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Everett, K.V., Chiosa, B.A., Georgouls, C., et al. (2008) Genome-wide high density SNP-based linkage analysis of infantile hypertrophic pyloric stenosis identifies loci on chromosomes 11q14-q22 and Xq23. American Journal of Human Genetics, 82, 756-762. doi:10.1016/j.ajhg.2007.12.023

has been cited by the following article:

• TITLE: New insights on the pathogenesis of pyloric stenosis of infancy. A review with emphasis on the hyperacidity theory

  AUTHORS: Ian M. Rogers

  KEYWORDS: Infantile Hypertrophic Pyloric stenosis (IHPS); Immunohistochemistry; Smooth Muscle Cells; Gastrin; Motilin; Gastrointestinal Motility; Erythromycin; Pyloromyotomy; Acidification of the Stomach; Pyloric Sphincter Function; Receptor Binding; Pathogenesis; Antral Motility; Gastric Outflow Obstruction; Linkage Analysis; Single Nucleotide Polymorphism: Interstitial Cells of Cahal; Nitric Oxide Synthetase

  JOURNAL NAME: Open Journal of Pediatrics, Vol.2 No.2, June 19, 2012

  ABSTRACT: A review is presented on the theories concerning the cause of pyloric stenosis with emphasis on the primary position of inherited hyperacidity in pathogenesis. Existing theories are critically analysed and the hyperacidity theory is precisely defined in the light of recent physiological insights into the gastrointestinal hormone motilin. The progressive fixed fasting hypergastrinaemia within the first few weeks of life will, in the baby who inherits acid secretion at the top of the normal range, produce hyperacidity of sufficient severity to trigger the process of acid-induced work hypertrophy of the pylorus. The potential contribution of motilin is discussed. The baby who inherits a normal gastric acidity will not reach acid levels severe enough to trigger sphincter hypertrophy despite the early gastrin stimulus. The potential threat will cease when gastrin naturally declines with age and the pyloric canal becomes wider. Genetic factors clearly must also be involved and these are separately discussed.