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The increasing prevalence of morbid obesity in Germany is associated with an increasing number of metabolic surgical interventions. Short-term surgical and long-term metabolic complications - such as nutrient deficiencies - are the main risks of metabolic surgery and the resulting malabsorption. Obesity, especially morbid obesity, is associated with a high incidence of female infertility. One important cause of female infertility in obese women is the polycystic ovary syndrome, with 6 - 10%. Metabolic surgery significantly increases the fertility of obese women. The positive effect of obesity surgery on weight loss, remission of comorbidities, psychological outcome and fertility (in comparison with the effect of conservative treatment) has led to an increase in the number of metabolic operations. Nutrient deficiencies after restrictive, combined and malabsorptive procedures must be considered. Prophylaxis of these deficiencies during pregnancy after obesity surgery must be based on intensive interdisciplinary treatment. The aim of this overview is to characterise the metabolic complications and their prophylaxis, which are specific for the various bariatric procedures and which, subsequently, require temporary or permanent surveillance and supplementation.Die zunehmende Prävalenz der morbiden Adipositas geht auch in Deutschland mit einer deutlichen Zunahme von adipositas- und metabolisch-chirurgischen Eingriffen einher. Die Adipositas ist häufig mit Fertilitätsstörungen assoziiert. Mit einer Häufigkeit von 6 – 10% stellt das polyzystische Ovarsyndrom (PCOS) eine häufige Ursache der Infertilität dar. Die damit assoziierten metabolischen und kardiovaskulären Folgen bedeuten ein erhebliches Gesundheitsproblem. Metabolisch-chirurgische Eingriffe können die Fertilität dieser Frauen deutlich verbessern. Aufgrund der Effektivität der metabolischen Chirurgie hinsichtlich der Gewichtsreduktion, der Rückbildung der Komorbiditäten sowie der Lebensqualität und der Fertilität im Vergleich mit konservativen Verfahren hat die Bedeutung der Adipositaschirurgie erheblich zugenommen. Metabolische Defizite können Folge diverser restriktiver, kombinierter und malabsorptiver Operationsmethoden sein. Ihre Prophylaxe bei Schwangerschaft nach bariatrischer Operation erfordert eine intensive und interdisziplinäre Versorgung der Schwangeren. Ziel der vorliegenden Arbeit ist es, die Problematik der nutritiven Mangelzustände und deren Prophylaxe in Zusammenhang mit einer Gravidität darzustellen.

Ein Diabetes in der Schwangerschaft liegt vor, wenn eine an Diabetes erkrankte Patientin schwanger wird oder wenn in der Schwangerschaft eine Glukosetoleranzstorung entsteht. Im zweiten Trimenon kommt es unter dem Einfluss plazentar gebildeter Hormone zur Ausbildung einer ausgepragten Insulinresistenz. Gleichzeitig stimuliert plazentares Laktogen eine Vermehrung der Betazellkapazitat im maternalen Pankreas mit gesteigerter Insulinproduktion. Plazentagrose und -funktion beeinflussen die Stoffwechselumstellung. Besteht bei der Mutter eine latente Insulinresistenz oder eine eingeschrankte Kapazitat zur Steigerung der Insulinsekretion, entsteht ein Gestationsdiabetes. Plazenten von Diabetikerinnen zeigen bei allen Krankheitsformen strukturelle Veranderungen. Haufig sind diese Plazenten voluminoser und zeigen Veranderungen in der Zottenvaskularisation und -reife. Eine fur Diabetes typische Morphologie ist nicht beschrieben. Ein Zusammenhang zur Stoffwechselkontrolle und zum Zeitpunkt der einsetzenden Hyperglykamie im Verlauf der Schwangerschaft wird vermutet, muss aber in systematischen Untersuchungen bestatigt werden.

Introduction Human maternal placentophagy, the behavior of ingesting the own raw or processed placenta postpartum, is a growing trend by women of western societies. This study aims to identify the impact of dehydration and steaming on hormone and trace element concentration as well as microbial contamination of placental tissue. Methods A total of nine placentas have been processed: six were studied for hormone and trace element concentrations; eight were studied for microbial contamination. The concentrations of CRH, hPL, oxytocin and ACTH in samples of raw, steamed dehydrated and raw dehydrated placental tissue were detected using ELISA. A yeast bioassay was performed in order to detect estrogen equivalent (EEQ) and gestagen equivalent (PEQ) active substances. Elements (As, Cd, Fe, Pb, Se, Hg) were analyzed using ICP-MS. Isolated colonies from tissue and placenta swab samples were identified using Vitek MS. Results Following mean hormone concentrations were detected in raw placental tissue: CRH (177.88 ng/g), hPL (17.99 mg/g), oxytocin (85.10 pg/g), ACTH (2.07 ng/g), estrogen equivalent active substances (46.95 ng/g) and gestagen equivalent active substances (2.12 μg/g). All hormones were sensitive to processing with a significant concentration reduction through steaming and dehydration. Microorganisms mainly from the vaginal flora were detected on placenta swab samples and samples from raw, steamed, dehydrated and steamed dehydrated tissue and mostly disappeared after dehydration. According to regulations of the European Union the concentrations of potentially toxic elements (As, Cd, Hg, Pb) were below the toxicity threshold for foodstuffs. Conclusion The commonly used protocols for preparation of placenta for its individual oral ingestion reduce hormone concentrations and bacterial contamination.

Aim: In pregnancies complicated by impaired utero-placental perfusion, pentaeritrithyltetranitrate (PETN) has been shown to reduce the risk of severe fetal growth restriction (FGR) and perinatal death by 39%. The effect is most likely related to the vasodilatative influence of PETN. To assess its impact on utero-placental and fetal perfusion, we analyzed the Doppler parameters measured during the PETN pilot-trial. Methods: One hundred and eleven pregnancies presenting impaired utero-placental resistance at mid-gestation were included in the trial. Fifty-four women received PETN, while 57 received a placebo. Doppler velocimetry measurements were monitored biweekly. Statistical analysis was performed using a mixed linear model. Results: Within the first week of treatment, the mean pulsatility index (PI) of the uterine artery (UtA) dropped more prominently in the PETN group [−0.20, 95% confidence interval (CI): −0.34 to −0.05, P=0.007). The adjusted relative risk (RR) for abnormal cerebro-placental ratio (CPR) was significantly reduced by PETN [RR 0.412 (95% CI: 0.181–0.941)]. Kaplan-Meier analysis demonstrates the postponement of absent end-diastolic flow (AED), absent or reverse end-diastolic flow (ARED), brain sparing and abnormal cerebroplacental ratio (CPR) in the PETN group. Conclusion: The demonstrated effect of PETN on utero-placental and feto-placental perfusion strengthens the evidence for a positive impact in pregnancies complicated by impaired placental perfusion and might explain the effect on neonatal outcome, as shown in the PETN-pilot trial.

Schistosomiasis is a widespread helminthic infection which sometimes may affect travelers to endemic areas. We report on a case of urogenital and placental schistosomiasis in a 28-year-old German woman who had been exposed to schistosomiasis in Lake Malawi one year earlier. She experienced painless macrohaematuria in her 21st week of pregnancy. Cystoscopy revealed vesical lesions typical for urogenital schistosomiasis. Histopathology confirmed ova of Schistosoma (S.) haematobium. The patient was treated with praziquantel 40 mg/kg/body weight/day for 3 days. After 285 days of gestation and 18 weeks post treatment, the patient delivered a healthy girl. Histopathology of placenta revealed eggs of S. haematobium in placental stroma. The infant proved negative for anti-Schistosoma spp. antibodies at the age of 15 months. This is the first report on placental schistosomiasis since 1980 and the first case occurring in a traveler.

The aim of this study was to evaluate possible associations of genetic polymorphisms predisposing to cardiovascular disease with the development and/or the severity of preeclampsia. A two hospital-based prospective case–control study was performed in Germany and Ghana. 470 blood samples of 250 Caucasian and 220 black African have been genotyped by pyrosequencing and fragment length analysis. We evaluated the distribution of the epoxide hydrolase 1 (EPHX1) polymorphism on exon 3, the endothelial nitric oxide synthase (eNOS) polymorphisms on exon 7 and on intron 4, the angiotensinogen polymorphism on exon 2 and the estrogen receptor 1 polymorphism in intron 1. 74 Caucasian and 84 African were classified as preeclampsia with 27 Caucasian developing a hemolysis, elevated liver enzymes and low platelets (HELLP) syndrome and 17 African women experiencing eclampsia. Multivariate logistic regression analysis adjusting for ethnicity, age and parity revealed for carriers of eNOSI4 VNTR4a a 1.7-fold increased (95 % CI 1.10–2.711, p = 0.016) risk to develop preeclampsia and a 3.6-fold increase for carriers of the EPHX1 113Tyr (95 % CI 1.366–8.750, p = 0.009) to develop severest preeclampsia. Our finding of eNOSI4 polymorphism predisposing to preeclampsia independently of ethnicity, age and parity supports the concept of NO being involved in the endothelial disorder preeclampsia. Since EPHX1 is highly expressed in the liver, can interact with various signaling pathways and is involved in central nervous system disorders, the association of EPHX1 polymorphism with the HELLP syndrome and eclampsia may hint to EPHX being a further key player in the pathogenesis of preeclampsia.

Zielsetzung: Die S3-Leitlinie zur Diagnostik und Therapie des Gestationsdiabetes empfiehlt die Einbeziehung sonografischer Parameter in die Therapieentscheidung. Die Zielbereiche fur die Blutglukose in der Stoffwechseleinstellung werden an das Wachstum des Feten angepasst. Entsprechend liegen die Zielbereiche der Blutglukose bei Patientinnen deren Feten einen Abdomenumfang (AU) uber der 75. Perzentile aufweisen niedriger, und bei Wachstum unterhalb der 10. Perzentile hoher, als bei normosom wachsenden Kindern. Die Dicke der kindlichen Bauchhaut (BHD) ist insbesondere von der Glukosezufuhr abhangig. Ziel der vorliegenden Studie war es die Assoziation von AU, Schatzgewicht (SG) und BHD im Verlauf der Schwangerschaft von Patientinnen mit GDM zu untersuchen. Methode: Prospektive Beobachtungsstudie der Schwangerschaften und Therapie bei 142 Patientinnen mit Gestationsdiabetes, die 2013 an unserem Kompetenzzentrum fur Diabetes und Schwangerschaft behandelt wurden. Ergebnisse: AU, SG und BHD zeigten eine lineare Zunahme mit steigendem Schwangerschaftsalter. Dabei nahm die BHD in unserem Kollektiv zwischen 24 und 40 SSW zwischen 2,4 mm und 4 mm linear zu. Eine Insulintherapie wurde bei 50% der Frauen notwendig und musste durchschnittlich in der 296 SSW begonnen werden. Zu diesem Zeitpunkt zeigte sich fur die BHD ein signifikant diskriminierender Unterschied zwischen Patientinnen mit Insulintherapie und solchen mit rein diatetischer Therapie. Zusammenfassung: Unsere Ergebnisse implizieren eine Bedeutung der Bestimmung der BHD zur Uberwachung und Kontrolle der Therapie von Patientinnen mit Gestationsdiabetes. Dies trifft insbesondre fur die Phase zwischen 28 und 30 SSW zu, in der eine Diskriminierung zwischen insulinpflichtigen und diatetisch fuhrbaren Patientinnen durch die Bestimmung der BHD unterstutzt werden konnte.

Workshops are an important part of the IFPA annual meeting as they allow for discussion of specialized topics. At IFPA meeting 2011 there were twelve themed workshops, three of which are summarized in this report. These workshops related to vascular systems and circulation in the mother, placenta and fetus, and were divided in to 1) angiogenic signaling and regulation of fetal endothelial function; 2) placental and fetal circulation and growth; 3) spiral artery remodeling.

Aim Affecting approximately 10% of pregnancies, intrauterine growth restriction (IUGR), is the most important cause of perinatal mortality and morbidity. Impaired placental function determined by insufficient transformation of the uterine arteries and mal-perfusion of the placenta is the leading cause of IUGR. So far there is no treatment option for pregnancy complicated by IUGR and the clinical management is restricted to close monitoring, assessing for the optimal time point of delivery the fetus threatened by intrauterine death. In a prospective randomized controlled trial we could demonstrate a risk reduction of 39% (relative risk RR = 0.609, 95% CI 0.367–1.011) for the development of IUGR and IUGR or death (RR = 0.615, 95% CI 0.378–1.000) by delivering the organic nitrate pentaerythrityl-tetranitrate (PETN) to patients recognized at risk for IUGR by impaired uterine artery Doppler at mid gestation (Schleussner, 2014). To confirm these results a prospective randomized placebo controlled double-blinded multicentre trial was now initiated. Approach Eligible patients are pregnant women at risk of developing IUGR meeting the inclusion criteria: abnormal uterine artery Doppler ultrasound, defined by a mean PI greater than 1.6, singleton pregnancy, informed consent and 190–226 weeks of gestation. Outcome measures Primary efficacy endpoint : Development of IUGR (defined by birth weight 1.6). Key secondary endpoint(s) : severe morbidity and mortality as composite of severe IUGR ( Results Patient enrollment will be started in July 2017. The proposed recruitment period is 18 month. Results are expected in the beginning of 2020.

The pathophysiology of preeclampsia includes an unbalanced syncytiotrophoblast renewal from the underlying cytotrophoblast and increased necrotic/aponecrotic shedding of syncytiotrophoblast particles into the maternal circulation. These non-apoptotic syncytiotrophoblast fragments cause the maternal endothelial dysfunction underlying the syndrome of preeclampsia. In order to understand the pathophysiological changes at the fetomaternal interface in preeclampsia we studied the expression of VE-cadherin and vascular endothelial growth factor receptor-2 (VEGFR2) in preeclampsia. We show that VE-cadherin is expressed in the syncytiotrophoblast and is upregulated in fusing BeWo cells, while inhibition of VE-cadherin expression by siRNA does not block BeWo cell fusion. Our immunohistochemistry data show lower VE-cadherin expression in early onset preeclampsia compared to early controls. In late onset preeclampsia VE-cadherin was significantly more expressed compared to late controls. Concurrently VE-cadherin expression decreased significantly in control pregnancies towards term, but not in pregnancies complicated by preeclampsia. VEGFR2 expression was significantly reduced in all cases of preeclampsia compared to control placentas. Because of their close interaction in barrier function regulation we speculate that sustained expression of VE-cadherin in late onset preeclampsia could counteract VEGFR2 deficiency by enhancing survival pathway stimulation in the syncytiotrophoblast, thus preventing further decompensation of unbalanced villous trophoblast turnover.

Mycological examination of sputum from 121 patients with cystic fibrosis by means of long-term cultures (4 weeks) revealed the occurrence of Candida albicans in low quantities in 70%, Aspergillus fumigatus in 30%, and Exophiala/Wangiella dermatitidis in 9% of the examined patients. A. fumigatus frequently causes the development of allergic bronchopulmonary aspergillosis in patients with cystic fibrosis. The predisposing factors for colonization with the otherwise seldom found fungus E. dermatitidis in these patients and the consequences of these findings are discussed. In conclusion, long-term fungal cultures are advocated for specimens from CF patients.

Preeclampsia (PE) is one of the leading causes of maternal and perinatal morbidity and mortality worldwide. Abnormal expression of microRNAs (miRNAs) occurs in several pregnancy diseases including PE. Placental trophoblast cells express a specific set of miRNAs which changes during pregnancy. These miRNAs can be released within extracellular vesicles (EVs) and mediate intercellular communication. miR-141 is a pregnancy-related miRNA which is expressed by trophoblast cells at increased levels in maternal plasma in the third trimester. We hypothesize that miR-141 is abnormally expressed in PE placentae, controls trophoblast, and immune cell functions and is involved in the intercellular communication between fetal trophoblast and maternal immune cells. Expression of miR-141 was analyzed by quantitative real-time PCR (qPCR) in normal and preeclamptic placentae and in 2 different trophoblastic cell lines, JEG-3 and HTR-8/SVneo. Changes in JEG-3 and HTR-8/SVneo cell proliferation and invasion were investigated after miR-141 inhibition and overexpression by MTS-, BrdU-, and Matrigel assays. EVs from miR-141 transfected cells were isolated from supernatants and characterized by NanoSight analysis and qPCR. Proliferation of Jurkat T cells and invasion of HTR-8/SVneo cells were investigated after treatment with EVs containing different miR-141 levels. miR-141 expression was higher in placentae from PE patients compared with those from normal pregnancies. miR-141 inhibition in trophoblastic cells resulted in decreased cell viability and reduced invasion capability. After transfection with miR-141-mimic, trophoblastic cells secreted EVs with increased miR-141 content. These vesicles did not exert effects on trophoblastic cell invasion but reduced Jurkat T cell proliferation. In conclusion, miR-141 regulates major functions of trophoblastic and immune cells. Trophoblast cells release EVs whose miRNA content can be modified by transfection of origin cells. Furthermore, elevated levels of miR-141 can be transferred from trophoblast to immune cells by release and internalization of EVs suggesting their role in the immune regulation of normal and pathologic pregnancies.

Introduction Preeclampsia (PE) is a potentially dangerous pregnancy pathology contributing to a higher worldwide mortality and morbidity. The negative influence of syncytiotrophoblastic microparticles (STBMs) on the placenta and maternal endothelia is thought to play a key role in generating the inflammatory effects that lead to PE symptoms. Doppler sonography of the uterine arteries assists in identifying a risk population, however, the positive predictive value for this method is low. Objectives Aim of this study is to evaluate whether STBMs can serve as an accessory marker to conventional Doppler sonography to better identify pregnant women who will actually develop PE. Methods Pregnant women between 19–21 gestational weeks (GW) with abnormal uterine perfusion were enrolled into this prospective study. Plasma samples were taken at inclusion (baseline) and at two further visits at 8 week intervals to follow STBM concentration alterations during pregnancy. The primary endpoint assessed is PE and/or hemolysis, elevated liver, low platelets (HELLP) syndrome. Other PE-associated pathologies (intrauterine growth retardation [IUGR], intrauterine fetal demise [IUFD], placental abruption, premature delivery) constitute the secondary endpoints. Maternal STBM concentrations were measured using a home made Enzyme Linked Sorbent Assay (ELSA) which specifically measures STBMs. The receiver operating characteristics (ROC) for baseline measures are graphically displayed and area under curve (AUC) is estimated including 95% confidence levels. Results Of the 73 women included in the study, 16 developed PE (cases) and 56 did not (control). After analyses of mid-gestational probes, the ROC curve was in close proximity to the line of no-discrimination. Conclusion Our preliminary results indicate that the maternal STBM concentration at mid-gestation does not predict the development of PE or associated pregnancy pathologies. Further analysis is underway to assess whether STBM measurements at later gestational time points can predict PE shortly before onset of disease.

ProblemThe pregnancy-associated disease preeclampsia is related to the release of syncytiotrophoblast extracellular vesicles (STBEV) by the placenta. To improve functional research on STBEV, reliable and specific methods are needed to quantify them. However, only a few quantification methods are available and accepted, though imperfect. For this purpose, we aimed to provide an enzyme-linked sorbent assay (ELSA) to quantify STBEV in fluid samples based on their microvesicle characteristics and placental origin.Method of StudyEx vivo placenta perfusion provided standards and samples for the STBEV quantification. STBEV were captured by binding of extracellular phosphatidylserine to immobilized annexin V. The membranous human placental alkaline phosphatase on the STBEV surface catalyzed a colorimetric detection reaction.Results and ConclusionThe described ELSA is a rapid and simple method to quantify STBEV in diverse liquid samples, such as blood or perfusion suspension. The reliability of the ELSA was proven by comparison with nanoparticle tracking analysis.

On page 1 “adjusted relative risk (RR)“ should be changed to “adjusted odds ratio (OR)”. On page 1, 3 and in the table head of table 2 “adjusted RR” should be changed to “adjusted OR”. On page 3 “Mantel-Haenszel estimates of relative risk” should be changed to “Mantel-Haenszel estimates of odds ratios”. In Table 2, caption b “Mantel-Haenszel estimate of relative risk” should be changed to “Mantel-Haenszel estimate of odds ratio”.