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This study was performed to evaluate the systemic oxidative stress balance in women with either ovarian or deep infiltrating endometriosis (DIE) and any alterations of the same during hormone therapy. Free oxygen radicals (FORT) and free oxidant radical defense (FORD) were measured in the capillary blood of 24 women without endometriosis, 26 women with endometrioma, and 26 women with DIE with or without endometrioma. Endometriosis was diagnosed by clinical and ultrasound assessment. Dietary factors, lifestyle habits, and intake of any substances interfering with the oxidative status were recorded. Women were prescribed contraceptive hormones, and the baseline assessments were repeated at the 3rd month of use, revealing a higher oxidative stress balance (FORT/FORD) in women with endometriosis than in controls (4.75 ± 4.4 vs. 2.79 ± 2.2; p = 0.05). The highest values were found in women with DIE (5.34 ± 4.6; p = 0.028 vs. controls). Regression analysis revealed an independent link between FORT/FORD and endometrioma (b 2.874, 95% CI 0.345, 5.403; p = 0.027) and DIE (b 4.419, 95% CI 1.775, 7.064; p = 0.001) but a negative correlation with HDL-cholesterol (b −0.063, 95% CI −0.125, −0.002; p = 0.043). In controls, the hormone therapy increased FORT (p = 0.003), but also FORD (p = 0.012), with the FORT/FORD balance remaining stable (2.72 ± 2.2 vs. 2.73 ± 1.8; p = 0.810). In women with endometriosis, FORT remained unchanged, but FORD increased (p = 0.004), and the FORT/FORD ratio significantly decreased (4.75 ± 4.4 vs. 2.57 ± 1.76; p = 0.002) to values similar to the control levels. These data indicate that systemic oxidative stress balance increased in women with endometriosis, particularly in those with DIE. The hormonal therapy did not change the oxidative stress balance in control women but significantly improved it in women with endometriosis, particularly those suffering from DIE.

Pregnancy can be considered as an allogeneic transplant and preeclampsia can be seen as a failure of the acceptance mechanisms of this transplant as occurs in acute organ transplant rejection. Some genetic polymorphisms may be involved in its pathogenesis. Since the kidney is one of the organs mainly involved in preeclampsia, our study attempted to determine the frequencies of single nucleotide polymorphisms of DNA (SNP) in 3 genes (adenosine triphosphate-binding cassette sub-family B member 1 (ABCB1)/multi drug reactivity 1 (MDR1) gene, interleukin 10 gene and tumor necrosis factor α gene) which are targets of immunosuppressive therapies and related to acute renal rejection. The study was an observational, monocentric, case-control study. We enrolled 20 women with severe preeclampsia and 10 women age-matched with regular pregnancy. Continuous variables were compared by the Student’s t- test for independent variables or using the Mann-Whitney test depending on their distribution. We used Fisher test to compare categorical variables between cases and controls, while we used logistic regression model to evaluate which risk factor was associated with preeclampsia. Although there was no statistically significant difference between the two groups, we found different percentages of two of the polymorphisms considered (rs1045642 and rs2032582 in the gene ABCB1). Despite these results, our work may be helpful for future research to better understand the pathogenesis of preeclampsia.

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