Min Yang

Sclerosing mesenteritis is a rare fibroinflammatory disorder of unknown etiology that primarily affects the mesentery of the small intestine during late adult life. Only about twenty pediatric cases have been reported to date, but none has been reported in Chinese children. A 5-year-old Chinese male presented with a 4-week history of recurrent bloating, abdominal pain, anorexia and vomiting. On admission, physical examination showed a severely distended abdomen. Biochemical investigations showed a slightly increased C-reactive protein, and normal serum levels of electrolytes and erythrocyte sedimentation rate. An abdominal film showed small intestine obstruction and massive ascites. An exploratory laparotomy revealed widespread inflammatory fibrotic adhesions between the bowel and the abdominal wall, thickening of the small bowel and massive ascites. During a prolonged hospital course, a 2nd surgery (4 months after 1st exploratory laparotomy) was performed in order to close the ileostomy and revealed that the bowel was still severely edematous, with very tight adhesions between the bowel and the abdominal wall. Histopathological examination of excised mesentery and nodules showed chronic inflammatory cell infiltration, fat necrosis and fibrosis. A diagnosis of sclerosing mesenteritis was finally established. Prednisolone at 2 mg/kg was started and he experienced rapid clinical improvement in 4 weeks. Sclerosing mesenteritis is extremely rare in children and often misdiagnosed due to its nonspecific clinical manifestation. It is important to be aware of sclerosing mesenteritis when evaluating a child with intractable abdominal pain, bloating, intestinal obstruction and massive ascites.

With increasing prevalence of childhood obesity, non-alcoholic fatty liver disease (NAFLD) has emerged as the most common cause of liver disease among children and adolescents in industrialized countries. It is generally recognized that both genetic and environmental risk factors contribute to the pathogenesis of NAFLD. Recently, there has been a growing body of evidence to implicate altered gut microbiota in the development of NAFLD through the gut-liver axis. The first line of prevention and treatment of NAFLD in children should be intensive lifestyle interventions such as changes in diet and physical activity. Recent advances have been focused on limitation of dietary fructose and supplementation of antioxidants, omega-3 fatty acids, and prebiotics/probiotics. Convincing evidences from both animal models and human studies have shown that reduction of dietary fructose and supplement of vitamin E, omega-3 fatty acids, and prebiotics/probiotics improve NAFLD.

Congenital sucrase-isomaltase deficiency (CSID) is a rare genetic disorder. The prevalence of CSID in Chinese population is unknown and no single case has been reported. Sucrose tolerance tests were performed in three children suspected of CSID. Glucose tolerance tests were performed to exclude glucose malabsorption. Blood glucose was measured at fasting and at 30 min, 60 min, 120 min, and 180 min of the study. Gastrointestinal symptoms were recorded up to 4 hours after the study. From December 2008 to June 2011, three children, ranging from 16 to 19 months old, were referred to our tertiary children’s hospital due to chronic watery diarrhea and failure to thrive. Laboratory investigations including complete blood counts, ESR, CRP, and serum immunoglobulins were normal. Routine stool culture for bacteria and exam for parasites were negative. Upper endoscopy, colonoscopy and histology were unremarkable. All children failed lactose-free and amino acid-based formulas. All three children had flat sucrose tolerance tests and began to have watery stool 2–4 hours after feeding sucrose test solution. The glucose tolerance tests were normal and no children developed watery stools up to 4 hours after feeding glucose test solution. This is the first case series of CSID in Chinese children. The diagnosis of CSID can be made based on clinical suspicion and sucrose tolerance test. CSID is probably an under-diagnosed or misdiagnosed disease in Chinese children and should be considered in children with chronic watery diarrhea.

Introduction: Duodenal duplication is a rare congenital malformation and has been reported as a rare cause of recurrent acute pancreatitis. Hemorrhagic ascites has been reported in only one case of duodenal duplication. Case presentation: An 11-year-old Chinese girl presented with abdominal pain, hematemesis and dark stools. On admission, an abdominal examination revealed a moderately distended abdomen with diffuse tenderness. Biochemical investigations showed increased serum levels of amylase, lipase, and urine amylase. An abdominal computed tomography scan and magnetic resonance imaging scan revealed an enlarged and heterogeneous pancreas with poorly delineated borders. There was a cystic lesion measuring 25mm × 48mm × 28mm, located between the descending portion of her duodenum and the head of her pancreas. There were massive effusion signals in her abdominal cavity. An exploratory laparotomy was performed. A tubular cyst measuring 32mm × 52mm × 30mm was found in the second part of the duodenum, next to the head of her pancreas. The anterior wall of the duplication cyst was resected and anastomosis of the remaining cyst to the duodenum was performed for drainage. Histopathological examination of the excised cyst wall showed duodenal mucosa, submucosa and muscle coats, indicative of a duodenal duplication. Conclusions: It is important to be aware of duodenal duplication when evaluating a patient with recurrent acute pancreatitis accompanied by massive hemorrhagic ascites.

Background: Numerous diagnostic tests are available to detect Helicobactor pylori (H. pylori). There has been no single test available to detect H. pylori infection reliably. We evaluated the accuracy of a new fluorescence quantitative PCR (fqPCR) for H. pylori detection in children. Methods: Gastric biopsy specimens from 138 children with gastritis were sent for routine histology exam, rapid urease test (RUT) and fqPCR. ¹³C-urea breath test (¹³C-UBT) was carried out prior to endoscopic procedure. Gastric fluids and dental plaques were also collected for fqPCR analysis. Results: 38 children (27.5%) were considered positive for H. pylori infection by gold standard (concordant positive results on 2 or more tests). The remaining 100 children (72.5%) were considered negative for H. pylori. Gastric mucosa fqPCR not only detected all 38 H. pylori positive patients but also detected 8 (8%) of the 100 gold standard-negative children or 11 (10.7%) of the 103 routine histology-negative samples. Therefore, gastric mucosa fqPCR identified 46 children (33.3%) with H. pylori infection, significantly higher than gold standard or routine histology (P13C-UBT alone or in combination to detect H. pylori infection in children with chronic gastritis. Either gastric fluid or dental plaque PCR is as reliable as ¹³C-UBT for H. pylori detection.