2006
DOI: 10.1097/01.ogx.0000206323.83912.31
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Predictors of Endothelial Dysfunction in Young Women With Polycystic Ovary Syndrome

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Cited by 52 publications
(91 citation statements)
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“…Therefore, we might speculate that some genetic abnormalities, such as polymorphisms in AR or other yet unidentified genetic abnormalities aggravated by the higher levels of androgens found in PCOS subjects, may be responsible for impaired endothelial function observed in our test group in comparison with our control group. Several lines of evidence, but not all [8,10,12,27,33], revealed an association between insulin resistance and endothelial dysfunction markers in PCOS women [4,7,9,11,34]. We observed however, significant correlations of FMD with insulin concentrations and HOMA-IR, but only in the entire population studied.…”
Section: Discussioncontrasting
confidence: 70%
See 1 more Smart Citation
“…Therefore, we might speculate that some genetic abnormalities, such as polymorphisms in AR or other yet unidentified genetic abnormalities aggravated by the higher levels of androgens found in PCOS subjects, may be responsible for impaired endothelial function observed in our test group in comparison with our control group. Several lines of evidence, but not all [8,10,12,27,33], revealed an association between insulin resistance and endothelial dysfunction markers in PCOS women [4,7,9,11,34]. We observed however, significant correlations of FMD with insulin concentrations and HOMA-IR, but only in the entire population studied.…”
Section: Discussioncontrasting
confidence: 70%
“…Up to the present, the results on this topic have been controversial as far as the presence of arterial structural and functional alterations or of chronic inflammation in PCOS are concerned. For example, there are reports which have demonstrated that PCOS is associated with endothelial dysfunction or increased CIMT even from a young age, while other reports have stated the contrary [3][4][5][6][7][8][9][10][11][12][13][14][15][16]. Additionally, there are authors who consider PCOS as a pro-inflammatory state due to elevated plasma concentrations of inflammatory mediators of atherogenesis, such as interleukin (IL)-6, IL-18, soluble intercellular adhesion molecule-1 (sICAM-1), sEselectin, high sensitivity C-reactive protein (hsCRP), tumoral necrosis factor-alpha (TNF-α), monocyte chemotactic protein-1 (MCP-1), and plasminogen activator inhibitor-1 (PAI-1) [17][18][19].…”
Section: Introductionmentioning
confidence: 98%
“…This theory is supported by studies showing impaired endothelial function in postmenopausal women with low testosterone levels 110 and increased carotid atherosclerosis and endothelial dysfunction in polycystic ovary syndrome women with supraphysiological testosterone levels. 111,112 Results from experimental studies show a similar pattern. Bruck et al 113 showed an increase in plaque size after testosterone treatment in female rabbits on an atherogenic diet.…”
Section: Atherosclerosismentioning
confidence: 63%
“…Other studies demonstrated increased pulse wave velocity of the brachial artery and increased stiffness of both internal and external carotid arteries (22,23). Alterations in both endothelium-dependent and independent vasodilator responses of the brachial artery in women with PCOS have been also reported (24)(25)(26)(27)(28). Further, morphological studies have shown that women with PCOS have increased carotid intima media thickness as well as higher incidence of coronary and aortic arterial calcification (29)(30)(31)(32).…”
Section: Markers Of Cardiovascular Risk In Pcosmentioning
confidence: 98%