Inflammatory and endothelial markers in women with polycystic ovary syndrome

Abstract

Background Women with polycystic ovary syndrome (PCOS) carry a pattern of cardiovascular risk factors. Endothelial dysfunction and chronic inflammation are early findings in the atherosclerotic process. The purpose of the study was to investigate the coexistence of active inflammation markers and endothelial dysfunction in young women with PCOS, and their relationship with metabolic and hormonal abnormalities of the syndrome. Materials and methods Twenty‐five young women with PCOS and 25 controls of similar age and body mass index (BMI) were studied. Endothelial function was assessed by flow‐mediated dilatation (FMD) on the brachial artery and smooth muscle cells injury was excluded by nitrate‐induced dilatation (NID). Plasma levels of endothelin‐1 (ET‐1), soluble intercellular adhesion molecule‐1 (sICAM‐1), soluble vascular cell adhesion molecule‐1 (sVCAM‐1) and high sensitivity C‐reactive protein (hsCRP) were measured. Hormonal and metabolic profiles were determined in both groups. Results Flow‐mediated dilatation (FMD) was statistically lower in PCOS (P < 0·001), whereas nitrate‐induced dilatation (NID) was similar within the two groups. Polycystic ovary syndrome (PCOS) had statistically higher levels of ET‐1 (P = 0·03), sICAM‐1 (P = 0·01), sVCAM‐1 (P = 0·02) and hsCRP (P = 0·01). Furthermore FMD was statistically higher in PCOS population with hsCRP 1 mg L−1 when compared with PCOS population with hsCRP > 1 mg L−1 (P = 0·02). Flow‐mediated dilatation (FMD) was negatively related to hsCRP (r = −0·512, P = 0·015); ET‐1 was positively related to free androgen index (r = 0·27, P = 0·05) and negatively to sex hormone‐binding globulin (r = −0·465, P = 0·022); sVCAM‐1 was positively related to total testosterone (r = 0·431, P = 0·036); hsCRP was positively related to BMI (r = 0·647, P = 0·001), and negatively related to FMD (r = −0·512, P = 0·015), quantitative insulin sensitivity check index (QUICKI) (r = −0·499, P = 0·018), and MATSUDA index (r = −0·445, P = 0·038). Conclusions The present study demonstrates that endothelial dysfunction coexists and is influenced by the presence of increased serum levels of inflammation and endothelial activation markers in young women with PCOS. These parameters appear to be interrelated with hyperandrogenaemia in this insulin‐resistant population.

The polycystic ovary syndrome (pcos) status and cardiovascular risk in young women

“…Consistent with our results, most of the studies, but not all [8,12], demonstrated impaired endothelial function in PCOS using either noninvasive endothelium-dependent (FMD) and-independent (glyceroltrinitrate, GTN) changes in the brachial artery or invasive methodology [4,6,10,11,24] compared with the controls. Among several circulating endothelium-derived vasoactive molecules, ET-1 is considered one of the best indices of abnormal vascular reactivity, playing an important role in the early events of endothelial dysfunction [4].…”

“…Among several circulating endothelium-derived vasoactive molecules, ET-1 is considered one of the best indices of abnormal vascular reactivity, playing an important role in the early events of endothelial dysfunction [4]. With regard to ET-1 levels, we confirm the other authors' results on increased levels of ET-1 in PCOS women [3,4,9,10]. Furthermore, impaired vascular reactivity and increased level of ET-1 were linked to markers of hyperandrogenism (TT, FAI).…”

“…The relationship with hyperandrogenemia is especially controversial, since the effect of the androgens was described as either adverse [10,25], neutral [24,26], or even protective in patients with PCOS [27]. However, the reports are more constant with regard to ET-1 and the deleterious effect that markers of hyperandrogenemia have on it [3,9,10]. The mechanisms by which hyperandrogenemia might affect endothelial function are complex and controversial.…”

“…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].…”

Arteriolar insulin resistance in a rat model of polycystic ovary syndrome

“…Human experiments have shown microvascular dysfunction in PCOS, as indicated by the inhibition of Ach-dependent vasodilation (5). Endothelial dysfunction and damage has been shown to be enhanced by increased inflammatory and soluble activation markers (24). Paraoxonase-1 and flow-mediated dilation have been shown to be useful predictors of endothelial dysfunction (25).…”