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1
Department of Pediatric Radiology, Vanderbilt Children's Hospital, Vanderbilt
University Medical Center-D-1120, Medical Center North, 21st Ave. S.,
Nashville, TN 37232-2675.
2
Department of Pathology, Vanderbilt Children's Hospital, Nashville, TN
37232-2675.
3
Department of Surgery, Vanderbilt Children's Hospital, Nashville, TN
37232-2675.
4
Department of Gastroenterology, Vanderbilt Children's Hospital, Nashville, TN
37232-2675.
OBJECTIVE. Infantile hypertrophic pyloric stenosis (IHPS) is a common condition which presents in infants at 2-12 weeks of postnatal life, and whose cause remains obscure. Multiple associated abnormalities have been recognized within the external hypertrophied pyloric muscle layer, but the internal component of the pyloric mucosa has received scant attention in the literature to date. Our purpose in this study was to show that pyloric mucosal redundancy is a constant finding in infants with IHPS, to discuss its possible cause, and to explore the hypothesis of a relationship between pyloric mucosal redundancy and the development of IHPS.
MATERIALS AND METHODS. We identified 102 consecutive infants with surgically confirmed IHPS and determined the thickness of the pyloric mucosa compared with the thickness of the surrounding hypertrophied muscle. Fifty-one infants who did not have pyloric stenosis served as controls.
RESULTS. Mean mucosal thickness in patients with IHPS approximated mean muscle thickness, with a ratio of 0.89. In infants with IHPS, the pyloric mucosa constitutes approximately one third of the cross-sectional diameter of the pyloric mass and fills and obstructs the pyloric canal.
CONCLUSION. Mucosal redundancy is a constant associated finding in IHPS. Although the origin of the redundancy and a cause-and-effect relationship are difficult to establish, our findings support the hypothesis that hypergastrinemia may be implicated in the pathogenesis of IHPS, and suggest that mucosal thickening could be implicated as one of the initiating factors in its development.
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