Abstract
“An ideal intestinal replacement would be derived from immunocompatible cells, would grow with the recipient, and be fully capable of performing all metabolic and physiologic functions of native small bowel.” Short bowel syndrome (SBS) is defined by both the metabolic and physiologic disturbances observed with significant truncation of normal bowel length. With a 70–75% reduction in small intestine length, alterations in fluid and nutrient bal ance occur with potentially life threatening consequences. These include profound decrease in the absorption of carbohydrates and protein as well as severe mineral and vitamin deficiencies. Additional sequalae include formation of renal and biliary calculi, low body weight, failure to thrive and death [1–3]. Both adults and children may be affected. In the adult population, bowel resection secondary to mesenteric ischemia, trauma, inflammatory bowel disease and malignancy are common etiologies. Children are susceptible to a wide range of congenital or acquired conditions such as intestinal atresia, volvulus and necrotizing enterocolitis. The incidence of SBS is estimated to be 24.5 per 100,000 live births and is associated with 30% 5-year mortality [2]. Current treatment options are inadequate and are focused on nutritional supplementation via total parenteral nutrition or intestinal replacement with transplanted allograft. The risks of hepatic failure and central line sepsis associated with prolonged total parenteral nutrition have been described [4]. Although outcomes for small intestine transplantation are improving, this therapy has disadvantages of supply shortages, rejection and lifelong immunosuppression. An ideal intestinal replacement would
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