Ovarian reserve in women with a previous history of severe pre-eclampsia.

PURPOSE: Severe pre-eclampsia affects maternal health with long-term consequences. It is postulated that during the process of implantation and cell differentiation, embryos resulting from the fertilization of ageing oocytes produce malfunctioning trophoectoderm leading to placental dysfunction. Therefore, severe pre-eclampsia may be associated with a decreased ovarian reserve. The objective of this study was to compare serum markers of ovarian reserve and function between women who had severe pre-eclampsia and those who had normal pregnancies. METHODS: Twenty women who had severe pre-eclampsia (PE) and 20 who had uncomplicated pregnancies (controls) matched for age and body mass index were included in the study. Fasting blood samples were taken during the follicular phase (day 5) of the menstrual cycle 6 months to 5 years after the delivery. Serum was separated and frozen at -70 °C until analyzed for anti-Mϋllerian hormone (AMH), total and free testosterone (TT), free-androgen index (FAI), luteinizing hormone (LH), and follicle-stimulating hormone (FSH) hormone to evaluate ovarian reserve and function, and the results were compared between two groups. RESULTS: The median AMH was 0.91 ng/mL in PE group compared to 0.72 ng/mL in controls (p = 0.995). No significant differences were found between the two groups in the levels of LH (5.65 vs. 5.4 IU/L, respectively, p = 0.897) and FSH (4.95 vs. 5.1 IU/L, respectively, p = 0.523). However, total and free-TT levels as well as FAI were significantly lower in the PE group compared to controls (p = 0.017, p = 0.006, and p = 0.011, respectively). CONCLUSIONS: Ovarian reserve and function are not altered significantly in women with a previous history of pre-eclampsia compared with women who had an uncomplicated pregnancy.

PP079. Ovarian reserve and function is preserved following severe preeclampsia.

INTRODUCTION: Preeclampsia is a multi-organ disorder that predominantly affects renal, cardiovascular, and endocrine systems with long-term consequences for the women's health. As advanced age and history of subfertility increase the risk of developing preeclampsia, reduced ovarian reserve may be associated with preeclampsia. However, long-term effect of preeclampsia on the ovarian function and reserve is not known. We hypothesized that the ovarian reserve and function are reduced in women with a previous history of severe preeclampsia. OBJECTIVE: To compare the plasma levels of markers of ovarian function (FSH, LH, SHBG, testosterone) and reserve (anti-Müllerian hormone, AMH) in women who previously had preeclampsia with their matched controls. METHOD: Twenty women who had severe preeclampsia (PE group) requiring delivery before 36 weeks of gestation and 20 controls were matched for age, parity, height and weight were included in the study. Women were not breast-feeding, they were having regular menstrual periods and were not using any hormonal contraception. Fasting blood samples were taken during the follicular phase. Plasma was separated and frozen at -70 degrees until analyzed. Comparison between groups was performed using paired sample t-test for parametric and Wilcoxon T-test for nonparametric data. A two-tailed p-value <0.05 was considered significant. RESULTS: The mean age was 36.4 years, height 164cm and weight 72kg in PE group, compared to 37.0 years, 165cm and 69kg, respectively in control group. The mean AMH was 1.34ng/mL in PE group compared to 1.55ng/mL in controls (p=NS). No significant differences were found in the levels of LH (6.72 versus 6.53 IU/L), FSH (5.27 versus 7.16 IU/L), LH/FSH ratio (1.39 versus 1.11), SHBG (63.65 versus 52.90 versus 52.90nmol/L), and testosterone (0.72 versus 1.01nmol/L) between groups. CONCLUSION: Ovarian reserve and function is not altered significantly in women with a previous history of preeclampsia.

A screening and intervention program aimed to reduce mortality and serious morbidity associated with severe neonatal alloimmune thrombocytopenia.

The study's objective was to identify HPA 1a-negative women and to offer them an intervention program aimed to reduce morbidity and mortality of neonatal alloimmune thrombocytopenia (NAIT). HPA 1 typing was performed in 100 448 pregnant women. The HPA 1a-negative women were screened for anti-HPA 1a. In immunized women, delivery was performed by Cesarean section 2 to 4 weeks prior to term, with platelets from HPA 1a-negative donors reserved for immediate transfusion if petechiae were present and/or if platelet count was less than 35 x 10(9)/L. Of the women screened, 2.1% were HPA 1a negative, and anti-HPA 1a was detected in 10.6% of these. One hundred seventy pregnancies were managed according to the intervention program, resulting in 161 HPA 1a-positive children. Of these, 55 had severe thrombocytopenia (< 50 x 10(9)/L), including 2 with intracranial hemorrhage (ICH). One woman with a twin pregnancy missed the follow-up and had one stillborn and one severely thrombocytopenic live child. In 15 previous prospective studies (136 814 women) there were 51 cases of severe NAIT (3 intrauterine deaths and 7 with ICH). Acknowledging the limitation of comparing with historic controls, implementation of our screening and intervention program seemed to reduce the number of cases of severe NAIT-related complications from 10 of 51 to 3 of 57.