Risk factors for necrotizing enterocolitis in small-for-gestational-age infants: a matched case-control study.

Few studies have focused on the risk factors for necrotizing enterocolitis (NEC) in small for gestational age (SGA) infants. The aim of this study was to identify the risk factors for NEC in SGA newborns. This study included consecutive SGA neonates admitted to a tertiary hospital in Jiangxi Province, China from Jan 2008 to Dec 2022. Patients with NEC (Bell's stage ≥ II) were assigned to the NEC group. Gestational age- and birth weight-matched non-NEC infants born during the same period at the same hospital were assigned to the control group. The risk factors associated with NEC were analyzed with univariate and logistic regression models. During the study period, 2,912 SGA infants were enrolled, 150 (5.15%) of whom developed NEC. In total, 143 patients and 143 controls were included in the NEC and control groups, respectively. Logistic regression analysis revealed that sepsis (OR 2.399, 95% CI 1.271-4.527, P = 0.007) and anemia (OR 2.214, 95% CI 1.166-4.204, P = 0.015) might increase the incidence of NEC in SGA infants and that prophylactic administration of probiotics (OR 0.492, 95% CI 0.303-0.799, P = 0.004) was a protective factor against NEC. Therefore, sepsis, anemia and a lack of probiotic use are independent risk factors for NEC in SGA infants.

Butyrate protects the intestinal barrier by upregulating Fut2 expression via MEK4-JNK signaling pathway activation.

BACKGROUND: Necrotizing enterocolitis (NEC) is a severe gastrointestinal inflammatory disease in neonates. Fucosyltransferase 2 (Fut2) regulates intestinal epithelial cell fucosylation. In this study, we aimed to investigate butyrate-mediated upregulation of Fut2 expression and the underlying mechanisms. METHODS: In vivo and in vitro models were established. SP600125 was used to inhibit the MEK4-JNK pathway, and anisomycin was used to activate the MEK4-JNK pathway. Fut2, occludin, and ZO-1 expressions were assessed. Furthermore, intestinal permeability was analyzed by FITC-Dextran. The expression of proteins in the MEK-4-JNK pathway was examined by western blotting. RESULTS: In vivo, the addition of exogenous butyrate notably upregulated Fut2, occludin, and ZO-1 expressions and reduced intestinal permeability in mice with NEC. Butyrate may increase the phosphorylation of MEK4, JNK, and c-jun, which are key components of the MEK4-JNK pathway. Additionally, SP600125 inhibited their phosphorylation, which was reversed by anisomycin treatment. In vitro, butyrate substantially increased occludin and ZO-1 expressions. Butyrate considerably increased Fut2 expression and markedly upregulated p-MEK4, p-JNK, and p-c-jun expressions. SP600125 administration decreased their expressions, while anisomycin administration increased their expressions. CONCLUSION: Butyrate upregulated Fut2 expression via activation of the MEK4-JNK pathway, improved intestinal barrier integrity, and protected neonatal mice from NEC. IMPACT: We found that exogenous butyrate could improve intestinal barrier integrity and protect against NEC in neonatal mice. Our data showed that exogenous butyrate supplementation upregulated Fut2 expression by activating the MEK4-JNK pathway. Our study provides novel insights into the pathogenesis of NEC, thereby laying an experimental foundation for future clinical research on the use of butyrate in NEC treatment.

Acute esophageal obstruction caused by reverse migration of gastric bezoars: A case report.

BACKGROUND: Bezoars can be found anywhere in the gastrointestinal tract. Esophageal bezoars are rare. Esophageal bezoars are classified as either primary or secondary. It is rarely reported that secondary esophageal bezoars caused by reverse migration from the stomach lead to acute esophageal obstruction. Guidelines recommend urgent upper endoscopy (within 24 h) for these impactions without complete esophageal obstruction and emergency endoscopy (within 6 h) for those with complete esophageal obstruction. Gastroscopy is regarded as the mainstay for the diagnosis and treatment of esophageal bezoars. CASE SUMMARY: A 59-year-old man was hospitalized due to nausea, vomiting and diarrhea for 2 d and sudden retrosternal pain and dysphagia for 10 h. He had a history of type 2 diabetes mellitus for 9 years. Computed tomography revealed dilated lower esophagus, thickening of the esophageal wall, a mass-like lesion with a flocculent high-density shadow and gas bubbles in the esophageal lumen. On gastroscopy, immovable brown bezoars were found in the lower esophagus, which led to esophageal obstruction. Endoscopic fragmentation was successful, and there were no complications. The symptoms of retrosternal pain and dysphagia disappeared after treatment. Mucosal superficial ulcers were observed in the lower esophagus. Multiple biopsy specimens from the lower esophagus revealed nonspecific findings. The patient remained asymptomatic, and follow-up gastroscopy 1 wk after endoscopic fragmentation showed no evidence of bezoars in the esophagus or the stomach. CONCLUSION: Acute esophageal obstruction caused by bezoars reversed migration from the stomach is rare. Endoscopic fragmentation is safe, effective and minimally invasive and should be considered as the first-line therapeutic modality.