Morbid obesity negatively influences inpatient hospitalization and is associated with adverse clinical outcomes, including mortality, organ failure, and health-care resource utilization. These observations and the increasing global prevalence of obesity justify ongoing efforts to understand the role of obesity-induced inflammation in the pathogenesis and management of AP.

AIMTo critically evaluate previous scientific evidence on Fusobacterium’s role in colorectal neoplasia development.METHODSTwo independent investigators systematically reviewed all original scientific articles published between January, 2000, and July, 2017, using PubMed, EMBASE, and MEDLINE. A total of 355 articles were screened at the abstract level. Of these, only original scientific human, animal, and in vitro studies investigating Fusobacterium and its relationship with colorectal cancer (CRC) were included in the analysis. Abstracts, review articles, studies investigating other colonic diseases, and studies written in other languages than English were excluded from our analysis. Ninety articles were included after removing duplicates, resolving disagreements between the two reviewers, and applying the above criteria.RESULTSStudies have consistently identified positive associations between Fusobacterium, especially Fusobacterium nucleatum (F. nucleatum), and CRC. Stronger associations were seen in CRCs proximal to the splenic flexure and CpG island methylator phenotype (CIMP)-high CRCs. There was evidence of temporality and a biological gradient, with increased F. nucleatum DNA detection and quantity along the traditional adenoma-carcinoma sequence and in CIMP-high CRC precursors. Diet may have a differential impact on colonic F. nucleatum enrichment; evidence suggests that high fiber diet may reduce the risk of a subset of CRCs that are F. nucleatum DNA-positive. Data also suggest shorter CRC and disease-specific survival with increased amount of F. nucleatum DNA in CRC tissue. The pathophysiology of enrichment of F. nucleatum and other Fusobacterium species in colonic tissue is unclear; however, the virulence factors and changes to the local colonic environment with disruption of the protective mucus layer may contribute. The presence of a host lectin (Gal-GalNAc) in the colonic epithelium may also mediate F. nucleatum attachment to CRC and precursors through interaction with an F. nucleatum protein, fibroblast activation protein 2 (FAP2). The clinical significance of detection or enrichment of Fusobacterium in colorectal neoplasia is ambiguous, but data suggest a procarcinogenic effect of F. nucleatum, likely due to activation of oncogenic and inflammatory pathways and modulation of the tumor immune environment. This is hypothesized to be mediated by certain F. nucleatum strains carrying invasive properties and virulence factors such as FadA and FAP.CONCLUSIONEvidence suggests a potential active role of Fusobacterium, specifically F. nucleatum, in CRC. Future prospective and experimental human studies would fill an important gap in this literature.

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Analysis of national level data demonstrates that morbidly obese patients have an increased CRC surgery peri-operative mortality with higher prevalence of co-morbidities, surgical complications, and more health care resource utilization. Future research efforts should concentrate on ameliorating these outcomes in morbidly obese patients.

OBJECTIVES: Strong evidence links obesity to esophageal cancer (EC), gastric cancer (GC), colorectal cancer (CRC), and pancreatic cancer (PC). However, national-level studies testing the link between obesity and recent temporal trends in the incidence of these cancers are lacking. METHODS: We queried the Surveillance, Epidemiology, and End Results (SEER) to identify the incidence of EC, GC, CRC, and PC. Cancer surgeries stratified by obesity (body mass index ≥30 kg/m2) were obtained from the National Inpatient Sample (NIS). We quantified trends in cancer incidence and resections in 2002–2013, across age groups, using the average annual percent change (AAPC). RESULTS: The incidence of CRC and GC increased in the 20–49 year age group (AAPC +1.5% and +0.7%, respectively, P < 0.001) and across all ages for PC. Conversely, the incidence of CRC and GC decreased in patients 50 years or older and all adults for EC. According to the NIS, the number of patients with obesity undergoing CRC resections increased in all ages (highest AAPC was +15.3% in the 18–49 year age group with rectal cancer, P = 0.047). This trend was opposite to a general decrease in nonobese patients undergoing CRC resections. Furthermore, EC, GC, and PC resections only increased in adults 50 years or older with obesity. DISCUSSION: Despite a temporal rise in young-onset CRC, GC, and PC, we only identify a corresponding increase in young adults with obesity undergoing CRC resections. These data support a hypothesis that the early onset of obesity may be shifting the risk of CRC to a younger age.

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ObjectiveWe investigated whether vertical sleeve gastrectomy (VSG) and Roux-en-Y gastric bypass surgery (RYGB) have a differential impact on post-operative risk of acute pancreatitis (AP).MethodsThis retrospective study uses the 2012–2014 National Readmission Database. We compared morbidly obese patients who underwent VSG (n = 205,251), RYGB (n = 169,973), and hernia repair (HR) control (n = 16,845). Our main outcome was rates of AP within 6 months post- vs. 6 months pre-surgery in VSG, RYGB, and HR. We also investigated risk factors and outcomes of AP after bariatric surgery.ResultsThe rates of AP increased post- vs. pre-VSG (0.21% vs. 0.04%; adjusted odds ratio [aOR] = 5.16, P < 0.05) and RYGB (0.17% vs. 0.07%; aOR = 2.26, P < 0.05) but not post-HR. VSG was associated with a significantly greater increase in AP risk compared to RYGB (aOR = 2.28; 95% CI: 1.10, 4.73). Furthermore, when compared to HR controls, only VSG was associated with a higher AP risk (aOR = 7.58; 95% CI: 2.09, 27.58). Developing AP within 6 months following bariatric surgery was mainly associated with younger age (18–29 years old: aOR = 3.76 for VSG and aOR: 6.40 for RYGB, P < 0.05) and gallstones (aOR = 85.1 for VSG and aOR = 46 for RYGB, P < 0.05). No patients developed “severe AP” following bariatric surgery.ConclusionsMore patients develop AP within 6 months after VSG compared to RYGB and controls. This risk is highest for younger patients and those with gallstones. Prospective studies examining mechanisms and prevention are warranted.

Prior bariatric surgery in patients hospitalized with AP is not adversely associated with in-hospital mortality, development of organ failure, or healthcare resource use. Bariatric surgery may mitigate the obesity-associated adverse prognostication in AP. These observations are pertinent for future research, because the prevalence of obesity and AP-related hospitalizations is increasing.