Stymulacja owulacji

Brak owulacji dotyczy około 15–25% kobiet z rozpoznaną niepłodnością. Stymulacja owulacji jest metodą leczeniazaburzeń owulacji i polega na pobudzeniu rozwoju pęcherzyka jajnikowego. Postępowanie to jest zarezerwowanedla kobiet z brakiem owulacji. Prawidłowo przeprowadzone leczenie daje dobre rezultaty. W ostatnich latachwprowadzono nowe metody leczenia zaburzeń owulacji. Cytrynian klomifenu pozostaje nadal lekiem pierwszegowyboru, ale wyniki aktualnych badań zdecydowanie przemawiają za zastąpieniem tego preparatu letrozolem.Metformina stosowana w monoterapii ma ograniczoną skuteczność, jednak w niektórych sytuacjach może miećzastosowanie jako lek zwiększający insulinowrażliwość. Gonadotropiny w tzw. protokole step-up pozostają lekamidrugiego wyboru.Zgodnie z aktualnymi badaniami stymulacja owulacji jest bezpieczną i skuteczną metodą leczenia niepłodnościspowodowanej brakiem owulacji

Perinatal and neonatal outcome in patients with preeclampsia

Objectives: Preeclampsia (PE) affects 2–5% of pregnant women. Hypertensive disorders of pregnancy are associated with adverse maternal and perinatal outcomes. Material and methods: This study included 88 women showing gestational hypertension (GH) or PE symptoms, and their newborns. Results: The rate of FGR was 43% for mothers with PE, compared to 8% with GH. The association was significant, p = < 0.001 but with moderate strength, Cramer’s V = 0.40. The risk of FGR increased nine times when PE occurred, as the odds ratio was 9.25 (CI: 2.46–34.83), p = 0.001. PE was associated with FGR risk if delivery time was less than 34 weeks compared to a delivery time of more than 34 weeks. This was 82% of FGR cases for < 34 weeks, compared with 35% of cases in > 34 group, (p = 0.001; Cramer’s V = 0.50). PE was also associated (p = 0.01, Cramer’s V = 0.27) with the type of delivery, as the caesarean section rate was 74%, compared to 50% in the GH group. This made it three times higher the likelihood of delivery by caesarean section, as the odds ratio was 3.10 (CI: 1.24–7.75), p=0,02. Delivery time was significantly (p < 0.001) shortened to 38 weeks (27–41), compared to 40 weeks (38–42) GH mothers. There was no distinction in median age for PE and GH mothers (p = 0.124). The overall clinical status of neonates was proportional despite the mother’s PE. The sum of Apgar points in the first, and then the second to third minute, did not differ significantly, p = 0.370 and 0.560, respectively. The number of peripheral blood platelets and leucocytes was not reduced (p = 0.821 and 0.534) in infants when the mother suffered from PE. Conclusions: The prediction of adverse maternal outcomes from hypertensive diseases of pregnancy is key to optimal management, including the timing of delivery and planning for the most appropriate place of care.

Cytokine Imprint in Preeclampsia

The hallmark of preeclampsia (PE) is a shift toward persistent inflammatory response, accompanied by endothelial dysfunction. The driving forces in PE are proinflammatory cytokine and growth factors, in parallel with reduced functionality of anti-inflammatory effectors, like regulatory T cells are observed. Unfortunately, no conclusive mechanism underlying preeclampsia has been identified. For this reason, research on preeclampsia is needed to provide a state of the art understanding of the pathophysiology, identification of new diagnostics tools and the development of targeted therapies. The 68 patients were divided into three groups: gestational hypertension (GH) group (n = 19) and PE group (n = 28) and a control group (n = 21). We have tested a set of 53 cytokines, chemokines and growth factors in preeclampsia and gestational hypertension, and then compared them with normal pregnancies. Using a diagnostic test assessment characteristic parameters (IL-22, MDC/CCL22, IL-2/IL-4 ratio) have been identified and cut-off values have been proposed to diagnose preeclampsia. All parameters had high negative or positive predictive values, above 80%. In conclusion, we have proposed a potential set of immune parameters to diagnose preeclampsia

Environmental exposure to non-persistent endocrine disrupting chemicals and semen quality: An overview of the current epidemiological evidence

Some of the recent publications have reported a decline in semen quality in the last few decades. This phenomenon is associated with environmental factors, particularly with exposure to endocrine disrupting chemicals (EDCs). The aim of this publication is to critically review the literature on exposure to the following 6 ubiquitous environmental non-persistent EDCs: bisphenol A, triclosan, parabens, synthetic pyrethroids, organophosphate pesticides and phthalates, and on their influence on semen quality measured as sperm concentration, sperm volume, total sperm count, motility, total motile count, morphology, sperm motion, sperm DNA damage (comet extent, tail length, tail distributed moment, percent of DNA located in the tail (tail%), DNA fragmentation index, high DNA stainability, X:Y ratio and aneuploidy. Several electronic databases were systematically searched until 31 August 2016. Studies were qualified for the review if they: linked environmental exposure to non-persistent EDCs to semen quality outcomes, were published in English after 2006 (and, in the case of phthalates, if they were published after 2009) and were conducted in the case of humans. Out of the 970 references, 45 articles were included in the review. This review adds to the body of evidence that exposure to non-persistent EDCs may affect semen quality parameters and decrease semen quality. Int J Occup Med Environ Health 2018;31(4):377–41

High maternal-fetal HLA eplet compatibility is associated with severe manifestation of preeclampsia

IntroductionPreeclampsia is responsible for more than 70 000 and 500 000 maternal and fetal deaths, respectively each year. Incomplete remodelling of the spiral arteries in placenta is the most accepted theory of preeclampsia pathogenesis. However, the process is complexed with immunological background, as pregnancy resembles allograft transplantation. Fetus expresses human leukocyte antigens (HLA) inherited from both parents, thus is semiallogeneic to the maternal immune system. Therefore, induction of fetal tolerance is crucial for physiological outcome of pregnancy. Noteworthy, the immunogenicity of discordant HLA antigens is determined by functional epitopes called eplets, which are continuous and discontinuous short sequences of amino acids. This way various HLA molecules may express the same eplet and some HLA incompatibilities can be more immunogenic due to different eplet combination. Therefore, we hypothesized that maternal- fetal HLA incompatibility may be involved in the pathogenesis of gestational hypertension and its progression to preeclampsia. We also aimed to test if particular maternal-fetal eplet mismatches are more prone for induction of anti- fetal HLA antibodies in gestational hypertension and preeclampsia.MethodsHigh resolution next-generation sequencing of HLA-A, -B, -C, -DQB1 and -DRB1 antigens was performed in mothers and children from physiological pregnancies (12 pairs) and from pregnancies complicated with gestational hypertension (22 pairs) and preeclampsia (27 pairs). In the next step HLA eplet identification and analysis of HLA eplet incompatibilities was performed with in silico approach HLAMatchmaker algorithm. Simultaneously maternal sera were screened for anti-fetal HLA class I, class II and anti-MICA antibodies with Luminex, and data were analyzed with HLA-Fusion software.ResultsWe observed that high HLA-C, -B, and DQB1 maternal-fetal eplet compatibility was associated with severe preeclampsia (PE) manifestation. Both quantity and quality of HLA epletmismatches affected the severity of PE. Mismatches in HLA-B eplets: 65QIA+76ESN, 70IAO, 180E, HLA-C eplets: 193PL3, 267QE, and HLA-DRB1 eplet: 16Y were associated with a mild outcome of preeclampsia if the complication occurred.ConclusionsHigh HLA-C, HLA-DQB1 and HLA-B eplet compatibility between mother and child is associated with severe manifestation of preeclampsia. Both quantity and quality of maternal-fetal HLA eplet mismatches affects severity of preeclampsia