Bone loss has been suggested as a possible marker for an excess risk of cardiovascular (CV) death or stroke [1, 2]. However, previously published studies did not fully characterize this association, which remains controversial. These controversies stem from small sample sizes, confounding by age or the limitations of bone mineral density (BMD) to evaluate the severity of the bone loss. Further, this question was primarily addressed within populations with a high prevalence of risk factors for CV diseases, such as in the USA [3], in which an independent association between osteoporosis and vascular calcification is potentially more challenging to uncover. Moreover, the association between the occurrence and distribution of fractures and vascular calcification remains to be fully documented. Finally, whilst osteoprotegerin has been suggested as a possible mechanistic link between osteoporosis and vascular calcification [4], there is limited data addressing its potential role in clinical studies addressing this issue. This study was undertaken to address these gaps in knowledge within a large cohort of French women, amongst whom the prevalence of atherosclerosis can be expected to be lower based on epidemiological studies [3]. Within the same population, we evaluated simultaneously abdominal aortic calcifications (an established indicator of CV diseases), BMD, fractures and osteoprotegerin levels. We tested the hypothesis that bone loss or fractures were associated with the presence of aortic calcifications. Between January 2000 and May 2004, all consecutive postmenopausal women evaluated during one office visit for osteoporosis were included in the study. The data collected included a comprehensive history of previous fractures, lifestyle habits (smoking habits, daily consumption of calcium), CV risk factors (diabetes mellitus, hypertension or hypercholesterolaemia) and medical therapy (hormonal replacement therapy, bisphosphonates, raloxifene, calcium, vitamin D). All patients underwent a detailed medical examination, conducted at least 6 months after fractures. Standardized measurements of the BMD were performed using dual energy X-ray absorptiometry (DEXA) with a DPX-MD + scanner (Lunar Company, Lambesc, France). BMD was analysed at the femoral site, because of known pitfalls with the measure of lumbar BMD in the presence of aortic calcifications. The presence or absence of abdominal aortic calcification was assessed by one single reader from lateral lumbar spine radiographs. Osteoprotegerin was measured with enzymelinked immunosorbent assay (ELISA) kits (Nordic Bioscience, 2730 Herlev, Denmark) in 79 randomly selected patients. Differences between groups were tested with chi-square tests for categorical variables and t-tests or rank sum tests for continuous variables. Logistic regression was used to examine the association between abdominal aortic calcifications and fractures or low BMD. A total of 327 consecutive women (mean age 64 years) were enrolled. Amongst them, 59% had a history of fractures (wrist Journal of Internal Medicine 2005; 257: 117–119
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