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Published on: September 10, 2021
Infantile hypertrophic pyloric stenosis: are viruses involved?
Jiad N Mcheik1, Isabelle Dichamp, Guillaume Levard
1Department of Pediatric Surgery, University Hospital, Poitiers, France.
Insights
Common respiratory and digestive viruses do not appear to cause infantile hypertrophic pyloric stenosis (IHPS). This study found no significant viral link in infants diagnosed with IHPS.
Area of Science:
- Pediatrics
- Virology
- Gastroenterology
Background:
- Infantile hypertrophic pyloric stenosis (IHPS) involves abnormal thickening of the pyloric muscle.
- The exact causes and pathophysiology of IHPS remain unclear, despite known genetic and environmental influences.
Purpose of the Study:
- To investigate the prevalence of common respiratory and digestive viruses in infants with IHPS.
- To determine if these viruses play a role in the development of IHPS.
Main Methods:
- Samples including nasopharyngeal fluids, stools, vomit, and pyloric muscle were collected from IHPS patients.
- Tests performed included cell culture, viral antigen assay, and PCR.
- Samples were analyzed for common respiratory and digestive tract viruses.
Main Results:
- No significant viral presence was detected in ear, nose, throat, or pyloric muscle samples.
- A single adenovirus type 3 was found in one stool sample.
- Enterovirus RNA was detected in one vomit sample via RT-PCR.
Conclusions:
- The study suggests that common respiratory and digestive viruses are unlikely to be the primary cause of IHPS.
- Further research is needed to elucidate the specific etiology of infantile hypertrophic pyloric stenosis.
Abstract:
Infantile hypertrophic pyloric stenosis (IHPS) is characterized by abnormal thickening of the internal circular muscle layer. IHPS is known to be due to a combination of genetic and environmental factors, but its precise causes and pathophysiology are poorly understood. The objective of the study is to determine the prevalence of the principal viruses targeting the respiratory and digestive tracts in children with IHPS. Nasopharyngeal fluids, stools, vomit, and surgical pyloric muscle fragments and swabs were tested by cell culture, viral antigen assay and PCR. IHPS was diagnosed in 23 boys and 8 girls with a mean (± SD) age of 42 ± 15 days (range 20-88 days). There was no seasonal pattern of diagnosis. Twenty-two children (71%) lost weight (mean 246 ± 164 g, range 30-600 g) after the onset of vomiting, and five (16.1%) were dehydrated. Seven (22.6%) infants had been exposed to an infectious contact within 15 days before admission, and one on the day of admission (3.2%). Ear, nose and throat samples and pyloric muscle specimens were negative for all the viruses tested. An adenovirus type 3 was recovered from one stool sample, and RT-PCR was positive for an enterovirus on one vomit sample. This study suggests that the principal viruses targeting the respiratory and digestive tracts are not responsible for IHPS.
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