ABSTRACT
Objectives To estimate the correlation between osteoporosis and vascular calcification in postmenopausal women and the influence of calcium/vitamin D supplements on vascular calcification.
Methods A cross-sectional study was performed including 29 women with osteoporosis (15 not taking supplements) and 18 age-matched, non-osteoporotic women. They were evaluated for cardiovascular risk factors and blood tests, lateral X-ray of lumbar spine (assessment of abdominal aorta calcification, AAC) and carotid ultrasound (increased intima media thickness (iIMT) or calcified plaques) were performed.
Results In univariate analysis, osteoporotic women were 16 times more likely to develop AAC (odds ratio (OR) 15.8, 95% confidence interval (CI) 1.9–135.4) and seven times more likely to develop iIMT (OR 6.8, 95% CI 1.8–25.4) compared to normal individuals. The odds of developing AAC and iIMT were increased each year after menopause (OR 1.11, 95% CI 1.01–1.2 and OR 1.18, 95% CI 1.05–1.3, respectively) and with aging (OR 1.27, 95% CI 1.1–1.47 and OR = 1.17, 95% CI 1.04–1.3, respectively). Calcified plaques were significantly correlated with osteoporosis (p = 0.014). In multivariate analysis, osteoporosis was an independent risk factor for AAC (OR 13.3, 95% CI 1.3–134.4) and iIMT (OR 4.7, 95% CI 1.1–19.9). Low doses of supplements did not appear to affect vascular calcification (p = 0.6).
Conclusions Osteoporosis is associated with increased calcification of the abdominal aorta and carotids. Low doses of supplements do not appear to cause any increase in vascular calcification in osteoporotic women.
Acknowledgements
We would like to thank Professor Haralampos M. Moutsopoulos for his observation about the relation between osteoporosis and vascular calcification and for the paternity of this project, as well as Dr Panagiotis Nikolarakos for his contribution to the design of the study.
Conflict of interest
The authors report no conflicts of interest. The authors alone are responsible for the content and writing of this paper.
Source of funding
Nil.