Conservative Management of Emphysematous Gastritis With Gastric Mucosal Ischaemia: A Case Report.

Emphysematous gastritis is a rare condition historically associated with high mortality. It is characterised by gastric mural pneumatosis and portal venous gas, secondary to bacterial or fungal invasion. Given the rarity of the condition, there is little evidence to guide clinical decisions regarding whether a patient requires surgical resection. We describe the case of a 72-year-old male diagnosed with emphysematous gastritis, with endoscopic evidence of gastric fundus mucosal ischaemia. As there was no evidence of ischaemia extending to the serosa on exploratory laparotomy, gastrectomy was not performed, and the patient was managed conservatively. He subsequently made a full recovery, and was discharged without any further complications. This case demonstrates that in the absence of full-thickness gastric ischaemia, patients with emphysematous gastritis may be appropriate for conservative management without surgical resection.

Liver-Secreted Hexosaminidase A Regulates Insulin-Like Growth Factor Signaling and Glucose Transport in Skeletal Muscle.

Nonalcoholic fatty liver disease (NAFLD) and impaired glycemic control are closely linked; however, the pathophysiological mechanisms underpinning this bidirectional relationship remain unresolved. The high secretory capacity of the liver and impairments in protein secretion in NAFLD suggest that endocrine changes in the liver are likely to contribute to glycemic defects. We identify hexosaminidase A (HEXA) as an NAFLD-induced hepatokine in both mice and humans. HEXA regulates sphingolipid metabolism, converting GM2 to GM3 gangliosides-sphingolipids that are primarily localized to cell-surface lipid rafts. Using recombinant murine HEXA protein, an enzymatically inactive HEXA(R178H) mutant, or adeno-associated virus vectors to induce hepatocyte-specific overexpression of HEXA, we show that HEXA improves blood glucose control by increasing skeletal muscle glucose uptake in mouse models of insulin resistance and type 2 diabetes, with these effects being dependent on HEXA's enzymatic action. Mechanistically, HEXA remodels muscle lipid raft ganglioside composition, thereby increasing IGF-1 signaling and GLUT4 localization to the cell surface. Disrupting lipid rafts reverses these HEXA-mediated effects. In this study, we identify a pathway for intertissue communication between liver and skeletal muscle in the regulation of systemic glycemic control.

Deep proteomic profiling unveils arylsulfatase A as a non-alcoholic steatohepatitis inducible hepatokine and regulator of glycemic control.

Non-alcoholic steatohepatitis (NASH) and type 2 diabetes are closely linked, yet the pathophysiological mechanisms underpinning this bidirectional relationship remain unresolved. Using proteomic approaches, we interrogate hepatocyte protein secretion in two models of murine NASH to understand how liver-derived factors modulate lipid metabolism and insulin sensitivity in peripheral tissues. We reveal striking hepatokine remodelling that is associated with insulin resistance and maladaptive lipid metabolism, and identify arylsulfatase A (ARSA) as a hepatokine that is upregulated in NASH and type 2 diabetes. Mechanistically, hepatic ARSA reduces sulfatide content and increases lysophosphatidylcholine (LPC) accumulation within lipid rafts and suppresses LPC secretion from the liver, thereby lowering circulating LPC and lysophosphatidic acid (LPA) levels. Reduced LPA is linked to improvements in skeletal muscle insulin sensitivity and systemic glycemic control. Hepatic silencing of Arsa or inactivation of ARSA's enzymatic activity reverses these effects. Together, this study provides a unique resource describing global changes in hepatokine secretion in NASH, and identifies ARSA as a regulator of liver to muscle communication and as a potential therapeutic target for type 2 diabetes.

Diagnostic accuracy of non-invasive tests for advanced fibrosis in patients with NAFLD: an individual patient data meta-analysis.

OBJECTIVE: Liver biopsy is still needed for fibrosis staging in many patients with non-alcoholic fatty liver disease. The aims of this study were to evaluate the individual diagnostic performance of liver stiffness measurement by vibration controlled transient elastography (LSM-VCTE), Fibrosis-4 Index (FIB-4) and NAFLD (non-alcoholic fatty liver disease) Fibrosis Score (NFS) and to derive diagnostic strategies that could reduce the need for liver biopsies. DESIGN: Individual patient data meta-analysis of studies evaluating LSM-VCTE against liver histology was conducted. FIB-4 and NFS were computed where possible. Sensitivity, specificity and area under the receiver operating curve (AUROC) were calculated. Biomarkers were assessed individually and in sequential combinations. RESULTS: Data were included from 37 primary studies (n=5735; 45% women; median age: 54 years; median body mass index: 30 kg/m2; 33% had type 2 diabetes; 30% had advanced fibrosis). AUROCs of individual LSM-VCTE, FIB-4 and NFS for advanced fibrosis were 0.85, 0.76 and 0.73. Sequential combination of FIB-4 cut-offs (<1.3; ≥2.67) followed by LSM-VCTE cut-offs (<8.0; ≥10.0 kPa) to rule-in or rule-out advanced fibrosis had sensitivity and specificity (95% CI) of 66% (63-68) and 86% (84-87) with 33% needing a biopsy to establish a final diagnosis. FIB-4 cut-offs (<1.3; ≥3.48) followed by LSM cut-offs (<8.0; ≥20.0 kPa) to rule out advanced fibrosis or rule in cirrhosis had a sensitivity of 38% (37-39) and specificity of 90% (89-91) with 19% needing biopsy. CONCLUSION: Sequential combinations of markers with a lower cut-off to rule-out advanced fibrosis and a higher cut-off to rule-in cirrhosis can reduce the need for liver biopsies.

Pathophysiological Mechanisms of Gastro-esophageal Reflux After Sleeve Gastrectomy.

OBJECTIVE: To evaluate the mechanisms associated with reflux events after sleeve gastrectomy (SG). SUMMARY BACKGROUND DATA: Gastro-esophageal reflux (GERD) post-SG is a critical issue due to symptom severity, impact on quality of life, requirement for reoperation, and potential for Barrett esophagus. The pathophysiology is incompletely delineated. METHODS: Post-SG patients, stratified into asymptomatic and symptomatic, underwent protocolized nuclear scintigraphy (n = 83), 24-hour esophageal pH monitoring, and stationary manometry (n = 143) to characterize reflux patterns. Ten patients underwent fasting and postprandial concurrent manometry and pH for detailed analysis of reflux events. RESULTS: Baseline demographics between cohorts were similar: Age 47.2 ± 11.6 versus 44.1 ± 11.3 years ( P = 0.121); females 73.2% versus 90.8% ( P = 0.005); excess weight loss 53.8 ± 28.1% versus 57.4 ± 25.5% ( P = 0.422), follow-up duration 12.3 versus 7.4 months ( P = 0.503). Nuclear scintigraphy delineated bolus-induced deglutitive reflux events (29.6% vs 62.5%, P = 0.005) and postprandial reflux events [4 (IQR2) versus 4 (IQR 3) events, P = 0.356]. Total acid exposure was significantly elevated in the symptomatic population (7.7% vs 3.6%, P < 0.001), especially fasting acid exposure (6.0% vs 1.3%, P < 0.001). pH/manometry analysis demonstrated acute elevations of the gastro-esophageal pressure gradient (>10 mm Hg) underpinned most reflux events. Swallow-induced intragastric hyper-pressur-ization was associated with individual reflux events in most patients (90% in fasting state and 40% postprandial). CONCLUSIONS: We found reflux to be strongly associated with SG and identified 3 unique categories. Bolus-induced deglutitive and postprandial reflux occurred in most patients. Elevated fasting esophageal acid exposure mediated symptoms. Frequent, significant elevation in the gastro-esophageal pressure gradient was the mechanism of reflux and seemed to relate to the noncompliant proximal stomach.

Proteome analysis of human adipocytes identifies depot-specific heterogeneity at metabolic control points.

Adipose tissue is a primary regulator of energy balance and metabolism. The distribution of adipose tissue depots is of clinical interest because the accumulation of upper-body subcutaneous (ASAT) and visceral adipose tissue (VAT) is associated with cardiometabolic diseases, whereas lower-body glutealfemoral adipose tissue (GFAT) appears to be protective. There is heterogeneity in morphology and metabolism of adipocytes obtained from different regions of the body, but detailed knowledge of the constituent proteins in each depot is lacking. Here, we determined the human adipocyte proteome from ASAT, VAT, and GFAT using high-resolution Sequential Window Acquisition of all Theoretical (SWATH) mass spectrometry proteomics. We quantified 4,220 proteins in adipocytes, and 2,329 proteins were expressed in all three adipose depots. Comparative analysis revealed significant differences between adipocytes from different regions (6% and 8% when comparing VAT vs. ASAT and GFAT, 3% when comparing the subcutaneous adipose tissue depots, ASAT and GFAT), with marked differences in proteins that regulate metabolic functions. The VAT adipocyte proteome was overrepresented with proteins of glycolysis, lipogenesis, oxidative stress, and mitochondrial dysfunction. The GFAT adipocyte proteome predicted the activation of peroxisome proliferator-activated receptor α (PPARα), fatty acid, and branched-chain amino acid (BCAA) oxidation, enhanced tricarboxylic acid (TCA) cycle flux, and oxidative phosphorylation, which was supported by metabolomic data obtained from adipocytes. Together, this proteomic analysis provides an important resource and novel insights that enhance the understanding of metabolic heterogeneity in the regional adipocytes of humans.NEW & NOTEWORTHY Adipocyte metabolism varies depending on anatomical location and the adipocyte protein composition may orchestrate this heterogeneity. We used SWATH proteomics in patient-matched human upper- (visceral and subcutaneous) and lower-body (glutealfemoral) adipocytes and detected 4,220 proteins and distinguishable regional proteomes. Upper-body adipocyte proteins were associated with glycolysis, de novo lipogenesis, mitochondrial dysfunction, and oxidative stress, whereas lower-body adipocyte proteins were associated with enhanced PPARα activation, fatty acid, and BCAA oxidation, TCA cycle flux, and oxidative phosphorylation.

Hepatic lipidomic remodeling in severe obesity manifests with steatosis and does not evolve with non-alcoholic steatohepatitis.

BACKGROUNDS & AIMS: Obesity often leads to non-alcoholic fatty liver disease (NAFLD), which can progress from simple steatosis (non-alcoholic fatty liver (NAFL)) to non-alcoholic steatohepatitis (NASH). The accumulation of certain lipid subtypes is linked with worsening metabolic and liver disease, however, specific changes during progression from No-NAFL to NAFL then NASH are unresolved. Herein, we characterise the liver, adipose tissue and plasma lipidome of worsening NAFLD in obesity, and evaluate the utility of plasma lipids as biomarkers of NAFLD. METHODS: Venous blood, liver, visceral and subcutaneous adipose tissue samples were obtained from 181 patients undergoing bariatric surgery. NAFLD severity was assessed histologically. Lipidomic analysis was performed using liquid chromatography-tandem mass spectrometry. RESULTS: The liver lipidome showed substantial changes with increasing steatosis, with increased triacylglycerols, diacylglycerols and sphingolipids including ceramide, dihydroceramide, hexosyl-ceramide and GM3 ganglioside species. These lipid species were also increased in plasma with increasing hepatic steatosis and showed strong correlations with liver lipids. Adipose tissue lipidomes showed no correlation with NAFLD. There were no significant changes in liver lipids with NASH compared to NAFL. The addition of plasma lipid variables to routine markers yielded significant improvements in diagnostic accuracy for NASH (AUROC 0.667 vs. 0.785, p = 0.025). CONCLUSION: Overall, these data provide a detailed description of the lipidomic changes with worsening NAFLD, showing significant changes with steatosis but no additional changes with NASH. Alterations in the liver lipidome are paralleled by similar changes in plasma. Further investigation is warranted into the potential utility of plasma lipids as non-invasive biomarkers of NAFLD in obesity. LAY SUMMARY: Non-alcoholic fatty liver disease (NAFLD) is characterised by distinct changes in the liver lipidome with steatosis. The development of non-alcoholic steatohepatitis (NASH) does not result in further changes in the lipidome. Lipids within body fat do not appear to influence the lipid profile of the liver or blood. Changes in liver lipids are paralleled by changes in blood lipids. This has potential to be developed into a non-invasive biomarker for NAFLD. CLINICAL TRIAL NUMBER: ACTRN12615000875505.

Ectodysplasin A Is Increased in Non-Alcoholic Fatty Liver Disease, But Is Not Associated With Type 2 Diabetes.

Ectodysplasin A (EDA) was recently identified as a liver-secreted protein that is increased in the liver and plasma of obese mice and causes skeletal muscle insulin resistance. We assessed if liver and plasma EDA is associated with worsening non-alcoholic fatty liver disease (NAFLD) in obese patients and evaluated plasma EDA as a biomarker for NAFLD. Using a cross-sectional study in a public hospital, patients with a body mass index >30 kg/m2 (n=152) underwent liver biopsy for histopathology assessment and fasting liver EDA mRNA. Fasting plasma EDA levels were also assessed. Non-alcoholic fatty liver (NAFL) was defined as >5% hepatic steatosis and nonalcoholic steatohepatitis (NASH) as NAFLD activity score ≥3. Patients were divided into three groups: No NAFLD (n=45); NAFL (n=65); and NASH (n=42). Liver EDA mRNA was increased in patients with NASH compared with No NAFLD (P=0.05), but not NAFL. Plasma EDA levels were increased in NAFL and NASH compared with No NAFLD (P=0.03). Plasma EDA was related to worsening steatosis (P=0.02) and fibrosis (P=0.04), but not inflammation or hepatocellular ballooning. ROC analysis indicates that plasma EDA is not a reliable biomarker for NAFL or NASH. Plasma EDA was not increased in patients with type 2 diabetes and did not correlate with insulin resistance. Together, we show that plasma EDA is increased in NAFL and NASH, is related to worsening steatosis and fibrosis but is not a reliable biomarker for NASH. Circulating EDA is not associated with insulin resistance in human obesity. Clinical Trial Registration: https://www.anzctr.org.au/Trial/Registration/TrialReview.aspx?ACTRN=12615000875505, identifier ACTRN12615000875505.

Diagnostic Criteria for Gastro-esophageal Reflux Following Sleeve Gastrectomy.

BACKGROUND: Gastro-esophageal reflux disease (GERD) post-sleeve gastrectomy (SG) is a controversial issue and diagnostic dilemma. Strong heterogeneity exists in the assessment of reflux post-SG, and better diagnostic tools are needed to characterize symptomatic reflux. We aimed to determine the discriminant factors of symptomatic reflux and establish diagnostic thresholds for GERD following SG. MATERIALS AND METHODS: Patients post-SG were categorized into asymptomatic and symptomatic cohorts and completed validated symptom questionnaires. All patients underwent stationary esophageal manometry and 24-h ambulatory pH monitoring. Univariate and multivariate analyses were conducted to determine the strongest discriminant factors for GERD. RESULTS: Baseline characteristics of the asymptomatic cohort (n = 48) and symptomatic cohort (n = 76) were comparable. The median post-operative duration was 7.3 (14.1) vs 7.5 (10.7) months (p = 0.825). The symptomatic cohort was more female predominant (90.8 vs 72.9%, p = 0.008). Reflux scores were significantly higher in the symptomatic group (36.0 vs 10.5, p = 0.003). Stationary manometry parameters were similar, including hiatus hernia prevalence and impaired esophageal motility. The symptomatic cohort had significantly higher total acid exposure, especially while supine (11.3% vs 0.6%, p < 0.001). Univariate and multivariate regressions delineated reflux score and supine acid exposure as discriminant factors for symptomatic reflux. The thresholds for distinguishing symptomatic reflux are as follows: reflux score of 11.5 (sensitivity 84.0%, specificity 68.2%) and supine acid exposure of 2.65% (sensitivity 67.1%, specificity 70.8%). CONCLUSION: A reflux score of 11.5 or more or supine acid exposure of 2.65% or more should be considered diagnostic in defining symptomatic reflux following SG.

Single Anastomosis Duodenal-Ileal Bypass with Sleeve Gastrectomy/One Anastomosis Duodenal Switch (SADI-S/OADS) IFSO Position Statement-Update 2020.

PreambleThe International Federation for the Surgery of Obesity and Metabolic Disorders (IFSO) has played an integral role in educating both the metabolic surgical and the medical communities at large about the role of innovative and new surgical and or endoscopic interventions in treating adiposity-based chronic diseases. The single anastomosis duodenal-ileal bypass with sleeve gastrectomy/one anastomosis duodenal switch (SADI-S/OADS) is a relatively new procedure that has been proposed as an alternative to the conventional duodenal switch (DS) procedure. The IFSO published a position paper on SADI-S/OADS in 2018 with which concluded that this procedure was likely to be a safe and efficacious treatment for adiposity and its related diseases. However, it noted that there was insufficient long-term data and minimal high-level evidence available. The position statement called for patients to be enrolled in long-term multidisciplinary care encouraged the registration of patients in national registries, and called for more randomized controlled trials (RCT) (Obes Surg 28:1207-16, 2018) involving the procedure. The following position statement is an update of the previous position statement. It is issued by the IFSO SADI-S/OADS task force and has been reviewed and approved by both the IFSO Scientific Committee and Executive Board. This statement is based on current clinical knowledge, expert opinion, and published peer-reviewed scientific evidence. It will be reviewed again in 2 years.

Evaluation of the histological variability of core and wedge biopsies in nonalcoholic fatty liver disease in bariatric surgical patients.

BACKGROUND: Liver biopsy remains the gold standard for characterizing and evaluating treatment response in nonalcoholic fatty liver disease (NAFLD). Liver heterogeneity and sampling variability can affect the reliability of results. This study aimed to compare histological variability of intraoperative wedge and core liver biopsies from different lobes in bariatric patients, to better inform surgeons on biopsy method and guide interpretation of results. METHODS: We prospectively recruited bariatric surgical patients. Intraoperative core biopsies were taken from the left and right lobe, with a wedge biopsy taken from the left. All biopsies were graded by a specialist liver pathologist, blinded to clinical details and biopsy site. Concordance of histological findings between sites was evaluated. RESULTS: There were 91 participants (72.2% female), mean age 46.8 ± 12.0 years, body mass index 45.9 ± 9.4 kg/m2. There was no significant pattern for up- or down-grading disease dependent on biopsy technique. Moderate to strong agreement was seen in the presence of NAFLD and nonalcoholic steatohepatitis (NASH, κ = 0.609-0.865, p < 0.001) between biopsy sites. Individual components (steatosis, inflammation, ballooning) showed weaker agreement (κ = 0.386-0.656, p < 0.01). Fibrosis showed particularly poor agreement (κ = 0.223-0.496, p < 0.01). Detection of pathology improved with a combination of biopsy techniques, compared to a single biopsy method. CONCLUSION: Overall diagnosis of NAFLD or NASH shows good agreement between biopsy sites, but individual components, particularly fibrosis stage, vary significantly. Clinicians should consider biopsies from varied sites, to better assess liver disease severity. These data have important implications in fibrosis assessment of NAFLD and are relevant in the interpretation of histological efficacy of investigational pharmacotherapies. TRIAL REGISTRATION: ACTRN12615000875505 (Australian Clinical Trials Register).

Mechanisms of Esophageal and Gastric Transit Following Sleeve Gastrectomy.

PURPOSE: Sleeve gastrectomy (SG) patients have substantially altered anatomy. The mechanism of rapid gastric emptying and the role of esophageal contractile function in esophago-gastric transit has not been defined. We aimed to determine the mechanisms of esophago-gastric transit and role of esophageal function following sleeve gastrectomy. METHODS: Prospective study of twenty-six asymptomatic participants post SG underwent nuclear scintigraphy and high-resolution manometry. Fourteen had semi-solid stress barium to model the emptying process. Concurrent video fluoroscopy and manometry were performed on 7 participants. RESULTS: Demographic data are as follows: age 45.3 ± 15.0 years, 73.1% female, excess weight loss 62.2 ± 28.1% at 8 months. Scintigraphy showed rapid gastric emptying (24.4 ± 11.4 vs. 75.80 ± 45.19 min in control, p < 0.001) with 35.24 ± 17.12% of bolus transited into small bowel on initial frame. Triggered deglutitive reflux was common (54.4% vs. 18.2%, p = 0.017). Stress barium delineated separate vertical and antral gastric compartments with cyclical emptying of 8 stages, including reflux-induced repeated esophageal peristalsis. During manometry, ramping effects were noted, with sequential swallows producing sustained isobaric pressurizations in proximal stomach (33.6 ± 29.5 mmHg). Video fluoroscopy showed individual esophageal peristalsis generating pressurizations at 5.0 ± 1.4 cm below lower esophageal sphincter (LES), at amplitude of 31.6 ± 13.1 mmHg, associated with intragastric transit. Pressurizations were sustained for 17.3 ± 8.2 s, similar to the prolonged LES contraction (18.5 ± 9.0 s, p = 0.355). CONCLUSIONS: Repeated esophageal peristaltic contractions induced isobaric pressurization of proximal stomach, thus providing the drive to pressurize and empty the vertical compartment of the gastric sleeve. Transit following SG appeared to be esophageal-mediated and followed a distinct cycle with strong associations with reflux.

Perioperative screening, management, and surveillance of Barrett's esophagus in bariatric surgical patients.

Obesity is a strong risk factor for Barrett's esophagus (BE), the only proven precursor lesion to esophageal adenocarcinoma (EAC). Bariatric surgery is currently the only reliable treatment that achieves long-term sustained weight loss; however, it can markedly affect the development of de novo BE, and the progression or regression of existing BE. Bariatric procedures may also have implications on future surgical management of any consequent EAC. In this review, we examine the current evidence and published guidelines for BE in bariatric surgery. Current screening practices before bariatric surgery vary substantially, with conflicting recommendations from bariatric societies. If diagnosed, the presence of BE may alter the type of bariatric procedure. A selective screening approach prevents unnecessary endoscopy; however, there is poor symptom correlation with disease. Studies suggest that sleeve gastrectomy predisposes patients to gastroesophageal reflux and de novo BE. Conversely, Roux-en-Y gastric bypass is associated with decreased reflux and potential improvement or resolution of BE. There are currently no guidelines addressing the surveillance for BE following bariatric surgery. BE is an important consideration in the management of bariatric surgical patients. Evidence-based recommendations are required to guide procedure selection and postoperative surveillance.

Impact of human visceral and glutealfemoral adipose tissue transplant on glycemic control in a mouse model of diet-induced obesity.

Regional distribution of adipose tissue is an important factor in conferring cardiometabolic risk and obesity-related morbidity. We tested the hypothesis that human visceral adipose tissue (VAT) impairs glucose homeostasis, whereas subcutaneous glutealfemoral adipose tissue (GFAT) protects against the development of impaired glucose homeostasis in mice. VAT and GFAT were collected from patients undergoing bariatric surgery and grafted onto the epididymal adipose tissue of weight- and age-matched severe, combined immunodeficient mice. SHAM mice underwent surgery without transplant of tissue. Mice were fed a high-fat diet after xenograft. Energy homeostasis, glucose metabolism, and insulin sensitivity were assessed 6 wk later. Xenograft of human adipose tissues was successful, as determined by histology, immunohistochemical evaluation of collagen deposition and angiogenesis, and maintenance of lipolytic function. Adipose tissue transplant did not affect energy expenditure, food intake, whole body substrate partitioning, or plasma free fatty acid, triglyceride, and insulin levels. Fasting blood glucose was significantly reduced in GFAT and VAT compared with SHAM, whereas glucose tolerance was improved only in mice transplanted with VAT compared with SHAM mice. This improvement was not associated with differences in whole body insulin sensitivity or plasma insulin between groups. Together, these data suggest that VAT improves glycemic control and GFAT does not protect against the development of high-fat diet-induced glucose intolerance. Hence, the intrinsic properties of VAT and GFAT do not necessarily explain the postulated negative and positive effects of these adipose tissue depots on metabolic health.

Colorectal peritoneal metastases: pathogenesis, diagnosis and treatment options - an evidence-based update.

Peritoneal metastases confer the worst survival among all sites in patients with metastatic colorectal cancer. They develop largely through transcoelomic spread, with a sequence of events that allow cells to first detach from primary tumours, survive in the peritoneal environment, attach to the peritoneal surface of organs and migrate into the submesothelial space to create a microenvironment conducive to metastatic growth. Diagnostic challenges have previously hindered early identification of peritoneal metastases. While advances in diagnostic modalities have improved our ability to identify peritoneal metastases, lesions under 0.5 cm remain challenging to detect. The advent of cytoreductive surgery with hyperthermic intraperitoneal chemotherapy (HIPEC) can offer selected patients with colorectal peritoneal metastases a favourable long-term survival. Recent trials, however, have cast doubts on the efficacy of HIPEC, with the recent PRODIGE 7 trial showing no benefit from oxaliplatin based HIPEC in addition to good quality cytoreductive surgery in resectable disease. While peritoneal recurrence can be reliably predicted from high-risk features in primary tumours such as a perforated cancer, ovarian metastases or T4a cancers, the use of prophylactic second look surgery with HIPEC or adjuvant HIPEC failed to demonstrate any survival benefit in high-risk cases in recent clinical trials, raising further questions about the efficacy of HIPEC. With high failure rates from systemic chemotherapy in unresectable disease, novel surgical techniques such as pressurized intraperitoneal aerolized chemotherapy are being investigated in clinical trials worldwide. Further collaborative research is needed to explore newer avenues of treatment for this poor prognostic cohort.

Long-Term Matched Comparison of Adjustable Gastric Banding Versus Sleeve Gastrectomy: Weight Loss, Quality of Life, Hospital Resource Use and Patient-Reported Outcome Measures.

BACKGROUND: Comparisons of bariatric procedures across a range of outcomes are required to better inform selection of procedures and optimally allocate health care resources. AIMS: To determine differences in outcomes between laparoscopic adjustable gastric banding (LAGB) and laparoscopic sleeve gastrectomy (LSG) across nine outcome domains. METHODS: Matched primary LSG or LAGB across age, weight and surgery date were recruited. Data were collected from a prospective database and patient-completed questionnaires. RESULTS: Patients (n = 520) were well-matched (LAGB vs. LSG; age 41.8 ± 11.2 vs. 42.7 ± 11.7 years, p = 0.37; male 32.4% vs. 30.2%, p = 0.57; baseline weight 131.2 ± 30.5 vs. 131.0 ± 31.1 kg, p = 0.94). Follow-up rate was 95% at a mean of 4.8 years. LAGB attended more follow-up visits (21 vs. 13, p < 0.05). Mean total body weight loss was 27.7 ± 11.7% vs. 19.4 ± 11.1% (LSG vs. LAGB, p < 0.001). LAGB had more complications (23.8% vs. 10.8%, p < 0.001), re-operations (89 vs. 13, p < 0.001) and readmissions (87 vs. 32, p < 0.001). However, early post-operative complications were higher post-LSG (2.6 vs. 9.2%, p = 0.007). Length of stay (LOS) was higher post-LSG compared with LAGB (5.2 ± 10.9 vs. 1.5 ± 2.2 days, p < 0.001). LSG patients reported better quality of life (SF-36 physical component score 54.7 ± 7.9 vs. 47.7 ± 10.8, p = 0.002) and satisfaction (9.2 ± 1.9 vs. 8.4 ± 1.6, p = 0.001) and less frequent regurgitation (1.2 ± 1.2 vs. 0.7 ± - 1.1, p = 0.032) and dysphagia (2.0 ± 1.3 vs. 1.3 ± 1.6, p = 0.007). CONCLUSION: This study showed high long-term follow-up rates in a large cohort of well-matched patients. Weight loss was greater with LSG. LAGB reported more re-operations and less satisfaction with the outcome. LOS was driven by patients with complications. This study has reinforced the need for comprehensive measurement of outcomes in bariatric surgery.

Correction to: Improving Compliance with Very Low Energy Diets (VLEDs) Prior to Bariatric Surgery-A Randomized Controlled Trial of Two Formulations.

In the original article the name of author Alexandra Klejn was misspelled.