
Hans G Schneider
Publications and source records attributed to Hans G Schneider.
Antioxidant vitamin supplements and markers of bone turnover in a community sample of nonsmoking women.
BACKGROUND: Whereas several epidemiological studies suggest that low dietary intake of vitamins C and E is linked to increased hip fracture in smokers and antioxidants (dietary and endogenous) are reduced in elderly osteoporotic women, none has demonstrated an effect of supplemental antioxidants on bone turnover. METHODS: In an observational study of 533 randomly selected women, we investigated the associations among the use of antioxidant supplements, vitamins C and E, serum levels of biochemical markers of bone turnover (C-telopeptide [CTx] and bone-specific alkaline phosphatase [BSAP]), and whole body bone mineral density (BMD). RESULTS: Twenty-two women were identified as current users of supplemental vitamin C or E. Duration of antioxidant supplement use was negatively associated with age-adjusted and weight-adjusted serum CTx, such that mean CTx levels (natural log transformed) were 0.022 units lower for each year of exposure. No significant differences were detected for adjusted serum BSAP or whole body BMD. CONCLUSIONS: Our results suggest that antioxidant vitamin E or C supplements may suppress bone resorption in nonsmoking postmenopausal women. Coupling of bone formation and resorption may explain the absence of an effect on bone formation markers, given evidence of enhanced effects of antioxidants on osteoblast differentiation; this warrants further investigation. This work adds to the growing body of evidence that antioxidants may play a role in preventing osteoporosis.
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Can the blood pressure effects of COX-2 selective inhibitors be explained by changes in plasma aldosterone levels?
OBJECTIVE: The increased cardiovascular risk associated with rofecoxib may relate to differential effects on blood pressure (BP) in comparison with other cyclooxygenase-2 (COX-2) selective inhibitors. Rofecoxib is uniquely metabolized by cytosol reductase and may compete with aldosterone for metabolism. We hypothesized that the effect of rofecoxib on BP may be due to an increase in aldosterone levels. DESIGN: Prospective, randomized, cross-over study. SETTING: Tertiary institution. PATIENTS: Eleven patients (all female, age 65 +/- 11 years) with osteoarthritis and hypertension. INTERVENTIONS: Patients received rofecoxib 50 mg once/day or celecoxib 400 mg once/day for 8 weeks, followed by cross-over after a 2-week wash-out period. OUTCOME MEASURES: Office BP, heart rate (HR), plasma aldosterone and aldosterone related-markers, markers of sympathetic and parasympathetic activity, catecholamines and heart rate variability (HRV) were measured. RESULTS: Rofecoxib caused an increase in BP compared to celecoxib; a change in recumbent systolic BP +/- SD (6.1 +/- 11.0 versus -7.0 +/- 12.5 mmHg, P < 0.05) and recumbent diastolic BP +/- SD (3.6 +/- 7.6 versus -1.7 +/- 5.7 mmHg). There was no difference in median change in plasma aldosterone levels between rofecoxib and celecoxib (-31 +/- 171.5 versus 43 +/- 147 pg/ml, P = 0.173). The other parameters measured were not different between the two agents. CONCLUSIONS: Rofecoxib therapy results in a significant increase in systolic BP compared to celecoxib. As plasma aldosterone levels were not different between the two drugs, the differential effect of rofecoxib on BP compared to celecoxib appears to be unlikely due to competition by rofecoxib for aldosterone metabolism.
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Seasonal periodicity of serum vitamin D and parathyroid hormone, bone resorption, and fractures: the Geelong Osteoporosis Study.
UNLABELLED: In this population-based study, seasonal periodicity was seen with reduced serum vitamin D, increased serum PTH, and increased bone resorption in winter. This was associated with an increased proportion of falls resulting in fracture and an increased risk of wrist and hip fractures. INTRODUCTION: In a population of women who reside in a temperate climate and do not generally receive dietary vitamin D supplementation, we investigated whether seasonal vitamin D insufficiency is associated with increased risk of fracture. MATERIALS AND METHODS: An observational, cross-sectional, population-based study set in southeastern Australia (latitude 38-39 degrees S). Participants were drawn from a well-defined community of 27,203 women >/=55 years old: 287 randomly selected from electoral rolls, 1635 with incident fractures, and 1358 presenting to a university hospital with falls. The main outcome measures were annual periodicities of ultraviolet radiation, serum 25-hydroxyvitamin D [25(OH)D], serum parathyroid hormone (PTH), serum C-telopeptide (CTx), BMD, falls, and fractures. RESULTS: Cyclic variations in serum 25(OH)D lagged 1 month behind ultraviolet radiation, peaking in summer and dipping in winter (p < 0.001). Periodicity of serum PTH was the inverse of serum 25(OH)D, with a phase shift delay of 1 month (p = 0.004). Peak serum CTx lagged peak serum PTH by 1-2 months. In late winter, a greater proportion of falls resulted in fracture (p < 0.001). Seasonal periodicity in 439 hip and 307 wrist fractures also followed a simple harmonic model (p = 0.078 and 0.002, respectively), peaking 1.5-3 months after the trough in 25(OH)D. CONCLUSIONS: A fall in 25(OH)D in winter is accompanied by increases in (1) PTH levels, (2) bone resorption, (3) the proportion of falls resulting in fracture, and (4) the frequency of hip and wrist fracture. Whether vitamin D supplementation in winter can reduce the population burden of fractures requires further investigation.
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Beta-blockers reduce bone resorption marker in early postmenopausal women.
BACKGROUND: There is evidence to suggest that beta-blockers used in the management of cardiovascular disease may also modulate bone metabolism and reduce bone fragility. AIM: The study aimed to determine the association between beta-blocker use, serum markers of bone turnover and bone loss in early postmenopausal women. SUBJECTS AND METHODS: In this observational study, we evaluated beta-blocker exposure in association with serum levels of C-telopeptide and bone-specific alkaline phosphatase, and rates of bone loss. Beta-blocker use, concomitant therapy and lifestyle were documented for 197 women (50-59 years), 175 of whom had changes in whole body bone mineral density monitored over a 2-year period. RESULTS: Twenty-four beta-blocker users were identified at baseline. After controlling for concomitant use of hormone therapy, C-telopeptide levels were 6.7% lower among beta-blocker users (p=0.02). No association was detected between bone-specific alkaline phosphatase and beta-blocker use. Analysis of 15 beta-blocker users and 152 non-users identified 2 years post-baseline showed that levels of C-telopeptide but not bone-specific alkaline phosphatase were predictors of adjusted rates of bone loss (p=0.008 and p>0.05, respectively). Adjusted rates of bone loss were-0.001+/-0.026 g cm(-2) over 2 years for the users and-0.004+/-0.025 g cm(-2) over 2 years for non-users, but this difference was not significant. CONCLUSION: Beta-blockers might suppress bone resorption with relative preservation of bone formation. A study with greater power is required to determine whether ss-blocker use is associated with lower rates of bone loss.
Adrenergic beta-Antagonists↗