Endocrine Abstracts

PCOS, the commonest endocrinopathy among reproductive-aged women, lies to the core of intensive research due to the multiplicity of its pathophysiologic and clinical aspects. Among the most intensively investigated fields,the clustering of metabolic abnormalities and cardiovascular risk factors in PCOS has been widely acknowledged. Functional, biochemical and morphological markers of subclinical cardiovascular disease have been explored in PCOS women. On balance the weight of evidence does not unveil clinically pronounced abnormalities, but points to the accelerated onset of vascular structural and functional lesions of in PCOS women. There is a growing body of literature identifying traditional vascular risk factors, mainly central adiposity, dyslipidemia, glucose intolerance, and diabetes in women with PCOS. Taken into account that these abnormalities are encountered as early as the second decade of life in patients with PCOS, these subjects represent significantly higher risk to develop cardiovascular incidents, in comparison to their age and BMI matched peers. Added to the detrimental metabolic profile, PCOS is characterized by low-grade systemic inflammation, as indicated by elevated serum levels of C-reactive protein and inflammatory cytokines (i.e. IL-6 and IL-18), increased leucocyte count, increased levels of Advanced Glycation End Products and amplified oxidative stress. Increased serum levels of the adhesion molecules sVCAM-1 and sE-selectin in women with PCOS reflect low-grade chronic inflammation of the endothelium. Increased levels of endothelin-1 and decreased flow-mediated dilatation,as determined by ultrasonography in conduit arteries, both indicate abnormal vascular tone, involved in the course of atherosclerosis. Morphological studies, in women with PCOS compared with matched controls, have been indicated by increased carotid wall thickness on B-mode ultrasonography and increased scores of coronary/aortic calcification on electron beam computed tomography. However, reflective of the pathophysiologic and clinical heterogeneity of PCOS, metabolic disturbances and vascular dysfunction are not universal findings in women with the syndrome.

Most importantly, risk factors and surrogate markers of subclinical cardiovascular disease have not been proved by epidemiological,mainly retrospective, studies to be translated into overt clinical disease or events. Prospective studies are required to address the end point of the cardiovascular events in this high-risk population. The course of cardiovascular abnormalities which starts from vascular risk factors and proceeds to subclinical disease, awaits further exploration in PCOS.