Influence of Helicobacter pylori infection on hormonal and metabolic indicators and chronic inflammation markers in women with polycystic ovary syndrome
Background. The purpose of this study was to evaluate the impact of Helicobacter pylori (H.pylori) infection on hormonal and metabolic parameters, markers of chronic inflammation in patients with polycystic ovary syndrome (PCOS). Materials and methods. Sixty patients with PCOS (26.4 ± 0.2 years) and 40 healthy women of corresponding age were examined. We have investigated blood lipid spectrum, parameters of carbohydrate metabolism, levels of total testosterone, estradiol, sex hormone-binding globulin, C-reactive protein, interleukin-6, IgG antibodies to H.pylori, homocysteine. Evaluation of these indicators was performed depending on the presence or absence of H.pylori infection. Results. It was found that in the control group, elevated levels of IgG antibodies to H.pylori were detected in 17.5 % of women, and they had a decrease in the concentration of sex hormone-binding globulin and an increase in the level of C-reactive protein and homocysteine. Among patients with PCOS, H.pylori infection was significantly more common (χ2 = 7.7; p < 0.01), and its presence exacerbated existing dyslipidemia, insulin resistance, hyperandrogenemia by increasing the levels of total testosterone and decreasing the content of sex hormone-binding globulin, it was accompanied by the formation of hyperhomocysteinemia and a significant increase in inflammatory markers. It was found that in patients with PCOS, increased concentration of C-reactive protein in the blood serum was associated with insulin resistance and dyslipidemia, and increased levels of interleukin-6 - with the severity of insulin resistance and hyperandrogenemia. Conclusions. The results indicate a strong relationship between PCOS and H.pylori infection, which enhances the existing metabolic and hormonal disorders characteristic of PCOS, leads to an increase in C-reactive protein and interleukin-6 levels. However, it cannot be said that this infection is a new pathogenic factor for the formation of PCOS.