Changes in ovarian function were evaluated in 43 women, before and after tubal ligation. Midluteal endocrine profiles and endometrial biopsies were investigated before and at 3, 6 and 12 months after the operations. During postoperative follow-up there was significant increase in luteal phase deficiency and midluteal FSH, LH and E2 levels (p < 0.001). Progesterone levels significantly decreased (p < 0.001) and anovulation was observed in 13 (30.2%) of 43 cases. Our data suggest that tubal sterilization carried increased risk in ovarian function, particularly luteal phase deficiency and anovulation.
We concluded that the elevated plasma levels of leptin and testosterone could contribute to the endothelial dysfunction involved in the pathogenesis of preeclampsia, and that estradiol might lead to an increase in the plasma levels of leptin.
Background. To clarify the role of leptin and androgens in the pathogenesis of preeclampsia, we wanted to assess role of maternal leptin in women with severe and mild preeclampsia and the effects of sex steroid hormones on leptin production. Methods. The groups consisted of 40 healthy pregnant women (HPW) as well as 55 pregnant women with severe preeclampsia (SPE) and 41 pregnant women with mild preeclampsia (MPE). No significant differences were observed between the three groups regarding age, gestational age and body mass index (BMI). Plasma leptin, total testosterone (T), estradiol (E 2 ), dehydroepiandrosterone sulfate (DHEAS) and androstenedione (A) levels were measured. Statistical analysis was achieved with one-way analysis of variance (ANOVA) followed by post hoc multiple comparisons with the Tukey honestly significant difference (HSD) test by using SPSS for Windows statistical computer program, and the Pearson's coefficient of correlation was calculated. Results. The plasma level of leptin was significantly increased in the SPE and MPE groups (p < 0.001), whereas the plasma level of T was significantly increased only in the SPE group (p < 0.001). However, there was no significant difference in plasma levels of DHEAS among the three groups (p < 0.05). The plasma level of A was significantly decreased in the MPE group (p < 0.05). There was no significant difference in the plasma level of E 2 in the MPE and SPE groups (p < 0.05). There was a significant positive correlation between the plasma levels of leptin and E 2 in the MPE group (r ¼ 0.41, p < 0.001). Conclusion. We concluded that the elevated plasma levels of leptin and testosterone could contribute to the endothelial dysfunction involved in the pathogenesis of preeclampsia, and that estradiol might lead to an increase in the plasma levels of leptin.
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