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Serum pepsinogen I in childhood Helicobacter pylori gastritis: its relation to mucosal peptic activity
J Yahav1, G Oderda, A Diver-Haber
1Pediatric Gastroenterology Unit, Chaim Sheba Medical Center, Tel-Hashomer, Israel.
Insights
Children with Helicobacter pylori gastritis show higher serum pepsinogen I (PG I) levels. This suggests H. pylori infection may cause pepsinogen leakage into the blood, not increased production.
Area of Science:
- Pediatric Gastroenterology
- Microbiology
- Biochemistry
Background:
- Helicobacter pylori (H. pylori) infection is a common cause of gastritis in children.
- Elevated serum pepsinogen I (PG I) levels are observed in children with H. pylori gastritis, but the underlying mechanism is unclear.
Purpose of the Study:
- To investigate whether increased serum PG I in H. pylori-infected children results from enhanced pepsin production or secretion.
- To determine the relationship between mucosal peptic activity and serum PG I levels in pediatric H. pylori gastritis.
Main Methods:
- Measurement of antrum and gastric body mucosal peptic activity in 122 children.
- Correlation of mucosal peptic activity with serum PG I levels.
- Comparison between children with and without H. pylori gastritis.
Main Results:
- Children with H. pylori gastritis exhibited decreased mucosal peptic activity compared to controls.
- Serum PG I levels were significantly increased in H. pylori-infected children (P < 0.001).
- A significant inverse relationship was found between serum PG I levels and mucosal peptic activity (P < 0.01).
Conclusions:
- H. pylori infection in children is associated with reduced gastric mucosal peptic activity.
- The findings suggest H. pylori gastritis promotes pepsinogen leakage into the circulation rather than increased production.
Abstract:
Serum pepsinogen I (PG I) levels are raised in children with Helicobacter pylori gastritis. To ascertain if this is due to increased production or to increased secretion of pepsin by chief cells, we measured mucosal peptic activity in antrum and gastric body mucosal homogenates and correlated it to serum PG I levels in 122 children with and without H. pylori gastritis. In patients infected with H. pylori, mucosal peptic activity was decreased when compared to control and to children with non H. pylori gastritis. Serum PG I levels were increased (P < 0.001) and were inversely related to mucosal peptic activity (P < 0.01). These findings suggest that H. pylori can promote a leakage of pepsinogen into the circulation.