United European Gastroenterology Journal

Endoscopic resection (ER) with or without ablation is the first choice treatment for early Barrett’s neoplasia. Adequate staging is important to assure a good oncological outcome.

The purpose of this study was to investigate the diagnostic accuracy of pre-operative biopsies in patients who undergo ER for high-grade dysplasia (HGD) or early adenocarcinoma (EAC) in Barrett’s oesophagus (BE) and the cardia.

Between November 2005–May 2012, 142 ERs performed in 137 patients were obtained. Worst pre-ER and ER histology were compared. Upgrading/downgrading was defined as any more/less severe histological grading on the ER specimen.

The accuracy of pre-ER biopsies in predicting final histology was 61%. ER changed the pre-treatment diagnosis in 55 of the 142 procedures (39%) with downgrading in 23 cases (16%) and upgrading from HGD to T1a or T1b in 32 cases (23%). In the majority of upgraded cases, a visible lesion according to the Paris classification could be detected (26/32, 81%).

The diagnostic accuracy of oesophageal biopsies alone in predicting final pathology in Barrett’s dysplasia is only 61%. The majority of upgraded lesions are detectable. When ablative therapy is considered in HGD Barrett's dysplasia a meticulous inspection for and removal of all small visible lesions is mandatory.

Low bone mineral density (BMD) remains a frequent problem in patients with inflammatory bowel diseases (IBD). There is no general agreement regarding osteoporosis screening in IBD patients.

Cases of low BMD and disease characteristics were retrieved from 3172 patients of the Swiss IBD cohort study. Multivariate logistic regression analysis was conducted for predictive modeling. In a subgroup of 877 patients, 253 dual-energy X-ray absorptiometry (DXA) scans were available for validation.

Low BMD was prevalent in 19% of patients. We identified seven predictive factors: type of IBD, age, recent steroid usage, low body mass index, perianal disease, recent high disease activity and malabsorption syndrome. Low BMD could be predicted with a sensitivity of 79% and a specificity of 64%, a positive predictive value (PPV) of 35% and a negative predictive value (NPV) of 93%. The area under the curve of the receiver operating characteristics was 0.78. In the validation cohort we calculated a PPV of 26% and an NPV of 88%.

We provide a comprehensive analysis of risk factors for low BMD and propose a predictive model with seven clinical variables. The high NPV of models such as ours might help in excluding low BMD to prevent futile investigations.

Sphingosine kinase 1 (SphK1)/sphingosine-1-phosphate (S1P)/sphingosine-1-phosphate receptors (S1PRs) signaling plays a key role in inflammatory responses. Lei et al. showed that SphK1 inhibition presented a hepatoprotective effect on acute liver damage via decreasing hepatic high-mobility group box 1 (HMGB1) cytoplasmic translocation.

We aim to determine whether SphK1 or S1PRs inhibition improves lipopolysaccharide (LPS)/D-galactosamine (GalN)-induced acute liver failure by inhibiting the mitogen-activated protein kinases (MAPKs) pathway.

A mouse model of acute liver failure was induced by LPS/GalN. Male C57BL/6J mice (6–8 weeks) were randomly distributed into five groups: control group, LPS/GalN group, SphK1 inhibition group (LPS/GalN+SKI-5c), S1PR1 inhibition group (LPS/GalN+W146), and S1PR3 inhibition group (LPS/GalN+CAY10444).

We confirmed the findings of Lei et al. that hepatic SphK1 expression was upregulated; serum transaminase activity (AST, ALT), as well as serum TNF-α and IL-6, were decreased by SphK1 inhibition. We further showed that the expression of S1PR1 and S1PR3 was augmented in response to LPS/GalN. SphK1 inhibition improves hepatic hemorrhage, and the activities of hepatic caspase-3 and myeloperoxidase (MPO). Furthermore, the activation of the MAPKs family (JNK, ERK and p38) was suppressed by SphK1 inhibition. However, S1PR1 or S1PR3 inhibition did not protect the mouse against liver damage, though S1PR1 or S1PR3 inhibition reduced serum TNF-α and IL-6, and partially attenuated the phosphorylation of the MAPKs signaling.

SphK1 inhibition improves LPS/GalN-induced liver injury by inhibiting activation of MAPKs signaling.

In Western countries the prevalence of Helicobacter pylori (H. pylori) infection may be declining but there is a lack of recent longitudinal population studies. We evaluated the changing epidemiology over a 23-year period in Sweden.

In 1989, the validated Abdominal Symptom Questionnaire (ASQ) was mailed to a random sample of inhabitants (ages 22–80 years) in a Swedish community, and 1097 (87%) responded. H. pylori serology was analysed in a representative subsample (n = 145). Twenty-three years later, the ASQ was mailed again using similar selection criteria, and 388 out of 1036 responders had an upper endoscopy with assessment of H. pylori and corpus atrophy status.

The prevalence of positive H. pylori serology decreased from 37.9% (1989) to 15.8% (2012), corresponding to a decrease in odds of 75% per decade (odds ratio (OR): 0.25; 95% confidence interval (CI): 0.11–0.59, p = 0.001) independent of age, gender, body mass index (BMI) and level of education, with a pattern consistent with a birth cohort effect. The prevalence increased with increasing age (p = 0.001). The prevalence of H. pylori on histology in 2012 was 11.4% (95% CI 8.6–15.0). The prevalence of corpus atrophy on serology and/or histology in 2012 was 3.2% (95% CI 1.8–5.5); all cases were ≥57 years old.

The stomach is healthier in 2012 compared with 1989. H. pylori prevalence in adults has decreased over the last two decades to a level where clinical management might be affected.

Evidence on small intestinal bacterial overgrowth (SIBO) in patients with chronic pancreatitis (CP) is conflicting.

The purpose of this study was to perform a systematic review and meta-analysis on the prevalence of SIBO in CP and to examine the relationship of SIBO with symptoms and nutritional status.

Case-control and cross-sectional studies investigating SIBO in CP patients were analysed. The prevalence of positive tests was pooled across studies, and the rate of positivity between CP cases and controls was calculated.

In nine studies containing 336 CP patients, the pooled prevalence of SIBO was 36% (95% confidence interval (CI) 17–60%) with considerable heterogeneity (I²= 91%). A sensitivity analysis excluding studies employing lactulose breath test gave a pooled prevalence of 21.7% (95% CI 12.7–34.5%) with lower heterogeneity (I²= 56%). The odds ratio for a positive test in CP vs controls was 4.1 (95% CI 1.6–10.4) (I²= 59.7%). The relationship between symptoms and SIBO in CP patients varied across studies, and the treatment of SIBO was associated with clinical improvement.

One-third of CP patients have SIBO, with a significantly increased risk over controls, although results are heterogeneous, and studies carry several limitations. The impact of SIBO and its treatment in CP patients deserve further investigation.

The surgical treatment of diverticulitis is in a state of evolution. Clinicians across many disciplines need to counsel patients regarding surgical choices.

A systematic review and meta-analysis was conducted to determine the mortality and complication rates following surgery for diverticulitis in both the emergent and elective setting.

We searched PubMed, Embase and the Cochrane Central Register of Controlled Trials (CENTRAL) for relevant articles published from 1980 to 2012. The primary outcome of interest was the point estimate of mortality, following surgery for diverticulitis.

Of the 289 citations reviewed, we included 59 studies. Overall, the point estimate for mortality was 3.05%, with a 95% confidence intereval (CI) of 1.73–5.32 and p < 0.001. Mortality following emergent surgery was 10.64% (95% CI 7.95–14.11; p < 0.001), versus 0.50% (95% CI 0.46–0.54; p < 0.001) following elective operations. A laparoscopic approach had an estimated mortality of 0.75% (95% CI 0.35–1.58; p < 0.001), compared to an open surgical approach, which had a mortality of 4.69% (95% CI 2.29–9.36, p < 0.001). The mortality following a resection with primary anastomosis was 1.96% (95% CI 1.22–3.13; p < 0.001) and for the Hartmann’s procedure was 14.18% (95% CI 9.83–20.03; p < 0.001). A comparative analysis found that the risk of post-operative mortality was significantly higher following emergent surgery, compared to elective surgery (odds ratio (OR): 6.12 with 95% CI 1.62–23.10; p = 0.008; Q = 2.56, p = 0.46 and I²= 0); the open approach, compared to a laparoscopic approach (OR: 36.43 with 95% CI 9.94–133.6; p = 0.13; and Q = 2.79, p = 0.25 and I²= 28.26); and for Hartmann’s procedure, compared to primary anastomosis without diversion (OR: 25.45 with 95% CI 15.13–42.81, p < 0.001; and Q = 23.34, p = 0.14 and I²= 27.16). The overall reported post-operative complication rate was 32.64% (95% CI 27.43–38.32; p < 0.00). The overall surgical and medical complication rates were 18.96% and 13.93%, respectively.

Urgent surgical treatment of diverticulitis has a significant complication rate. Even elective surgery has a significant complication rate that needs to be considered when doing the clinical decision-making for recurrent diverticulitis.