MALABSORPTION AND VILLOUS ATROPHY IN PATIENTS RECEIVING ENTERAL FEEDING

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 int estine. Methods: Studies were performed of patients at the time of PEG placement, in a cross-sectional group after a period of feeding and i n a smaller longitudinal subgroup. Enteral feeds were adjusted in volu me 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 de termined 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 inc rease in duodenal bacteriology, and abnormal lactuloserhamnose sugar p ermeability due to rhamnose malabsorption. These changes were also pre sent in 38 similar patients before enteral feeding. A second study bef ore enteral feeding showed lowered maltase activity (24 patients), and similar intestinal permeability findings (22 patients). Twelve of the se patients were followed longitudinally for 3 months of enteral feedi ng that maintained but did not improve nutrition, as assessed by body mass index and mid-arm muscle circumference, and there was no change i n duodenal morphometry (11 patients), rhamnose malabsorption (4 patien ts), or disaccharidases (11 patients). Conclusions: These studies sugg est villous atrophy was not due to an inflammatory enteropathy but res ulted from a poor luminal ''drive'' associated with the enteral feedin g. Enteral feeding maintained but did not improve nutrition status.