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By C. G. Dervenis, Herbert Lochs

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Extra info for Nutrition in Gastrointestinal and Liver Diseases (Special Issue: Digestive Diseases 2003, 3)

Sample text

Bacterial overgrowth also induces vitamin B12 deficiency. Finally, medical treatment (therapeutic fasting, steroids, cholestyramine) [16, 17] and self- or medically-recommended dietary restrictions may also contribute the development of nutritional deficiencies in IBD patients [10, 17]. Nutritional derangement may influence adult IBD outcome, since it may increase the need for surgical treatment [1] and its complications [17]. However, it has been in children and adolescents where malnutrition, in its wider sense, together with steroid treatment (by IGF-1 suppression) have been blamed as inducing one of the most severe IBD complications in this population – linear growth and sexual maturation failure [18–20].

The lower limit of remaining gut length compatible with successful weaning from enteral feeding is estimated to be ^30 cm in children. In adults, on the other hand, the extent of compensatory hypertrophy is becoming very limited (the lower limit of remaining intestinal length is said to be at least 50–70 cm) [4]. Recovery of intestinal function can be expected from efficient use of certain factors stimulating regeneration and hypertrophy of the remnant intestinal mucosa, in addition to prolonged nutritional management with enteral and parenteral nutritional regimens.

66] further showed that a synthetic, protease-resistant form of GLP-2 was a potent agent for increasing small and large intestine mass in normal rats. Findings in other similar studies showed that GLP-2 increases mucosal mass and absorptive function in intestine after MSBR [67]. In experiments on massive bowel resection or ischemia/reperfusion injury, administration of GLP-2 significantly increased DNA and protein content of the intestinal mucosa [59]. However, such effects have not been confirmed in humans.

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