A Szarszewski1, M Korzon, B Kamiñska, P Lass. 1. Department of Paediatrics, Paediatric Gastroenterology and Oncology, Medical University of Gdañsk, ul. Nowe Ogrody 1/6, 80-803 Gdañsk, Poland.
Abstract
BACKGROUND: Duodenogastric reflux is believed to cause damage to gastric mucosa. Most reports on this disorder concern adult patients. PATIENTS AND METHODS: 1120 children with abdominal pain were studied; endoscopic features of duodenogastric reflux were found in 92 patients. To confirm the diagnosis of duodenogastric reflux, cholescintigraphy (Tc99-HEPIDA) was performed. Children with confirmed duodenogastric reflux by scintigraphy were given a prokinetic drug (cisapride). RESULTS: Endoscopic features of duodenogastric reflux were found in 92 children; the diagnosis was confirmed by scintigraphy in 59 patients. There was no significant difference in the severity of inflammation in gastric mucosa compared with the control group, whereas significantly fewer of these patients were infected with Helicobacter pylori. There was no correlation between regions of isotope accumulation and inflammatory lesions in the stomach. The prokinetic drug (cisapride) helped eliminate or greatly reduce duodenogastric reflux in children. CONCLUSIONS: When endoscopic features of duodenogastric reflux are found the final diagnosis should be based on an examination that does not itself influence the motility of the gastrointestinal tract: cholescintigraphy seems to be a useful method. However, because the use of milk as a test meal affects the scintigraphic image, there was no correlation between the area of isotope accumulation and the localisation of inflammatory lesions in the stomach. Duodenogastric reflux seems to be less important as a cause of inflammatory lesions than other factors (such as genetic predisposition, stress, etc). Prokinetic drugs have a beneficial influence on treatment results in children with inflammatory lesions of gastric mucosa with duodenogastric reflux.
BACKGROUND: Duodenogastric reflux is believed to cause damage to gastric mucosa. Most reports on this disorder concern adult patients. PATIENTS AND METHODS: 1120 children with abdominal pain were studied; endoscopic features of duodenogastric reflux were found in 92 patients. To confirm the diagnosis of duodenogastric reflux, cholescintigraphy (Tc99-HEPIDA) was performed. Children with confirmed duodenogastric reflux by scintigraphy were given a prokinetic drug (cisapride). RESULTS: Endoscopic features of duodenogastric reflux were found in 92 children; the diagnosis was confirmed by scintigraphy in 59 patients. There was no significant difference in the severity of inflammation in gastric mucosa compared with the control group, whereas significantly fewer of these patients were infected with Helicobacter pylori. There was no correlation between regions of isotope accumulation and inflammatory lesions in the stomach. The prokinetic drug (cisapride) helped eliminate or greatly reduce duodenogastric reflux in children. CONCLUSIONS: When endoscopic features of duodenogastric reflux are found the final diagnosis should be based on an examination that does not itself influence the motility of the gastrointestinal tract: cholescintigraphy seems to be a useful method. However, because the use of milk as a test meal affects the scintigraphic image, there was no correlation between the area of isotope accumulation and the localisation of inflammatory lesions in the stomach. Duodenogastric reflux seems to be less important as a cause of inflammatory lesions than other factors (such as genetic predisposition, stress, etc). Prokinetic drugs have a beneficial influence on treatment results in children with inflammatory lesions of gastric mucosa with duodenogastric reflux.