Eosinophilic Enterocolitis: Gastric Outlet Obstruction.

Eosinophilic enterocolitis is a rare condition representing the least frequent manifestation of eosinophilic gastrointestinal disorders. We report a 49-year-old man who presented with abdominal pain, diarrhea, and intractable vomiting for 2 weeks. Abdominal computed tomography demonstrated gastric wall thickening with mural wall thickening of the small intestine and colon. Endoscopy revealed gastric outlet obstruction because of luminal stenosis from duodenal edema. Peripheral eosinophilia, endoscopic mucosal biopsies, and exclusion of differential diagnoses confirmed eosinophilic enterocolitis. The patient was successfully treated with a 4-week prednisone taper.

Temporal Trends in Incidence and Outcomes of Acute Pancreatitis in Hospitalized Patients in the United States From 2002 to 2013.

OBJECTIVES: We sought to examine temporal trends in incidence and outcomes of acute pancreatitis (AP) in hospitalized adult patients in the United States. METHODS: Subjects were obtained from the Healthcare Cost and Utilization Project-Nationwide Inpatient Sample database using International Classification of Diseases, Ninth Revision, Clinical Modification codes for the years 2002-2013. Incidence of AP, all-cause mortality, cost, and duration of hospitalization were assessed. RESULTS: We identified 4,791,802 cases of AP. A significant increase in the incidence of AP was observed from 9.48 cases per 1000 hospitalizations in 2002 to 12.19 per 1000 hospitalizations in 2013 (P < 0.001). In-hospital mortality decreased from 2.99 cases per 100 cases in 2002 to 2.04 cases per 100 cases in 2013 (P < 0.001). Mean length of stay decreased from 6.99 (standard deviation [SD], 9.37) days in 2002 to 5.74 (SD, 7.94) days in 2013 (P < 0.001). Cost of hospitalization increased from $27,827 (SD, $54,556) in 2002 to $49,772 (SD, $106,205) in 2013 (P < 0.001). CONCLUSIONS: Hospital admissions for AP in adults increased significantly in the United States from 2002 to 2013. In-hospital all-cause mortality and mean length of stay significantly decreased. In contrast, total cost of hospitalization rose.

Ulcerative Colitis in Colonic Interposition for Esophageal Atresia.

A 38-year-old male with a history of colonic interposition for esophageal atresia as an infant presented with dysphagia and abdominal pain. On the basis of endoscopy findings, pathology, and response to therapy, he was found to have ulcerative colitis of the colonic conduit.

Plasma citrulline concentration as a marker for disease activity in patients with Crohn's disease.

BACKGROUND: Citrulline is a nitrogen end product produced from the intermediary metabolism of glutamine through the enzymatically mediated urea cycle, almost exclusively in the enterocytes of small intestinal epithelium, with some synthesis in colonocytes. Intestinal dysfunction resulting from intestinal diseases or injuries affects intermediary metabolism, which includes citrulline synthesis. We sought to determine whether plasma citrulline was a biomarker for disease activity in patients with Crohn's disease with the hypothesis that citrulline concentration would be reduced during active disease. METHODS: A total of 81 outpatients aged 18 to 65 years (mean, 40.6±15.4 y) with a known history of Crohn's disease were studied prospectively. Patients with prior small intestinal resection, or renal or hepatic insufficiency were excluded. Crohn's disease activity was measured by Harvey-Bradshaw Index (HBI) and was correlated to the plasma citrulline concentration measured simultaneously (ion chromatography). Spearman correlation coefficients were used to assess for an association between the 2 variables. Subgroup analyses of patients with isolated small intestinal disease and endoscopically or radiologic verified disease activity were also performed. RESULTS: Twenty-two patients had isolated colonic disease and 59 had small intestinal involvement. Twenty-six of these patients had concurrent endoscopy and/or computed tomography or magnetic resonance imaging. On the basis of HBI scores, 32 patients had active disease (HBI ≥5) and 49 patients had inactive disease. The mean HBI scores were 4.8±5.5. The mean plasma citrulline concentration was normal, although was below normal in some patients. However, it failed to distinguish between active and inactive patients based on the HBI (active 27.8±8.8 µmol/L, inactive 27.8±11.1 µmol/L, P=0.991). There was no significant linear association between the ranks of citrulline and ranks of HBI (rs=0.012, P=0.915). Of the 59 patients with isolated small intestinal disease, there was no association between plasma citrulline concentration and the HBI (Spearman correlation coefficient, 0.073; P=0.583). There was no difference in plasma citrulline concentrations among those with confirmed inflammation by imaging or endoscopy (confirmed, 26.2±11.8; negative, 28.0±10.0; independent t test P=0.583). CONCLUSIONS: Plasma citrulline concentration was not a marker of disease activity in patients with Crohn's disease. However, all patients studied were outpatients and it is possible that plasma citrulline concentration may be depressed only in patients with more severe disease or extensive small bowel involvement. In addition, plasma citrulline may be increased in the postabsorptional state, and for the most part, our patients were nonfasting. More studies are needed to further elucidate the role of citrulline as a marker of disease activity in patients with Crohn's disease. The possibility also exists that citrulline may be a better marker in patients with previous resection, and this group will require specific evaluation.

Serum B12 concentration is elevated in patients receiving chronic parenteral nutrition, but is not a marker of intestinal failure-associated liver disease.

BACKGROUND: Cobalamin is released during hepatic cytolysis associated with liver injury. Serum B12 concentration is frequently elevated in patients that receive long-term parenteral nutrition (PN). We hypothesized that serum B12 concentration would become elevated in intestinal failure-associated liver disease and would reflect in disease severity. METHODS: We retrospectively evaluated 13 patients with short bowel syndrome (<200 cm residual small intestine) that included complete terminal ileum resection (3 male and 10 female, aged 42 to 78 y) that had received parenteral nutrition (PN) 6.1+/-3 years. All 13 patients had received at least 1 liver biopsy for presumed intestinal failure-associated liver disease. At the time of biopsy, patients had received PN between 2 and 7 days a week (4.7+/-1.9 d). The liver biopsies were evaluated and prospectively scored for pathology using 3 independent scoring systems validated for nonalcoholic steatohepatitis and nonalcoholic fatty liver disease [Brunt, NAFLD activity score (NAS) and Dixon methods], whereby numeric values were assigned to degrees of steatosis, inflammation, and fibrosis. Serum B12 concentration and hepatic chemistries (aspartate transaminase, alanine transaminase, alkaline phosphatase, and bilirubin) were recorded within 1 week of the biopsies. RESULTS: Thirteen biopsies were available for analysis. Serum B12 concentration and hepatic chemistries were available for all biopsy times. The mean serum B12 concentration was 619+/-222 pg/mL. The mean daily parenteral B12 dose was 3.3+/-1.3 mcg. Mean NAS, Brunt, and Dixon scores were 2, 1, and 1, respectively. The Spearman correlation coefficients between serum B12 concentration and liver biopsy scores were 0.15, 0.1, and 0.1 for the NAS, Brunt, and Dixon scores, respectively, indicating that there was no correlation between serum B12 concentration and liver pathology. The Spearman correlation coefficient between the NAS inflammation subscore and serum B12 concentration was 0.02. B12 concentration also failed to correlate with hepatic chemistries. There was surprisingly little correlation between serum B12 concentration and exogenous B12 daily dose through PN (r=0.19, P=0.45). CONCLUSIONS: Elevated serum B12 concentration is commonly encountered in patients who receive long-term parenteral nutrition. This does not seem to be an indicator of hepatic pathology; rather it may reflect the provision of excessive intravenous vitamin B12 and other as yet unknown factors.