Rationale: In response to the global coronavirus infectious disease 2019 (COVID-19) pandemic, several vaccines against severe acute respiratory syndrome coronavirus 2 have been developed. Although many infrequent side effects of COVID-19 mRNA vaccine have been reported, only a few cases of pancreatitis have been reported. Patient concerns: A 71-year-old woman was presented to the hospital with upper abdominal pain and vomiting. She had no history of alcohol consumption, pancreatitis, or allergic reactions to vaccines. She had received the first dose of the Pfizer/BioNTech COVID-19 mRNA vaccine 2 days prior to her current presentation. Laboratory tests revealed elevated serum pancreatic enzymes. An abdominal computed tomography scan showed diffuse enlargement of the pancreas with fat stranding extending to below the kidneys bilaterally. Diagnosis: The patient was diagnosed with acute pancreatitis. Interventions: The patient was treated with the administration of intravenous antimicrobials, proteolytic enzyme inhibitors, and proton pump inhibitors. Outcomes: The patient had an uneventful recovery with no complications. Lessons: Acute pancreatitis can develop shortly after COVID-19 mRNA vaccination. Therefore, of great importance to differentiate acute pancreatitis when abdominal pain occurs after COVID-19 mRNA vaccination.

Chikungunya fever is a mosquito‐borne disease cause of persistent arthralgia. The current diagnosis of Chikungunya virus (CHIKV) relies on a conventional reverse transcription polymerase chain reaction assay. Reverse transcription loop‐mediated isothermal amplification (RT‐LAMP) is a rapid and simple tool used for DNA‐based diagnosis of a variety of infectious diseases. In this study, we established an RT‐LAMP system to recognize CHIKV by targeting the envelope protein 1 (E1) gene that could also detect CHIKV at a concentration of 8 PFU without incorrectly detecting other mosquito‐borne viruses. The system also amplified the E1 genome in the serum of CHIKV‐infected mice with high sensitivity and specificity. Moreover, we established a dry RT‐LAMP system that can be transported without a cold chain, which detected the virus genome in CHIKV‐infected patient samples with high accuracy. Thus, the dry RT‐LAMP system has great potential to be applied as a novel CHIKV screening kit in endemic areas.

Antibiotics sometimes exert adverse effects on the pathogenesis of colitis due to the dysbiosis resulting from the disruption of gut homeostasis. However, the precise mechanisms underlying colitogenic effects of antibiotic‐induced colitis are largely unknown. Here, we show a novel murine fecal occult bleeding model induced by the combinatorial treatment of ampicillin and vancomycin, which is accompanied by an enlarged cecum, upregulation of pro‐inflammatory cytokines IL‐6 and IL‐12, a reduction in Ki‐67‐positive epithelial cell number and an increase in the apoptotic cell number in the colon. Moreover, gas chromatography–tandem mass analysis showed that various kinds of metabolites, including glutamic acid and butyric acid, were significantly decreased in the cecal contents. In addition, abundance of butyric acid producer Clostridiales was dramatically reduced in the enlarged cecum. Interestingly, supplementation of monosodium glutamate or its precursor glutamine suppressed colonic IL‐6 and IL‐12, protected from cell apoptosis and prevented fecal occult blood indicating that the reduced level of glutamic acid is a possible mechanism of antibiotic‐induced fecal occult bleeding. Our data showed a novel mechanism of antibiotic‐induced fecal occult bleeding providing a new insight into the clinical application of glutamic acid for the treatment of antibiotic‐induced colitis.

Objectives. Differentiating gastrointestinal stromal tumor (GIST) from other submucosal tumors (SMTs) is important in diagnosing SMT. GIST is an immunohistological diagnosis that cannot be made from images alone. Tissue sampling of tumor sites is thus becoming increasingly important. In this study, the utility and associated complications of mucosal cutting biopsy (MCB) for gastric SMTs were investigated. Methods. This was a case series study. The subjects were patients aged ≥20 years old in whom an SMT was seen on esophagogastroduodenography and who underwent MCB between January 2012 and December 2016. Patient information, endoscopy findings, gastric SMT size, pathological diagnosis, and other information were gathered from medical records. The SMT size was the maximum diameter that could be visualized on EUS. The pathological diagnosis was made with hematoxylin-eosin staining, with immunostaining added to diagnose GIST. The endpoint was the histopathological diagnostic yield. Risk assessment using the Miettinen classification and modified Fletcher classification was also done for GISTs treated with surgery. Results. The mean tumor diameter was 15.4 mm. The tumor diameter was ≥20 mm in seven patients and <20 mm in 23 patients. The tissue-acquiring rate was 93.3%. A histological diagnosis could not be made in two patients. The only complication was that bleeding required endoscopic hemostasis during the procedure in one patient, but no subsequent bleeding or no postoperative bleeding was seen. Conclusions. MCB is an appropriate and safe procedure in the diagnosis of gastric SMTs. Many hospitals will be able to perform MCB if they have the environment, including skills and equipment, to perform endoscopic submucosal dissection.

Inflammatory bowel disease (IBD) is a chronic inflammatory disorder in the intestine, and the dysfunction of intestinal epithelial barrier (IEB) may trigger the onset of IBD. Secretory leukocyte protease inhibitor (SLPI) is a serine protease inhibitor that has been implicated in the tissue‐protective effect in the skin and lung. We found that SLPI was induced in lipopolysaccharides‐treated colon carcinoma cell line and in the colon of dextran sulfate sodium (DSS)‐treated mice. SLPI‐deficient mice were administered DSS to induce colitis and sustained severe inflammation compared with wild‐type mice. The colonic mucosa of SLPI‐deficient mice showed more severe inflammation with neutrophil infiltration and higher levels of proinflammatory cytokines compared with control mice. Moreover, neutrophil elastase (NE) activity in SLPI‐deficient mice was increased and IEB function was severely impaired in the colon, accompanied with the increased number of apoptotic cells. Importantly, we demonstrated that DSS‐induced colitis was ameliorated by administration of protease inhibitor SSR69071 and recombinant SLPI. These results suggest that the protease inhibitory activity of SLPI protects from colitis by preventing IEB dysfunction caused by excessive NE activity, which provides insight into the novel function of SLPI in the regulation of gut homeostasis and therapeutic approaches for IBD.