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Intestinal damage in rotavirus and adenovirus gastroenteritis assessed by d-xylose malabsorption
Insights
Infants with acute gastroenteritis and rotavirus in the small intestine showed D-xylose malabsorption. Adenovirus in the small intestine also correlated with low D-xylose levels, suggesting viral-induced mucosal damage.
Area of Science:
- Pediatrics
- Infectious Diseases
- Gastroenterology
Background:
- Acute gastroenteritis is a common illness in infants.
- Viral infections are frequently implicated in infantile gastroenteritis.
- D-xylose absorption is a measure of small intestinal function.
Purpose of the Study:
- To assess D-xylose absorption in infants with acute gastroenteritis.
- To investigate the relationship between viral presence in the small intestine and D-xylose malabsorption.
- To explore the potential role of adenovirus in infantile gastroenteritis.
Main Methods:
- Infusion of D-xylose into the duodenum.
- Measurement of 1-hour blood-xylose levels.
- Analysis of small intestinal aspirates for viral particles (rotavirus, adenovirus).
- Stool analysis for viral detection.
Main Results:
- Low 1-hour blood-xylose levels were observed in infants with rotavirus in their small intestine.
- Infants without small intestinal viruses had normal D-xylose levels.
- Adenovirus in the small intestine was associated with low D-xylose levels in infants with acute gastroenteritis.
Conclusions:
- Rotavirus and adenovirus in the small intestine may cause D-xylose malabsorption in infants.
- Findings support adenovirus as a potential causative agent of acute infantile gastroenteritis.
- Viral presence in the small intestine might indicate associated mucosal damage, leading to malabsorption.
Abstract:
The absorption of D-xylose infused into the duodenum was assessed in infants with acute gastroenteritis. 1-hour blood-xylose levels were low in 6 patients found to harbour rotavirus in the small intestinal aspirate. Normal levels (greater than 1-26 mmol/l) were obtained in the absence of virus particles in the small intestine in a further 6 patients: in 3 of these adenovirus or rotavirus was recovered from the stools. Three patients with adenovirus in the small intestinal juice and ill with acute gastroenteritis also had low xylose levels. This finding supports earlier epidemiological studies that adenovirus may be a causative agent of acute infantile gastroenteritis. The association between virus in the small intestine and xylose malabsorption may indicate mucosal damage. Formal proff of this is awaited.