Abstract
AbstractTo elucidate the etiological role of big gastrin in hypertrophic pyloric stenosis (HPS), the pattern of plasma gastrins, the response of plasma big gastrin aftermilk feeding and the gastric secretion were investigated in 22 infants with HPS. In addition, histochemical study of the antral gastrin cells was carried out.The pattern of plasma gastrins in HPS was closely similar to that in the normal infant and big gastrin was a dominant component of circulating gastrins. The mean big gastrin level in HPS was significantly higher than that of the controls both fasting and after feeding. The HPS also had hypersecretion, of gastric juice, acid and pepsin before and after pentagastrin stimulation, Therefore, the HPS had both hypersecretion of gastric acid and hypergastrinemia. The number and the distribution of gastrin cells in the antral mucosa in HPS were similarly found by immunostainings with two antisera, anti‐big gastrin serum and anti‐gastrin serum. These gastrin cells were not different in number from those of infants and children with other diseases.These data suggest that the HPS has an incomplete negative feedback mechanism between plasma gastrin level and gastric acid secretion, and generally has hypergastrinemia whose trophic effect may play a role in the pathogenesis of this disease
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