The Impact of Pregnancy on Outcomes After Bariatric Surgery.

BACKGROUND: Bariatric surgery is performed mostly on obese women of reproductive age. Many studies have analyzed pregnancy outcomes after bariatric surgery, but only a small number have studied the impact of pregnancy on the postoperative outcomes. PURPOSE: To study the effect of pregnancy on outcomes after bariatric surgery in women of childbearing age. METHODS: From January 2010 to October 2017, a retrospective study of a prospectively maintained database was conducted at the University Hospital of Geneva (HUG), where 287 women between the ages of 18 and 45 years had undergone Roux-en-Y gastric bypass (RYGB). A comparison of the results during a 5-year follow-up was performed between women who became pregnant after their bariatric surgery (pregnancy group, n = 40) and postoperative non-pregnant women (non-pregnancy group, n = 247). The two groups were compared for weight loss, complications, and nutritional deficiencies. RESULTS: The pregnancy group was significantly younger (29.2 ± 5.5 vs. 36.4± 6.3 years, p < 0.001) and heavier (124.0 ± 18.0 kg vs. 114.7 ± 17.1, p < 0.001) compared with the non-pregnancy group at the time of surgery. The percentage of excess BMI loss (%EBMI loss) was similar in both groups during the 5-year follow-up. Complications after RYGB and nutritional deficiencies were nearly identical in the two groups. The interval of time between bariatric surgery and first pregnancy was a median of 20.8 months. Out of 40 first pregnancies, 28 women completed pregnancy successfully with live birth. CONCLUSION: Pregnancy after bariatric surgery is safe and does not adversely affect outcomes after RYGB.

[Surgical strategy for early stage carcinoma of the esophagus]. / Chirurgische Strategie bei Frühkarzinomen des Ösophagus.

Early stage carcinomas of the esophagus are histologically differentiated into adenocarcinomas and squamous cell carcinomas and subdivided into mucosal (m1-3) and submucosal (sm1-3) carcinomas depending on the infiltration depth. While the prevalence of lymph node metastases in mucosal carcinomas is very low, the probability of lymph node metastases increases from submucosal infiltration with increasing depth. According to the current German S3 guidelines endoscopic resection is the recommended treatment strategy for mucosal adenocarcinoma without histological risk factors (lymphatic invasion [L1], venous invasion [V1], poorly differentiated [>G2], microscopic residual disease [R1] at the deep resection margin). For superficial submucosal infiltration (sm1) without histological risk factors endoscopic resection can also be carried out, whereby in this case the guidelines make a stronger recommendation for esophagectomy. For squamous cell carcinoma endoscopic resection is indicated for an infiltration depth up to middle layer mucosal carcinoma (m2) without histological risk factors. Outside of these criteria an esophageal resection should always be carried out. The surgical gold standard is a subtotal abdominothoracic esophagectomy with two-field lymphadenectomy. Alternative procedures are total esophagectomy in proximal esophageal carcinoma and transhiatal extended gastrectomy for carcinoma of the cardia. Limited proximal or distal esophageal resections can be performed in proximal or distal mucosal carcinoma without the possibility of endoscopic resection; however, partial resections are not superior in terms of functional results and are not oncologically equivalent due to limited lymphadenectomy. Minimally invasive procedures show good oncological results and reduce the morbidity of radical esophagectomy. Reduced morbidity might be an argument for surgical resection in borderline cases between endoscopic and surgical resection.

Increased neuronal nitric oxide synthase dimerisation is involved in rat and human pancreatic beta cell hyperactivity in obesity.

AIMS/HYPOTHESIS: Pancreatic beta cell hyperactivity is known to occur in obesity, particularly in insulin-resistant states. Our aim was to investigate whether changes in neuronal nitric oxide synthase (nNOS) function affect beta cell compensation in two relevant models: the Zucker fa/fa rats and pancreatic islets from obese humans. METHODS: Glucose-induced insulin response was evaluated in the isolated perfused rat pancreas and in human pancreatic islets from obese individuals. Expression of nNOS (also known as NOS1) and subcellular localisation of nNOS were studied by quantitative RT-PCR, immunoblotting, immunofluorescence and electron microscopy. RESULTS: Pancreatic beta cells from Zucker fa/fa rats and obese individuals were found to be hyper-responsive to glucose. Pharmacological blockade of nNOS was unable to modify beta cell response to glucose in fa/fa rats and in islets from obese individuals, suggesting an abnormal control of insulin secretion by the enzyme. In both cases, nNOS activity in islet cell extracts remained unchanged, despite a drastic increase in nNOS protein and an enhancement in the dimer/monomer ratio, pointing to the presence of high amounts of catalytically inactive enzyme. This relative decrease in activity could be mainly related to increases in islet asymmetric dimethyl-arginine content, an endogenous inhibitor of nNOS activity. In addition, mitochondrial nNOS level was decreased, which contrasts with a strongly increased association with insulin granules. CONCLUSIONS/INTERPRETATION: Increased nNOS production and dimerisation, together with a relative decrease in catalytic activity and relocalisation, are involved in beta cell hyperactivity in insulin-resistant rats but also in human islets isolated from obese individuals.