Early Tube Feeding after Percutaneous Endoscopic Gastrostomy (PEG): An Observational Study

This study investigated whether enteral nutrition by early tube feeding led to changes in clinical parameters compared to tube feeding after 24 h. Starting on 1 January 2021, and following the latest update of the ESPEN guidelines on enteral nutrition, patients with percutaneous endoscopic gastrostomy (PEG) received tube feeding 4 h after tube insertion. An observational study was conducted to analyze whether the new scheme affected patient complaints, complications, or hospitalization duration compared to the previous procedure of tube feeding starting after 24 h. Clinical patient records from one year before and one year after the introduction of the new scheme were examined. A total of 98 patients were included, and of those 47 received tube feeding 24 h after tube insertion, and 51 received tube feeding 4 h after tube insertion. The new scheme did not influence the frequency or severity of patient complaints or complications related to tube feeding (all p-values > 0.05). However, the study showed that the length of stay in hospital was significantly shorter when following the new scheme (p = 0.030). In this observational cohort study an earlier start of tube feeding did not produce any negative consequences but did reduce the duration of hospitalization. Therefore, an early start, as suggested in the recent ESPEN guidelines, is supported and recommended

Early Tube Feeding after Percutaneous Endoscopic Gastrostomy (PEG): An Observational Study.

This study investigated whether enteral nutrition by early tube feeding led to changes in clinical parameters compared to tube feeding after 24 h. Starting on 1 January 2021, and following the latest update of the ESPEN guidelines on enteral nutrition, patients with percutaneous endoscopic gastrostomy (PEG) received tube feeding 4 h after tube insertion. An observational study was conducted to analyze whether the new scheme affected patient complaints, complications, or hospitalization duration compared to the previous procedure of tube feeding starting after 24 h. Clinical patient records from one year before and one year after the introduction of the new scheme were examined. A total of 98 patients were included, and of those 47 received tube feeding 24 h after tube insertion, and 51 received tube feeding 4 h after tube insertion. The new scheme did not influence the frequency or severity of patient complaints or complications related to tube feeding (all p-values > 0.05). However, the study showed that the length of stay in hospital was significantly shorter when following the new scheme (p = 0.030). In this observational cohort study an earlier start of tube feeding did not produce any negative consequences but did reduce the duration of hospitalization. Therefore, an early start, as suggested in the recent ESPEN guidelines, is supported and recommended

Serum Amyloid Beta42 Is Not Eliminated by the Cirrhotic Liver: A Pilot Study.

Amyloid-beta (Aβ) deposition in the brain is the main pathological hallmark of Alzheimer disease. Peripheral clearance of Aβ may possibly also lower brain levels. Recent evidence suggested that hepatic clearance of Aβ42 is impaired in liver cirrhosis. To further test this hypothesis, serum Aβ42 was measured by ELISA in portal venous serum (PVS), systemic venous serum (SVS), and hepatic venous serum (HVS) of 20 patients with liver cirrhosis. Mean Aβ42 level was 24.7 ± 20.4 pg/mL in PVS, 21.2 ± 16.7 pg/mL in HVS, and 19.2 ± 11.7 pg/mL in SVS. Similar levels in the three blood compartments suggested that the cirrhotic liver does not clear Aβ42. Aβ42 was neither associated with the model of end-stage liver disease score nor the Child-Pugh score. Patients with abnormal creatinine or bilirubin levels or prolonged prothrombin time did not display higher Aβ42 levels. Patients with massive ascites and patients with large varices had serum Aβ42 levels similar to patients without these complications. Serum Aβ42 was negatively associated with connective tissue growth factor levels (r = -0.580, p = 0.007) and a protective role of Aβ42 in fibrogenesis was already described. Diabetic patients with liver cirrhosis had higher Aβ42 levels (p = 0.069 for PVS, p = 0.047 for HVS and p = 0.181 for SVS), which is in accordance with previous reports. Present analysis showed that the cirrhotic liver does not eliminate Aβ42. Further studies are needed to explore the association of liver cirrhosis, Aβ42 levels, and cognitive dysfunction

Predictors and management of post-banding ulcer bleeding in cirrhosis: A systematic review and meta-analysis.

BACKGROUND AND AIMS Post-banding ulcer bleeding (PBUB) is an understudied complication of oesophageal varices endoscopic band ligation (EBL). This systematic review with meta-analysis aimed at: (a) evaluating the incidence of PBUB in patients with cirrhosis treated with EBL in primary or secondary prophylaxis or urgent treatment for acute variceal bleeding and (b) identifying predictors of PBUB. METHODS We conducted a systematic review of articles in English published in 2006-2022 using the Preferred Reporting Items for Systematic Reviews and Meta-analyses guidelines. Searches were made in eight databases including Embase, PubMed and Cochrane Library. Random-effects meta-analysis was used to determine the incidence, mean interval and predictors of PBUB. RESULTS Eighteen studies (9034 patients) were included. The incidence of PBUB was 5.5% (95% CI 4.3-7.1). The mean time for it to occur was 11 days (95% CI 9.94-11.97). Model for End-stage Liver Disease (MELD) score (OR 1.162, 95% CI 1.047-1.291) and EBL done in emergency setting (OR 4.902, 95% CI 2.99-8.05) independently predicted post-ligation ulcer bleeding. Treatment included drugs, endoscopic procedures and transjugular intrahepatic portosystemic shunt. Refractory bleeding was treated with self-expandable metallic stents or balloon tamponade. Mortality was on average 22.3% (95% CI 14.1-33.6). CONCLUSIONS Patients with high MELD score and receiving EBL in an emergency setting are more prone to develop PBUB. Prognosis is still poor and the best therapeutic strategy to address remains to be ascertained

Rapid Decline of Serum Proprotein Convertase Subtilisin/Kexin 9 (PCSK9) in Non-Cirrhotic Patients with Chronic Hepatitis C Infection Receiving Direct-Acting Antiviral Therapy.

Direct-acting antivirals (DAAs) efficiently eradicate the hepatitis C virus (HCV). Low-density lipoprotein (LDL) levels increase rapidly upon DAA treatment. Proprotein convertase subtilisin/kexin 9 (PCSK9) induces degradation of the hepatic LDL receptor and thereby elevates serum LDL. The aim of this study was to determine serum PCSK9 concentrations during and after DAA therapy to identify associations with LDL levels. Serum PCSK9 was increased in 82 chronic HCV-infected patients compared to 55 patients not infected with HCV. Serum PCSK9 was low in HCV patients with liver cirrhosis, but patients with HCV-induced liver cirrhosis still exhibited higher serum PCSK9 than patients with non-viral liver cirrhosis. Serum PCSK9 correlated with measures of liver injury and inflammation in cirrhotic HCV patients. In patients without liver cirrhosis, a positive association of serum PCSK9 with viral load existed. Serum PCSK9 was not different between viral genotypes. Serum PCSK9 did not correlate with LDL levels in HCV patients irrespective of cirrhotic status. Serum PCSK9 was reduced, and LDL was increased at four weeks after DAA therapy start in non-cirrhotic HCV patients. Serum PCSK9 and LDL did not change upon DAA treatment in the cirrhotic group. The rapid decline of PCSK9 after the start of DAA therapy in conjunction with raised LDL levels in non-cirrhotic HCV patients shows that these changes are not functionally related

Familienpolitik: Förderung von Familien - nach welchem Konzept?

Familienpolitik hat Konjunktur und ist ins Zentrum der politischen Agenda gerückt, weil sie eng mit Demographie- und Wachstumspolitik verbunden ist. Über die Notwendigkeit einer wirksamen Familienpolitik herrscht Einigkeit, aber welches Konzept ist das richtige? Christa Stewens, Bayerische Staatsministerin für Arbeit und Sozialordnung, Familie und Frauen, unterstreicht, dass Familienpolitik "ganzheitlich und nachhaltig angelegt sein" muss. Auch Malte Ristau, Bundesministerium für Familie, Senioren, Frauen und Jugend, verweist darauf, dass eine nur auf monetäre Hilfe angelegte Familienpolitik ein zu enger Ansatz sei. Reiner Klingholz, Berlin-Institut für Bevölkerung und Entwicklung, zeigt, dass interessanterweise nicht die Länder, in denen ein traditionelles Frauen- und Familienbild vorherrscht, sondern jene, in denen die Gleichstellung der Geschlechter am weitesten fortgeschritten ist, die höchste Fertilität aufweisen. Bertram Wiest und Stefan Schaible, Roland Berger Strategy Consultants, betonen das hohe Finanzvolumen, das in Deutschland vom Staat für Leistungen für Familien ausgegeben wird: "Es mangelt also nicht an Geld, sondern am zielgerichteten Mitteleinsatz". Für Michael Steiner, Michael Böhmer und Christian Böllhoff, Prognos AG, Basel, muss sich die Familienpolitik an das neue Familienbild anpassen und sowohl Gestaltungsfreiräume für Familie einrichten, als auch Chancengleichheit gewährleisten. Auch für Christel Humme, familienpolitische Sprecherin der SPD-Bundestagsfraktion, kommt es vor allem auf die richtige Mischung zwischen "Infrastruktur, Zeit und Geld für Familien" an.Familienpolitik, Konjunktur, Demographie, Wachstumspolitik, Kinder, Familie, Deutschland

Dysbiotic microbiota interactions in Crohn's disease.

Crohn's disease (CD) is a major form of inflammatory bowel disease characterized by transmural inflammation along the alimentary tract. Changes in the microbial composition and reduction in species diversity are recognized as pivotal hallmarks in disease dynamics, challenging the gut barrier function and shaping a pathological immune response in genetically influenced subjects. The purpose of this review is to delve into the modification of the gut microbiota cluster network during CD progression and to discuss how this shift compromises the gut barrier integrity, granting the translocation of microbes and their products. We then complete the scope of the review by retracing gut microbiota dysbiosis interactions with the main pathophysiologic factors of CD, starting from the host's genetic background to the immune inflammatory and fibrotic processes, providing a standpoint on the lifestyle/exogenous factors and the potential benefits of targeting a specific gut microbiota

Gastroesophageal Junction and Pylorus Distensibility Before and After Sleeve Gastrectomy-pilot Study with EndoFlipTM.

Sleeve gastrectomy (SG) is the most frequently performed bariatric surgical intervention worldwide. Gastroesophageal reflux disease (GERD) is frequently observed after SG and is a relevant clinical problem. This prospective study investigated the gastroesophageal junction (GEJ) and pyloric sphincter by impedance planimetry (EndoFlipTM) and their association with GERD at a tertiary university hospital center. Between January and December 2018, patients undergoing routine laparoscopic SG had pre-, intra-, and postoperative assessments of the GEJ and pyloric sphincter by EndoFlipTM. The distensibility index (DI) was measured at different volumes and correlated with GERD (in accordance with the Lyon consensus guidelines). Nine patients were included (median age 48 years, preoperative BMI 45.1 kg/m2, 55.6% female). GERD (de novo or stable) was observed in 44.4% of patients one year postoperatively. At a 40-ml filling volume, DI increased significantly pre- vs. post-SG of the GEJ (1.4 mm2/mmHg [IQR 1.1-2.6] vs. 2.9 mm2/mmHg [2.6-5.3], p VALUE=0.046) and of the pylorus (6.0 mm2/mmHg [4.1-10.7] vs. 13.1 mm2/mmHg [7.6-19.2], p VALUE=0.046). Patients with postoperative de novo or stable GERD had a significantly increased preoperative DI at 40 ml of the GEJ (2.6 mm2/mmHg [1.9-3.5] vs. 0.5 mm2/mmHg [0.5-1.1], p VALUE=0.031). There was no significant difference in DI at 40 mL filling in the preoperative pylorus and postoperative GEJ or pylorus. In this prospective study, the DI of the GEJ and the pylorus significantly increased after SG. Postoperative GERD was associated with a significantly higher preoperative DI of the GEJ but not of the pylorus

Microbiota-driven gut vascular barrier disruption is a prerequisite for non-alcoholic steatohepatitis development.

BACKGROUND & AIMS Fatty liver disease, including non-alcoholic fatty liver (NAFLD) and steatohepatitis (NASH), has been associated with increased intestinal barrier permeability and translocation of bacteria or bacterial products into the blood circulation. In this study, we aimed to unravel the role of both intestinal barrier integrity and microbiota in NAFLD/NASH development. METHODS C57BL/6J mice were fed with high-fat diet (HFD) or methionine-choline-deficient diet for 1 week or longer to recapitulate aspects of NASH (steatosis, inflammation, insulin resistance). Genetic and pharmacological strategies were then used to modulate intestinal barrier integrity. RESULTS We show that disruption of the intestinal epithelial barrier and gut vascular barrier (GVB) are early events in NASH pathogenesis. Mice fed HFD for only 1 week undergo a diet-induced dysbiosis that drives GVB damage and bacterial translocation into the liver. Fecal microbiota transplantation from HFD-fed mice into specific pathogen-free recipients induces GVB damage and epididymal adipose tissue enlargement. GVB disruption depends on interference with the WNT/β-catenin signaling pathway, as shown by genetic intervention driving β-catenin activation only in endothelial cells, preventing GVB disruption and NASH development. The bile acid analogue and farnesoid X receptor agonist obeticholic acid (OCA) drives β-catenin activation in endothelial cells. Accordingly, pharmacologic intervention with OCA protects against GVB disruption, both as a preventive and therapeutic agent. Importantly, we found upregulation of the GVB leakage marker in the colon of patients with NASH. CONCLUSIONS We have identified a new player in NASH development, the GVB, whose damage leads to bacteria or bacterial product translocation into the blood circulation. Treatment aimed at restoring β-catenin activation in endothelial cells, such as administration of OCA, protects against GVB damage and NASH development. LAY SUMMARY The incidence of fatty liver disease is reaching epidemic levels in the USA, with more than 30% of adults having NAFLD (non-alcoholic fatty liver disease), which can progress to more severe non-alcoholic steatohepatitis (NASH). Herein, we show that disruption of the intestinal epithelial barrier and gut vascular barrier are early events in the development of NASH. We show that the drug obeticholic acid protects against barrier disruption and thereby prevents the development of NASH, providing further evidence for its use in the prevention or treatment of NASH