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Infantile hypertrophic pyloric stenosis: genes and environment
Correspondence to:
Dr E Chung, General and Adolescent Paediatric Unit, Institute of Child Health, University College London, The Rayne Building, 5 University Street, London WC1E 6JJ, UK; eddie.chung@ucl.ac.uk
| The first 150 words of the full text of this article appear below. |
Most paediatricians take great pleasure in making a diagnosis of infantile hypertrophic pyloric stenosis (IHPS; OMIM 179010
[OMIM]
). It is a most satisfying experience to observe the dramatic gastric peristalsis and to palpate the pyloric "tumour" during a positive test feed. Over 120 years after the condition has become a clinical entity,1 its aetiology remains unclear. The condition has an interesting age-specific and tissue-specific nature. IHPS is never seen beyond the age of 3 months except in reports of premature infants in whom enteral feeding had been started late. This suggests that a period of enteral feeding is required for the condition to become clinically evident. Either the defect is only critical to the infant in the first 3 months of life and/or there are compensatory mechanisms that will circumvent the pyloric obstruction over time. The main reported pathology is restricted to the pylorus associated with smooth muscle hypertrophy, and
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