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Disaccharidase deficiency in infants with cow's milk protein intolerance. Response to treatment
Insights
Infants with cow's milk protein intolerance show severe intestinal damage and disaccharidase deficiencies. A milk-protein-free diet improved these symptoms, highlighting its importance in managing infant gut health.
Area of Science:
- Pediatric Gastroenterology
- Gastrointestinal Pathology
- Nutritional Science
Background:
- Cow's milk protein intolerance (CMPI) in infants can cause chronic diarrhea and failure to thrive.
- Intestinal mucosal damage and disaccharidase deficiencies are associated with CMPI.
- Histological findings in CMPI can mimic gluten-sensitive enteropathy.
Purpose of the Study:
- To investigate the histological and functional changes in the small intestinal mucosa of infants with CMPI.
- To assess the impact of a milk-protein-free diet on these changes.
Main Methods:
- Small intestinal biopsies were performed on 7 infants (5 weeks to 11 months) before and after a milk-protein-free diet.
- Histological examination using light microscopy.
- Assay of disaccharidase activities (lactase, sucrase, maltase, palatinase).
Main Results:
- All infants presented with moderate to severe mucosal damage, inflammation, and brush border injury.
- Marked depression of all measured disaccharidase activities was observed.
- After 3-5 months on a milk-protein-free diet, 6 infants showed significant improvement in disaccharidase activity and histological recovery.
Conclusions:
- Intestinal mucosal lesions in infants with CMPI are histologically similar to gluten-sensitive enteropathy.
- CMPI is associated with significant secondary disaccharidase deficiencies.
- Dietary withdrawal of cow's milk protein leads to functional and morphological recovery of the small intestinal mucosa in infants.
Abstract:
7 infants, aged 5 weeks to 11 months, with clinically documented intolerance to cow's milk protein, chronic diarrhea, and failure to thrive, underwent small intestinal (peroal, suction) biopsy before and after withdrawal of milk proteins. Mucosal specimens were examined by light microscopy and assayed for disaccharidase activities. In all patients, moderate to severe mucosal changes were presented, associated with marked inflammation of lamina propria and damages to the brushborder. Disaccharidase activities (lactase, sucrase, maltase and palatinase) were markedly depressed in all. Follow-up biopsies were obtained in 6 infants, after 3-5 months on a milk-protein-free diet. At the time of the second biopsy, the disaccharidase activities had risen significantly and histologic improvement had occurred in each instance. In infancy, intestinal mucosal lesions due to intolerance to cow's milk protein are histologically indistinguishable from those seen in gluten-sensitive enteropathy and are associated with marked secondary disaccharidase deficiencies. Following therapy, the activity of the disaccharidases become normal or near normal prior to the complete morphologic recovery of the small intestinal mucosa.