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Journal of Pediatric Biochemistry 2016; 06(03): 146-151
DOI: 10.1055/s-0036-1597606
Original Article
Georg Thieme Verlag KG Stuttgart · New York

The Cause of Pyloric Stenosis of Infancy: Primary Hyperacidity and Biochemistry Combined

Ian Munro Rogers
1   Faculty of Medicine, Asian Institute of Medical, Science and Technology, Kedah, Malaysia
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Publication History

24 March 2016

08 June 2016

Publication Date:
26 December 2016 (online)

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Abstract

The cause of pyloric stenosis (PS) of infancy is at present unknown. A theory of causation is proposed, which is consistent with all the known clinical features of this condition. It is based on the knowledge that babies with PS are hypersecretors of acid, which predates the development of PS and is an inherited constitutional feature. This acidity becomes dangerously high due to a temporary insensitivity of the negative feedback between gastrin and gastric acidy within the first few weeks of life. Normal babies with normal acidity levels will also experience peak acidity at that time but not dangerously so. Acid entering the duodenum causes contraction of the pyloric sphincter. Hyperacidity will naturally lead to repeated pyloric sphincter contractions with resulting work hypertrophy of the sphincter and PS. Should the baby with PS survive beyond the age of approximately 6 weeks, the matured negative feedback between gastrin and acid will ensure that dangerous hyperacidity is kept in check. Thus, the passage of time allows the physiological control of hyperacidity. When associated with an age-related widening of the pyloric canal control, a long-term cure is the natural outcome. This theory explains satisfactorily all the known and hitherto unexplained features of this condition.

Keywords

neonatal hypergastrinemia - hyperacidity - etiology of pyloric stenosis of infancy
 

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