Metabolically Healthy Obesity and the Risk of Erosive Esophagitis: A Cohort Study OBJECTIVES: Obesity is an established risk factor of erosive esophagitis, and metabolic unhealthiness has been implicated in the pathogenesis of erosive esophagitis. Yet, the risk of erosive esophagitis among obese individuals without obesity-related metabolic unhealthiness, a condition referred to as “metabolically healthy obese (MHO)”, remains unclear. We examined the association between body mass index (BMI) categories and the development of erosive esophagitis in a cohort of metabolically healthy individuals. METHODS: We conducted a cohort study of 14,725 asymptomatic adults free of erosive esophagitis and metabolic abnormalities, who underwent repeated health checkups including screening endoscopy. A metabolically healthy state was defined as having no metabolic syndrome components and a homeostasis model assessment of insulin resistance <2.5. The presence of erosive esophagitis was determined using endoscopy. RESULTS: During 81,385.2 person-years of follow-up, 1,865 participants developed erosive esophagitis (incidence rate, 22.9 per 1,000 person-years). The multivariable adjusted hazard ratios (95% confidence intervals) for incident erosive esophagitis comparing overweight (BMI 23.0–24.9) and obese (≥25) with normal-weight participants (18.5–22.9) were 1.12 (1.00–1.25) and 1.29 (1.14–1.47), respectively. In dose-response analyses, increasing BMI also showed positive association with overall and LA-B grade or higher. The association persisted in MHO individuals without central obesity. The association between waist circumference categories and the development of erosive esophagitis was also evident. DISCUSSION: In a large cohort of strictly defined metabolically healthy men and women, the MHO phenotype was associated with an increased incidence of erosive esophagitis, providing evidence that the MHO phenotype is not protective from gastroesophageal reflux disease.

Long-Term Natural History of Microscopic Colitis: A Population-Based Cohort OBJECTIVES: Data on long-term natural history of microscopic colitis (MC), including collagenous (CC) and lymphocytic colitis (LC), are lacking. METHODS: All new cases of MC diagnosed in the Somme area, France, between January 1, 2005, and December 31, 2007, were prospectively included. Colonic biopsies from all patients were reviewed by a group of 4 gastrointestinal pathologist experts to assess the diagnosis of CC or LC. Demographic and clinical data were retrospectively collected from diagnosis to February 28, 2017. RESULTS: One hundred thirty cases of MC, 87 CC and 43 LC, were included (median age at diagnosis: 70 [interquartile range, 61–77] and 48 [IQR, 40–61] years, respectively). The median follow-up was 9.6 years (7.6; 10.6). By the end of the follow-up, 37 patients (28%) relapsed after a median time of 3.9 years (1.2; 5.0) since diagnosis, without significant difference between CC and LC (30% vs 26%; P = 0.47). Twenty patients (15%) were hospitalized for a disease flare, and 32 patients (25%) presented another autoimmune disease. Budesonide was the most widely used treatment (n = 74, 59%), followed by 5-aminosalicylic acid (n = 31, 25%). The median duration of budesonide treatment was 92 days (70; 168), and no adverse event to budesonide was reported. Sixteen patients (22%) developed steroid dependency and 4 (5%) were corticoresistant. No difference in the risk of digestive and extradigestive cancer was observed compared with the general population. None of the death (n = 25) observed during the follow-up were linked to MC. In multivariate analysis, age at diagnosis (HR, 1.03; 95% confidence interval, 1.00–1.06; P = 0.02) and budesonide exposure (HR, 2.50; 95% confidence interval, 1.11–5.55; P = 0.03) were significantly associated with relapse. DISCUSSION: This population-based study showed that after diagnosis, two-third of the patients with MC observed long-term clinical remission. Age at diagnosis and budesonide exposure were associated with a risk of relapse.

Development and Validation of a Model to Predict Acute Kidney Injury in Hospitalized Patients With Cirrhosis OBJECTIVES: Acute kidney injury (AKI) is a common complication in hospitalized patients with cirrhosis which contributes to morbidity and mortality. Improved prediction of AKI in this population is needed for prevention and early intervention. We developed a model to identify hospitalized patients at risk for AKI. METHODS: Admission data from a prospective cohort of hospitalized patients with cirrhosis without AKI on admission (n = 397) was used for derivation. AKI development in the first week of admission was captured. Independent predictors of AKI on multivariate logistic regression were used to develop the prediction model. External validation was performed on a separate multicenter cohort (n = 308). RESULTS: In the derivation cohort, the mean age was 57 years, the Model for End-Stage Liver Disease score was 17, and 59 patients (15%) developed AKI after a median of 4 days. Admission creatinine (OR: 2.38 per 1 mg/dL increase [95% CI: 1.47–3.85]), international normalized ratio (OR: 1.92 per 1 unit increase [95% CI: 1.92–3.10]), and white blood cell count (OR: 1.09 per 1 × 109/L increase [95% CI: 1.04–1.15]) were independently associated with AKI. These variables were used to develop a prediction model (area underneath the receiver operator curve: 0.77 [95% CI: 0.70–0.83]). In the validation cohort (mean age of 53 years, Model for End-Stage Liver Disease score of 16, and AKI development of 13%), the area underneath the receiver operator curve for the model was 0.70 (95% CI: 0.61–0.78). DISCUSSION: A model consisting of admission creatinine, international normalized ratio, and white blood cell count can identify patients with cirrhosis at risk for in-hospital AKI development. On further validation, our model can be used to apply novel interventions to reduce the incidence of AKI among patients with cirrhosis who are hospitalized.

Factors That Affect Prevalence of Small Intestinal Bacterial Overgrowth in Chronic Pancreatitis: A Systematic Review, Meta-Analysis, and Meta-Regression OBJECTIVES: Small intestinal bacterial overgrowth (SIBO) can complicate chronic pancreatitis (CP) and interfere with management. Its predisposing factors in CP and treatment response are unknown. In this review, we evaluated factors affecting disease burden. METHODS: A computerized search of PubMed and EMBASE databases from inception through May 2019 was done for studies correlating SIBO with CP. Studies were screened, and relevant data were extracted and analyzed. Pooled prevalence, odds ratio (OR), and meta-regression were performed using the random effects model as classically described by Borenstein et al. (2009). SIBO's relation to diabetes mellitus (DM), pancreatic exocrine insufficiency (PEI), narcotic use, and proton-pump inhibitor use was investigated. Treatment response was pooled across studies. P value < 0.05 was considered significant. RESULTS: In 13 studies containing 518 patients with CP, SIBO prevalence was 38.6% (95% confidence interval [CI] 25.5–53.5). OR for SIBO in CP vs controls was 5.58 (95% CI 2.26–13.75). Meta-regression showed that PEI and the diagnostic test used were able to explain 54% and 43% of the variance in SIBO prevalence across studies, respectively. DM and PEI were associated with increased SIBO in CP with OR (2.1, 95% CI 1.2–3.5) and OR (2.5, 95% CI 1.3–4.8), respectively. Symptomatic improvement was reported in 76% of patients after SIBO treatment. DISCUSSION: SIBO complicates 38% of CP with OR of 5.58 indicating a predisposition for this condition. PEI correlates with SIBO in CP and might play a role in pathophysiology. DM and PEI are associated with increased SIBO in CP. Treatment of SIBO may lead to symptomatic improvement.

Role of Autoimmune Gastritis in Gastric Cancer No abstract available

IgG4-Related Disease: A Growing Appreciation of Follicular Helper T Cell Expansion No abstract available