[Pathophysiology of hypertrophic pyloric stenosis in infants (author's transl)].
A review of the publications on mediators of pyloric contraction, together with experimental lesions in animals, suggest that the lesions characteristic of hypertrophic pyloric stenosis in infants (hypertrophy of Torgersen's circular muscle and degenerative changes in Auerbach's myenteric plexus) are probably functional in nature. The hypothesis of a double mechanism is discussed. The primary defect would be an excess of pyloric contraction agonists, such as duodenal hormones and acetylcholine. This would be followed by self-maintenance of the lesions, where pyloric spasm and subsequent distension of the antrum would induce gastrin release with secondary stimulation of duodenal hormone release by oxyntic secretion and acidification of the duodenum.
D005755:Gastrins / Q000097:blood / Q000502:physiology; D006801:Humans; D006984:Hypertrophy / Q000503:physiopathology; D007223:Infant; D011707:Pyloric Stenosis / Q000503:physiopathology*
D005755:Gastrins
Physiopathologie de la sténose hypertrophique du pylore du nourrisson.