The development of hypertrophic pyloric stenosis in a patient with prostaglandin-induced foveolar hyperplasia

• Published in: Pediatric radiology 1999-10, Vol.29 (10), p.748-751
• Main Authors: CALLAHAN, M. J, MCCAULEY, R. G. K, PATEL, H, HIJAZI, Z. M
• Format: Article
• Language: English
• Subjects: Biological and medical sciences; Female; Gastric Mucosa - pathology; Gastric Outlet Obstruction - diagnosis; Gastric Outlet Obstruction - diagnostic imaging; Gastric Outlet Obstruction - etiology; Gastroenterology. Liver. Pancreas. Abdomen; Humans; Hypertrophy - chemically induced; Hypertrophy - diagnostic imaging; Infant, Newborn; Malformations; Medical sciences; Prostaglandins - adverse effects; Prostaglandins - therapeutic use; Pulmonary Atresia - drug therapy; Pyloric Antrum - diagnostic imaging; Pyloric Antrum - pathology; Pyloric Stenosis - diagnosis; Pyloric Stenosis - diagnostic imaging; Pyloric Stenosis - etiology; Stomach. Duodenum. Small intestine. Colon. Rectum. Anus; Ultrasonography
• ISSN: 0301-0449; 1432-1998
• DOI: 10.1007/s002470050688

Hypertrophic pyloric stenosis (HPS) has been described in association with several obstructive antropyloric lesions including idiopathic foveolar hyperplasia (gastric mucosal hypertrophy), feeding tubes, eosinophilic gastroenteritis, and hypertrophic antral polyps. Non obstructive antral webs have also been described with HPS. We present a case of gastric-outlet obstruction in association with HPS, namely, prostaglandin-induced foveolar hyperplasia. This entity has been previously described, but rarely in association with HPS. We report a female infant requiring prostaglandin therapy for pulmonary atresia who developed dose-related prostaglandin-induced foveolar hyperplasia and symptoms of progressive non-bilious vomiting. Initially, ultrasonography demonstrated evidence of antral mucosal hypertrophy as the cause for gastric-outlet obstruction. The patient subsequently developed progressive thickening of the antropyloric muscle, resulting in sonographic appearances of hypertrophic pyloric stenosis. Pyloromyotomy was eventually required for treatment of HPS. A common denominator of most of the above-described entities is thickening and/or hypertrophy of the antral mucosa. We suggest that the antropyloric musculature may hypertrophy in an effort to overcome the gastric-outlet obstruction caused by the adjacent thickened antral mucosa. In other words, these entities may represent examples of "secondary" hypertrophic pyloric stenosis.