Growth Hormone, Glutamine and Glucagon-like Peptide 2 in Short Bowel Syndrome

37 INTRODUCTION Rapid gastric emptying, gastric hypersecretion and intestinal malabsorption are key findings in patients with short bowel syndrome (SBS) (1–2). Fecal losses of fluids, electrolytes, and nutrients will, if not compensated for by increased oral intake (hyperphagia), lead to diminished body stores, subclinical and eventually clinical nutritional deficiencies. By definition, intestinal failure prevails when oral compensation is no longer feasible and parenteral nutrition (PN) support is necessary to maintain nutritional equilibrium (3) (Figure 1). Large fecal losses and the need for PN impair the quality of life in SBS patients (4). In addition, PN is associated with complications such as recurrent infections, increased risk of venous thrombosis and parenteral nutrition (PN) associated liver failure (4–6). In the past, research has mainly focused on “making the most of what the short bowel syndrome (SBS) patient still has” by optimizing remnant intestinal function through dietary interventions (7), antiGrowth Hormone, Glutamine and Glucagon-like Peptide 2 in Short Bowel Syndrome NUTRITION ISSUES IN GASTROENTEROLOGY, SERIES #68