Epidermal growth factor is critical for intestinal adaptation following small bowel resection

The loss of small intestinal mucosal surface area is a relatively common cl inical situation seen in both the pediatric and adult population. The most frequent causes include mesenteric ischemia, trauma, inflammatory bowel dis ease, necrotizing enterocolitis, and volvulus. Following surgical resection , the remnant intestine compensates or adapts to the loss of native bowel b y increasing its absorptive surface area and functional capacity. Unfortuna tely, many patients fail to adapt adequately, and are relegated to lifelong intravenous nutrition. Research into intestinal adaptation following small bowel resection (SBR) has evolved only recently from the gross and microsc opic level to the biochemical and genetic level. As understanding of this p rocess has increased, numerous therapeutic strategies to augment adaptation have been proposed. Epidermal growth factor (EGF) is an endogenous peptide that is secreted into the gastrointestinal tract and able to influence gut ontogeny, as well as mucosal healing. Early studies have demonstrated its ability to augment the adaptive process. Focusing on a murine model of mass ive intestinal loss, the morphological, structural, biochemical, and geneti c changes that occur during the intestinal adaptive process will be reviewe d. The role of EGF and its receptor as critical mediators of the adaptive p rocess will be discussed. Additionally, the ability of EGF to augment intes tinal proliferation and diminish programmed cell death (apoptosis) followin g SBR will be examined. Enhancing adaptation in a controlled manner may all ow patients to transition off parenteral nutrition to enteral feeding and, thereby, normalize their lifestyle. (C) 2000 Wiley-Liss, Inc.