Scuto S, Mangione D, de Angelis G L, Banchini G, Gregori G, Molina E, Ghinelli C
Pediatr Med Chir. 1984 Nov-Dec;6(6):791-3.
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.
