In vivo visualization of pyloric mucosal hypertrophy in infants with hypertrophic pyloric stenosis: Is there an etiologic role?

Citation
M. Hernanz-schulman et al., In vivo visualization of pyloric mucosal hypertrophy in infants with hypertrophic pyloric stenosis: Is there an etiologic role?, AM J ROENTG, 177(4), 2001, pp. 843-848
Citations number
37
Categorie Soggetti
Radiology ,Nuclear Medicine & Imaging","Medical Research Diagnosis & Treatment
Journal title
AMERICAN JOURNAL OF ROENTGENOLOGY
ISSN journal
0361803X → ACNP
Volume
177
Issue
4
Year of publication
2001
Pages
843 - 848
Database
ISI
SICI code
0361-803X(200110)177:4<843:IVVOPM>2.0.ZU;2-8
Abstract
OBJECTIVE. Infantile hypertrophic pyloric stenosis (IHPS) is a common condi tion which presents in infants at 2-12 weeks of postnatal life, and whose c ause remains obscure. Multiple associated abnormalities have been recognize d within the external hypertrophied pyloric muscle layer, but the internal component of the pyloric mucosa has received scant attention in the literat ure to date. Our purpose in this study was to show that pyloric mucosal red undancy is a constant finding in infants with IHPS, to discuss its possible cause, and to explore the hypothesis of a relationship between pyloric muc osal redundancy and the development of IHPS. MATERIALS AND METHODS. We identified 102 consecutive infants with surgicall y confirmed IHPS and determined the thickness of the pyloric mucosa compare d with the thickness of the surrounding hypertrophied muscle. Fifty-one inf ants who did not have pyloric stenosis served as controls. RESULTS. Mean mucosal thickness in patients with IHPS approximated mean mus cle thickness, with a ratio of 0.89. In infants with IHPS, the pyloric muco sa constitutes approximately one third of the cross-sectional diameter of t he pyloric mass and fills and obstructs the pyloric canal. CONCLUSION. Mucosal redundancy is a constant associated finding in IHPS. Al though the origin of the redundancy and a cause-and-effect relationship are difficult to establish, our findings support the hypothesis that hypergast rinemia may be implicated in the pathogenesis of IHPS, and suggest that muc osal thickening could be implicated as one of the initiating factors in its development.