Pentraxin 3 as a marker of endothelial dysfunction in young women with polycystic ovary syndrome (PCOS).

One of the consequences of polycystic ovary syndrome (PCOS) is an increased risk of early development of cardiovascular diseases. Pentraxin-3 (PTX-3) is a new potential marker of endothelial dysfunction. The aim of the study was to assess PTX3 and other markers of endothelial dysfunction in PCOS women. The study enrolled 99 stable body mass PCOS women (17 normal weight, 21 overweight and 61 obese). Anthropometric measurements and serum/plasma levels of glucose, insulin, lipids, estradiol, testosterone, sex hormone binding globulin, 17-OH progesterone, free androgen index, pentraxin-3 (PTX3), soluble intercellular (sICAM-1) and vascular cell adhesion molecule 1 (sVCAM-1), endothelin-1 and total nitric oxide metabolites (tNO) concentrations were assessed. Groups were divided into tercile-subgroups according to PTX3 serum levels. Serum PTX3 tercile-subgroups significantly differed in respect to tNO, endothelin-1 and sVCAM-1, but not sICAM-1. The levels of tNO, endothelin-1 and sVCAM-1 were significantly decreased in the subgroup with the lowest PTX3 levels compared to both middle (tNO and endothelin 1) and upper tercile subgroups (all of them). There were significant positive correlations between log10(PTX3) and log10(tNO) (r = 0.34, p < .001), log10(endothelin-1) (r = 0.41, p < .001) as well as sVCAM-1 levels (r = 0.22, p < .05). Circulating PTX-3 levels seem to be a marker of endothelial dysfunction in PCOS women.

Pentraxin 3 Levels in Young Women with and without Polycystic Ovary Syndrome (PCOS) in relation to the Nutritional Status and Systemic Inflammation.

OBJECTIVE: The aim of the study was to assess PTX3 levels in PCOS and non-PCOS women in relation to nutritional status and circulating markers of inflammation. METHODS: The study enrolled 99 stable body mass PCOS women (17 normal weight, 21 overweight, and 61 obese) and 61 non-PCOS women (24 normal weight, 19 overweight, and 18 obese). Body composition was assessed by bioimpedance, and plasma levels of pentraxin 3 (PTX3), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and monocyte chemoattractant protein 1 (MCP-1) were measured. Homeostatic model assessment of insulin resistance (HOMA-IR) was made. RESULTS: Plasma PTX3, TNF-α, and IL-6 levels and HOMA-IR were higher in PCOS than in non-PCOS group (p < 0.001). There were positive correlations between log10 (PTX3) and log10 (BMI), waist circumference and fat percentage, as well as log10 (HOMA-IR) and free androgen index but negative between log10 (estradiol) levels in PCOS. While in the non-PCOS group, the correlations between log10 (PTX3) and log10 (BMI), waist circumference and fat percentage, as well as log10 (HOMA-IR) were negative. The positive correlations between PTX3 and MPC-1 and log10 (IL-6) were shown in the PCOS group only. In multivariate regression analyses, variability in PTX3 levels in the PCOS group was proportional to log10 (BMI), waist circumference, and fat percentage, but inversely proportional to log10 (estradiol) levels. While in the non-PCOS group, PTX3 levels were inversely proportional to all anthropometric parameters. CONCLUSIONS: Our results show that the decrease in PTX3 levels observed in obese is distorted in PCOS by microinflammation, and possibly, dysfunction of stroma adipose tissue and liver steatosis is reflected by enhanced insulin resistance.