A modified Nissen fundoplication: subjective and objective midterm results

Purpose: The failure rate of laparoscopic anti-reflux surgery is approximately 10\u201320%. The aim of our prospective study was to investigate whether a modified Nissen fundoplication (MNF) can improve reflux symptoms and prevent surgical treatment failure in the midterm. Methods: The MNF consisted of (1) suturing the esophagus to the diaphragmatic crura on each side using four non-absorbable stitches, (2) reinforcing clearly weak crura with a tailored Ultrapro mesh, and (3) fixing the upper stitch of the valve to the diaphragm. Forty-eight consecutive patients experiencing typical gastroesophageal reflux disease (GERD) symptoms at least three times per week for 6 months or longer were assessed before and after surgery using validated symptom and quality of life (GERD-HRQL) questionnaires, high-resolution manometry, 24-h impedance-pH monitoring, endoscopy, and barium swallow. Results: Mortality and perioperative complications were nil. At median follow-up of 46.7 months, the patients experienced significant improvements in symptom and GERD-HRQL scores. One patient presented with severe dyspepsia and another complained of dysphagia requiring a repeat surgery 12 months after the first operation. Esophageal acid exposure (8.8 vs 0.1; p < 0.0001), reflux number (62 vs 8.5; p < 0.0001), and symptom-reflux association (19 vs 0; p < 0.0001) significantly decreased postoperatively. The median esophagogastric junction contractile integral (EGJ-CI) from 31 cases (8.2 vs 21.2 mmHg cm; p = 0.0003) and the abdominal length of the lower esophageal sphincter (LES) (0 vs 16 mm; p = 0.01) increased postoperatively. Conclusions: Our data demonstrate that the MNF is a safe and effective procedure both in the short term and midterm. \ua9 2018, Springer-Verlag GmbH Germany, part of Springer Nature

Oxidative stress in pregnancies complicated by diabetes

The placenta is essential for normal foetal metabolism and growth. However, maternal diabetes is an unfavourable environment for embryonic and fetoplacental development, which may disrupt normal foetal programming, leading later to metabolic disease. Additionally, an adverse in utero environment may lead to foetal congenital anomalies. Existing diabetes before pregnancy (pregestational type 1 and or type 2 diabetes mellitus) may have negative effects on the embryonic development, while gestational diabetes mellitus (GDM) that occurs during late stages of pregnancy may affect the growth and maturation of the foetus. Many of the damaging effects of diabetes in pregnancy have been attributed to oxidative stress. Reactive oxygen and nitrogen species are by-products of a number of important biological pathways of pregnancy, including embryo development, implantation, angiogenesis, placental development and function. In healthy pregnancies, these reactive oxygen and nitrogen species can be controlled to ensure no damage ensues. However, in pregnancies complicated by diabetes, their excessive production and/or a reduction in antioxidant defence mechanisms results in a number of damaging outcomes. Animal models of diabetes in pregnancy have provided supportive evidence of reactive oxygen and nitrogen species generation and their damaging effects, which are dependent on the developmental stage. In this chapter, we will review the available data on oxidative stress in human diabetic pregnancies as well as in animal models of diabetes in pregnancy during early gestation, fetoplacental development and the perinatal period, as well as on its postnatal consequences. Human and animal data supportive of antioxidant treatments will be also discussed