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Gastrin Secretion in Infancy and Childhood|Part I: Response to a Gastrin Secretion Test and G‐Cell in Infantile Hypertrophic Pyloric Stenosis
Author(s) -
Mayama Haruki
Publication year - 1986
Publication title -
pediatrics international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.49
H-Index - 63
eISSN - 1442-200X
pISSN - 1328-8067
DOI - 10.1111/j.1442-200x.1986.tb00698.x
Subject(s) - gastrin , medicine , antrum , endocrinology , g cell , hormone , gastroenterology , parietal cell , secretion , stomach , gastric acid
To examine the etiological role of gastrin in infantile hypertrophic pyloric stenosis (IHPS), fasting levels of serum gastrin and the response in the serum levels of this hormone to oral milk feeding were investigated in 10 infants with IHPS aged 18 to 125 days before treatment (untreated group) and in the convalescent stage (improved group) following conservative management. Distribution of the antral gastrin cells (G‐cell) was also studied electron microscopically. Seven pairs of the parents of patients investigated took part in the fasting serum gastrin measurement to investigate the genetic effects. Mean fasting serum gastrin concentration was significantly elevated in patients of the untreated group (254±44 pg/ml, p<0.05) and in patients of the improved group (191±35 pg/ml, p<0.05) compared with the mean value (115±20 pg/ml) for the control group (n=6). The maximum peak gastrin response and the duration of hypergastrinemic response to milk feeding in order of magnitude or length were observed in the untreated, improved and control groups. There was no difference of numbers of antral G‐cell among the 3 groups but G‐cells of untreated patients tended to have vacuoles near the Golge apparatus which is consistent with hyperfunction of the cell. Hypergastrinemia was found in 4 out of 7 mothers (54.3%), 2 of whom were extremely hypergastrinemic (329 pg/ml, 732 pg/ml), and in 3 out of 7 fathers (42.8%) including 2 pairs of the parents (28.5%). These results support the view that gastrin may play a role together with the genetic endowment within a susceptible population in the pathogenesis of IHPS.