Nutrition support of infants with short bowel syndrome.

Short bowel syndrome (SBS) is a clinically complex disorder resulting from alterations of normal intestinal anatomy and physiology and producing a variety of nutritional, infectious, and metabolic complications. It is usually defined functionally and is considered to be present when the patient has malabsorption in conjunction with a shortened small intestine.1 After resection, the residual small bowel undergoes intestinal adaptation, a process characterized by mucosal hyperplasia, villus lengthening, increased crypt depth, and bowel dilatation.2,3 Oral nutrients and hormones stimulate this intestinal adaptation. Among the hormones, enteroglucagon is an important growth-promoting agent in addition to other growth factors such as epidermal growth factor, prostaglandin E2, and human growth hormone analogs. The intestinal enterocyte is the target of these factors and, within the cell, the synthesis of polyamines responsible for rapid growth is the most essential step for the development of hyperplasia after resection.4 The prognosis of patients with SBS has changed in recent decades. Although the presence of an ileocecal valve markedly improves prognosis, some children have survived massive resection and adapted well even in the absence of an ileocecal valve.5 This disorder, which used to be fatal, is now often compatible with long-term survival and potentially even a normal life course. The establishment of surgical techniques and intestinal transplantation is currently further improving the future of these patients. Nevertheless, the main clinical challenge in SBS lies in managing the many nutritional problems that occur as a result of malabsorption secondary to the reduced absorptive surface area.