Signaling factors for gut adaptation.

Abstract

With the increasing number of patients safely receiving long-term total parenteral nutrition (TPN), it has become clear that there is a group of patients, in whom treatment is totally dependent on TPN for a prolonged period of time. This disease entity is referred to as ‘intestinal failure’, well defined as ‘conditions, which lack a functioning intestine necessary for adequate digestion and absorption’ [1]. Intestinal failure may roughly be divided into two types: one characterized by an absolute reduction in normally functioning gut mass (short bowel syndrome), and the other marked by an intestine with extensive lesions or functional insufficiency (intestinal dysfunction). Possible etiologic diseases or disorders are listed in Table 1. Short bowel syndrome occurs when the length of bowel available to achieve digestion and absorption has become inadequate as a result of massive bowel resection or congenital short bowel. Intestinal dysfunctions occur, when a large part of the intestinal tract does not function normally due to reduced motility or impaired digestion and absorption. Regarding survival following massive bowel resection in humans, an extensive review was made by Wilmore [2] in 1972. This indicates that, in infants with an intact ileocecal valve, none with small intestinal segment measuring less than 15 cm survived, while, in infants receiving ileocecal resection, this length is extended to 40 cm. However, patients with an even shorter length of remaining intestine can nowadays be maintained and successfully weaned from parenteral nutrition, if an appropriate nutritional regimen is administered concomitantly. The lower limit of remaining gut length compatible