Malabsorption and villus atrophy in patients receiving enteral feeding
Date
1995
Authors
Cummins, A.
Chu, G.
Faust, L.
Chandy, G.
Argyrides, J.
Robb, T.
Wilson, P.
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Journal article
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Journal of Parenteral and Enteral Nutrition, 1995; 19(3):193-198
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Adrian Cummins, Geoff Chu, Logan Faust, George Chandy, John Argyrides, Trevor Robb, and Peter Wilson
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Abstract
Background: The purpose of this study was to assess the structure and function of the small intestine before and after enteral feeding given via a percutaneous feeding gastrostomy (PEG). It is not known whether this method of feeding provides a good luminal drive to the small intestine. Methods: Studies were performed of patients at the time of PEG placement, in a cross-sectional group after a period of feeding and in a smaller longitudinal subgroup. Enteral feeds were adjusted in volume and caloric content for each patient. Duodenal biopsies were taken during endoscopy for quantitative morphometry, and lactulose-rhamnose permeability tests were performed during the next day. Duodenal fluid was cultured quantitatively in the first study, and disaccharidases determined in the second study. Results: The first study of 15 patients, who had enteral feeding for a median (range) period of 13 (8 to 104) weeks, showed partial villous atrophy with normal crypt length, no increase in duodenal bacteriology, and abnormal lactulose-rhamnose sugar permeability due to rhamnose malabsorption. These changes were also present in 38 similar patients before enteral feeding. A second study before enteral feeding showed lowered maltase activity (24 patients), and similar intestinal permeability findings (22 patients). Twelve of these patients were followed longitudinally for 3 months of enteral feeding that maintained but did not improve nutrition, as assessed by body mass index and mid-arm muscle circumference, and there was no change in duodenal morphometry (11 patients), rhamnose malabsorption (4 patients), or disaccharidases (11 patients). Conclusions: These studies suggest villous atrophy was not due to an inflammatory enteropathy but resulted from a poor luminal "drive" associated with the enteral feeding. Enteral feeding maintained but did not improve nutrition status.
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© 1995 by The American Society for Parenteral and Enteral Nutrition