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Gastrin, somatostatin and infantile hypertrophic pyloric stenosis
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Despite multiple and often contradictory research, no firm conclusions regarding the role of hypergastrinaemia in infantile hypertrophic pyloric stenosis (IHPS) have been established. Evaluation of somatostatin, the main physiological antagonist of gastrin, has not been assessed in previous studies. Long‐term evaluation following pyloromyotomy suggests persistent abnormalities in gastrin and somatostatin in IHPS. The objective of this case‐controlled study was to compare fasting serum gastrin and somatostatin levels in IHPS. Serum sample were collected from 39 children with IHPS at the time of pyloromyotomy and 20 age‐matched controls with no evidence of gastrointestinal disease. Standard radioimmunoassay techniques were used to detect circulating levels of the hormones. A two‐tailed t‐test was used for statistical analysis. The levels of the two hormones (mean ± SEM) revealed that there was no evidence of hypergastrinaemia in IHPS compared with controls (75.6 ±16.1 and 68.1 ± 7.8 ng l−1, respectively), but that the level of somatostatin was significantly elevated (38.9 ±6.4 and 30.5 ± 5 8 ng l−1, p = 0.016). An inverse trend in the gastrin/somatostatin levels could not be identified in IHPS.Conclusion: Somatostatin but not gastrin is raised in IHPS. Somatostatin is known to inhibit the actions of inhibitory neurotransmitters in the pylorus and may explain the development of pylorospasm, which is believed to be important in the development of pyloric tumours. These results do not agree with a previous long‐term follow‐up study, but reflect the hormonal imbalance at the time of pyloric hypertrophy.
Title: Gastrin, somatostatin and infantile hypertrophic pyloric stenosis
Description:
Despite multiple and often contradictory research, no firm conclusions regarding the role of hypergastrinaemia in infantile hypertrophic pyloric stenosis (IHPS) have been established.
Evaluation of somatostatin, the main physiological antagonist of gastrin, has not been assessed in previous studies.
Long‐term evaluation following pyloromyotomy suggests persistent abnormalities in gastrin and somatostatin in IHPS.
The objective of this case‐controlled study was to compare fasting serum gastrin and somatostatin levels in IHPS.
Serum sample were collected from 39 children with IHPS at the time of pyloromyotomy and 20 age‐matched controls with no evidence of gastrointestinal disease.
Standard radioimmunoassay techniques were used to detect circulating levels of the hormones.
A two‐tailed t‐test was used for statistical analysis.
The levels of the two hormones (mean ± SEM) revealed that there was no evidence of hypergastrinaemia in IHPS compared with controls (75.
6 ±16.
1 and 68.
1 ± 7.
8 ng l−1, respectively), but that the level of somatostatin was significantly elevated (38.
9 ±6.
4 and 30.
5 ± 5 8 ng l−1, p = 0.
016).
An inverse trend in the gastrin/somatostatin levels could not be identified in IHPS.
Conclusion: Somatostatin but not gastrin is raised in IHPS.
Somatostatin is known to inhibit the actions of inhibitory neurotransmitters in the pylorus and may explain the development of pylorospasm, which is believed to be important in the development of pyloric tumours.
These results do not agree with a previous long‐term follow‐up study, but reflect the hormonal imbalance at the time of pyloric hypertrophy.
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