Child ; Humans ; Intestinal Polyps ; genetics ; Molecular Biology

Child ; Gastroesophageal Reflux ; diagnosis ; therapy ; Humans

Bilirubin ; Child ; Duodenogastric Reflux ; diagnosis ; Esophageal Diseases ; diagnosis ; Esophagus ; metabolism ; Gastroesophageal Reflux ; diagnosis ; Humans

Adolescent ; Bilirubin ; metabolism ; Child ; Child, Preschool ; Duodenogastric Reflux ; metabolism ; Esophageal pH Monitoring ; Female ; Humans ; Male ; Stomach ; physiopathology

The manifestations of pediatric gastroesohageal reflux (GER) are varied and complex. Extra-oesophageal symptoms, including GER-related respiratory diseases, ear, nose and throat diseases, oral diseases and neuropsychiatric symptoms, are thought to be major manifestations of pediatric GER, but the causal relationship between GER and these extra-oesophageal symptoms is still unclear. Therefore, we describe the progress of research on the relationship between GER and asthma, chronic cough, laryngitis, pharyngitis, laryngeal papilloma, sinusitis, otitis media, dental erosion, apparent life-threatening event, and the crying baby syndrome in this review. It provides new strategies for the diagnosis and treatment of GER-related diseases in children.
Asthma ; etiology ; Cough ; etiology ; Gastroesophageal Reflux ; complications ; Humans ; Laryngitis ; etiology ; Sinusitis ; etiology ; Tooth Erosion ; etiology

Gastroesophageal reflux (GER) and cow's milk allergy (CMA) are common disorders in infants. In recent years, more and more research has investigated the relationship between these two diseases. Some studies reported that about half of the cases of GER in infants younger than 1 year may be an association with CMA. Therefore, overall understanding the role of CMA on the pathogenesis of GER has a great importance on improving clinical level of diagnosis and therapy. This review article tried to elaborate advances in research on the relationship between CMA and GER in infants, including epidemiology, pathogenesis, clinical manifestations, diagnosis and treatment.
Gastroesophageal Reflux ; diagnosis ; etiology ; Humans ; Infant ; Milk Hypersensitivity ; complications

Helicobacter pylori (Hp) infection is an important cause of chronic gastritis and peptic ulcer, but their pathogenesis is unclear. The role of gastric mucosal barrier dysfunction induced by impaired structure and function of tight junction in the pathogenesis of Hp-associated gastric diseases has received considerable attention in recent years. Tight junction is composed of a variety of proteins and molecules, including 3 integral membrane proteins (occludin, claudins, and junctional adhesion molecules) and a cytoplasmic protein (zonula occludens). This paper mainly describes the composition and function of various tight junction proteins, changes in tight junction protein function induced by Hp infection and their relationship with the incidence of gastric diseases, and the significance of enhancing the tight junction protein function in the prevention and treatment of Hp-associated gastric diseases.
Helicobacter Infections ; complications ; Helicobacter pylori ; pathogenicity ; Humans ; Oxidative Stress ; Stomach Diseases ; etiology ; Stomach Neoplasms ; etiology ; Tight Junction Proteins ; analysis ; chemistry ; physiology

Zinc oxide nanoparticle (nano-ZnO) has a size between 1 and 100 nm. Nano-ZnO has some special effects, such as small size effect, surface effect, quantum size effect, which makes it different from the ordinary ZnO, and is widely used in rubber industry, food processing, cosmetics and pharmaceutical fields. It has been reported that nano-ZnO has toxic effects in vitro and in vivo, but the mechanism of toxicity is still unclear. Therefore, it is important to evaluate the safety nano-ZnO by studying its biological toxic effects and related mechanisms. In this paper, we summarize the characterization, ingestion pathway, metabolism, systematic toxicity of nano-ZnO and its mechanisms, which may provide us with new strategy for the toxic research of nano-ZnO.
Animals ; Humans ; Metal Nanoparticles ; toxicity ; Zinc Oxide ; toxicity

OBJECTIVEDuodenogastric reflux (DGR) is a reverse flow of duodenal juice into stomach through pylorus composed of bile acid, pancreatic secretion, and intestinal secretion. The increased entero-gastric reflux results in mucosal injury that may relate not only to reflux gastritis but also esophagitis, gastric ulcers, carcinoma of stomach and esophagus. However, the exact mechanisms of gastric mucosal damage caused by DGR are still unknown. The objective of the present study is to investigate the pathogenic effect of primary DGR on gastric mucosa in children, and to explore the correlation of DGR with clinical symptoms, Hp infection and intragastric acidity.

METHODTotally 81 patients with upper gastrointestinal manifestations were enrolled and they were graded according to the symptom scores and underwent endoscopic, histological examinations and 24-hour intra-gastric bilirubin was monitored with Bilitec 2000. Of the 81 cases, 51 underwent the 24-hour intra-gastric pH monitoring by ambulatory pH recorder simultaneously. The total fraction time of bile reflux was considered as a marker to evaluate the severity of DGR. The total fraction time of bile reflux was compared between the patients with positive and negative results under endoscopy and histologically, respectively. The correlations of the total fraction time of bile reflux with clinical symptom score, Hp infection, intragastric acidity were analyzed respectively.

RESULTThe total fraction time of bile reflux in the patients with hyperemia and yellow stain gastric antral mucosa under endoscopy was significantly higher than that without those changes [17.1% (0.5% approximately 53.2%) vs. 6.5% (0 approximately 58.6%), Z = -1.980, P < 0.05; 19.8% (0.5% approximately 58.6%) vs. 8.8% (0 approximately 38.0%), Z = -2.956, P < 0.01 respectively]. Histologically, the cases with intestinal metaplasia had significantly higher total fraction time of bile reflux than in the cases without intestinal metaplasia [29.0% (1.9% approximately 58.6%) vs. 14.3% (0 approximately 53.7%), Z = -2.026, P < 0.05], but no significant difference was found either between the cases with and without chronic inflammation (P > 0.05) or between the cases with and without active inflammation (P > 0.05). The severity of bile reflux was positively correlated with the score of abdominal distention (r = 0.258, P < 0.05), but no correlation with either the severity of intragastric acid (r = -0.124, P > 0.05), or Hp infection (r = 0.016, P > 0.05) was found.

CONCLUSIONPrimary DGR could cause gastric mucosal lesions manifested mainly as hyperemia and bile-stained gastric antral mucosa under endoscopy and the gastric antral intestinal metaplasia histologically in children. There was no significant correlation between DGR and gastric mucosal inflammatory infiltration. DGR had no relevance to Hp infection and intragastric acidity. We conclude that DGR is probably an independent etiological factor and might play a synergistic role in the pathogenesis of gastric mucosal lesions along with gastric acid and Hp infection.

Adolescent ; Bile Reflux ; pathology ; physiopathology ; Child ; Child, Preschool ; Duodenogastric Reflux ; microbiology ; pathology ; physiopathology ; Female ; Gastric Mucosa ; microbiology ; pathology ; Helicobacter Infections ; Helicobacter pylori ; Humans ; Hydrogen-Ion Concentration ; Male