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[Exogenous and endogenous gastric secretion in children with primary duodenal ulcer]
Insights
Children with duodenal ulcers exhibit higher pepsinogen I levels and increased gastric acid secretion, suggesting a genetic predisposition. These findings indicate elevated acid production is a cause, not a consequence, of pediatric duodenal ulcers.
Area of Science:
- Pediatric Gastroenterology
- Gastrointestinal Physiology
- Genetics
Background:
- Duodenal ulcer disease in children is less common than in adults.
- The underlying pathophysiology and etiological factors in pediatric duodenal ulcers require further elucidation.
Purpose of the Study:
- To investigate the differences in gastric acid secretion and related biomarkers between children with duodenal ulcers and healthy controls.
- To explore the potential role of genetic factors in the development of duodenal ulcers in children.
Main Methods:
- Comparative study involving 12 children with duodenal ulcers (Group 1) and 20 healthy children (Group 2).
- Assessment of serum gastrin and pepsinogen I levels after a standardized protein meal.
- Evaluation of gastric acid secretion using the pentagastrin test to determine maximal acid output (MAO) and peak acid output (PAO).
Main Results:
- Children with duodenal ulcers showed significantly higher basal and postprandial serum pepsinogen I levels compared to controls (p < 0.01).
- The pentagastrin test revealed significantly higher MAO (p < 0.001) and PAO (p < 0.005) in the duodenal ulcer group.
- Serum gastrin levels did not differ significantly between the two groups.
Conclusions:
- Elevated gastric acid secretion is a significant factor in pediatric duodenal ulcer disease, appearing to be a causative element.
- The presence of family histories of duodenal ulcers supports a potential inherited basis for the condition in children.
Abstract:
Twelve cases of duodenal ulcer were studied in children, 11 male and 1 female (mean age 10 +/- 2.7 years) (mean weight 30 +/- 3.7 Kg.) (Group 1). All were submitted to x-ray examination and/or digestive endoscopy. Twenty healty children, matched by weight, age and sex were chosen as controls (Group 2). All children underwent a standardizet protein meal to evaluate serum gastrin and pepsinogen I response and the pentagastrin test for gastric acid secretion. The serum gastrin levels were found to be without significative differences in the two groups, both in the fasting state (Group 1: 77 +/- 16 pg/ml vs. Group 2: 58 +/- 12 pg/ml) and after food stimulation (Group 1: 110 +/- 22 pg/ml vs. Group 2: 88 +/- 47 pg/ml), whereas the basal serum pepsinogen I (Group 1: 74 +/- 10 ng/ml vs. Group 2: 43 +/- 1.8 ng/ml) and after meal (Group 1: 83 +/- 14 ng/ml vs. Group 2: 49 +/- 2.1 ng/ml) values were statistically higher in the duodenal ulcer group (p less than 0.01). The pentagastrin test showed a statistically difference in MAO (Group 1: 0.370 +/- 0.10 mmol/H+/hr./Kg. vs. Group 2: 0.210 +/- 0.11 mmol/H+/hr./Kg. - p less than 0.001) and PAO (Group 1: 0.480 +/- 0.13 mmol/H+/hr./Kg. vs. Group 2: 0.351 +/- 0.12 mmol/H+/hr./Kg. - p less than 0.005) between the groups. The results confirm that elevated gastric acid response is already present in duodenal ulcer of children and seems to be its cause rather than its consequence. Our finding of an already reported family histories of the disease, further support an inherited basis for duodenal ulcer in children.