No association between dehydroepiandrosterone sulfate and development of atherosclerosis in a prospective population study (Bruneck Study)

被引:60
作者
Kiechl, S
Willeit, J
Bonora, E
Schwarz, S
Xu, QB
机构
[1] Univ Innsbruck, Dept Neurol, A-6020 Innsbruck, Austria
[2] Univ Innsbruck, Inst Gen & Expt Pathol, A-6020 Innsbruck, Austria
[3] Univ Verona, Div Endocrinol & Metab, I-37100 Verona, Italy
[4] Austrian Acad Sci, Inst Biomed Aging Res, Innsbruck, Austria
关键词
dehydroepiandrosterone; atherosclerosis; aging; insulin resistance; risk factors;
D O I
10.1161/01.ATV.20.4.1094
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Antiatherogenic properties of dehydroepiandrosterone (DHEA) have been postulated For >40 years. Large-scale epidemiological studies on this important issue, however, are still sparse, and those available have yielded contradictory results. The Bruneck Study involved a large random sample of men and women aged 40 to 79 years that were enrolled in 1990 and reevaluated 5 years later. Baseline DHEA sulfate (DHEAS) levels were measured in 867 subjects after an overnight fast. Development and progression of carotid atherosclerosis was monitored by high-resolution duplex ultrasound. DHEAS levels declined with advancing age (29% and 44% per decade in men and women) and showed a complex sex-specific association with various vascular risk attributes and factors conferring protection against atherosclerosis, Age- anti sex-adjusted DHEAS baseline levels did not differ between subjects with or without incident/progressive atherosclerosis (geometric mean 1161 versus 1253 mu g/L), After adjustment for vascular risk factors and potential confounders, the odds ratio of incident/progressive atherosclerosis comparing a 50% increase in DHEAS levels was 0.99 (95% CI 0.89 to 1.11). Lack of an association between DHEAS and atherogenesis was confirmed in sex-specific and a variety of supplementary analyses. Statistical power would be high enough to detect differences in DHEAS between outcome categories as low as 15% (alpha=0.05). This prospective community-based study does not support a role for endogenous DHEA(S) in the development of human atherosclerosis.
引用
收藏
页码:1094 / 1100
页数:7
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