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Pediatric Intestinal Failure: Nutrition, Pharmacologic, and Surgical ApproachesChildren's Hospital of Boston, Boston, Massachusetts Correspondence: Correspondence: Y. Avery Ching, Children's Hospital of Boston, Department of Surgery, Fegan 3, 300 Longwood Avenue, Boston, MA 02115. Electronic mail may be sent to yching{at}bidmc.harvard.edu. Intestinal failure (IF) is a condition where there is insufficient functional bowel to allow for adequate nutrient and fluid absorption to sustain adequate growth in children. Several etiologies can predispose to IF, including necrotizing enterocolitis, gastroschisis, and intestinal atresias. Intestinal rehabilitation can be seen as a 3-pronged strategy merging nutrition, pharmacologic, and surgical approaches to achieve the ultimate goal of enteral nutrition. Nutrition approaches should seek to facilitate transition from parenteral nutrition (PN) to enteral nutrition because prolonged use of PN is associated with severe morbidity and mortality. Enteral nutrition, on the other hand, promotes and enhances an adaptive response in the intestine. Medications used in the treatment of IF may help alleviate symptoms of diarrhea, bacterial overgrowth, and gastrointestinal dysmotility. Surgical procedures, such as longitudinal intestinal lengthening and tapering (LILT) or serial transverse enteroplasty (STEP), can increase mucosal surface area and may enhance intestinal adaptation. IF is a difficult disease process with a complex patient population and is best guided through this 3-pronged approach by a multidisciplinary team featuring surgeons, gastroenterologists, dietitians, pharmacists, and nurses.
Various definitions of intestinal failure (IF) have been proposed. Perhaps the simplest is that IF is a condition of malabsorption of fluid and nutrients, necessitating parenteral nutrition (PN) to sustain adequate growth in children. Etiologies of IF are detailed in Table 1. Many of these conditions do not intrinsically cause IF, but their natural histories often mandate surgical resection of bowel.
This article reviews the 3 primary modalities in managing IF in pediatric patients: nutrition, pharmacologic, and surgical approaches. A multimodality treatment program, using all 3 approaches in conjunction, enhances and facilitates overall intestinal rehabilitation.
PN Arguably, there has been no greater advancement in managing IF than the use of PN in patients with enteral intolerance. IF patients are susceptible to significant fluid losses and electrolyte imbalances. Emesis, stomal output, and diarrhea are several symptoms that alter fluid balance. Care must be taken to adjust the PN content, and replenish the patient with additional hydration fluid. Typically, PN should be maintained as a standard formula, whereas additional losses are replaced on an individual basis. Measurement of electrolytes in urine and stomal output is helpful in assessing electrolyte supplementation. Acute electrolyte deficiencies can be supplemented in replacement fluids as an adjunct to PN. When the patient's fluid and electrolyte status has stabilized, these supplements can be incorporated into the PN components.
Management of PN-Associated Liver Disease (PNALD)
It has been demonstrated that lipids are metabolized differently depending
on their route of
administration.2
Enteral lipids are absorbed by the enterocyte in the form of a micelle and
packaged into chylomicrons for ultimate disposal in the liver. In the
bloodstream, these particles rapidly acquire apolipoproteins from circulating
high-density lipoproteins and subsequently can be metabolized by the liver.
The emulsified particles of commercially made and IV-administered lipid
emulsions, such as Intralipid (Kabi Pharmacia, Clayton, NC), mimic the size
and structure of chylomicrons but differ in their content. In contrast to
chylomicrons, artificial lipid particles primarily contain essential fatty
acids, such as There are several methods that clinicians can use to reduce the risk of PN-associated cholestasis. In neonates and infants, PN caloric intake should be limited to 90–100 kcal/kg to avoid overfeeding. In addition, attempts should be made to cycle PN 2–6 hours a day, which promotes the cyclic release of gastrointestinal (GI) hormones. Patients that exhibit signs and symptoms of infections, bacterial overgrowth, or line sepsis should be aggressively treated. Last, efforts should be made to encourage and advance enteral nutrition.5 An exciting and recently published case report discusses the potential role of IV fat emulsion to treat infants receiving prolonged courses of PN complicated by PNALD.6 Clinicians should consider stopping all conventional lipid emulsions and instead providing 1 g/kg/d as parenteral fish oil. Lower doses of Omegaven may not be effective and may predispose patients to essential fatty acid deficiency, which has also been linked to the development of fatty liver.
Enteral Nutrition Oral feedings of infants can prevent feeding aversion, as a result of learning how to suck and swallow. Continuous enteral feedings achieve total and constant saturation of intestinal transporters, thus using the full extent of the remaining absorptive surface area.9 Bolus feedings are another method of providing enteral nutrition in older children, but are poorly tolerated in infants. Multiple administration routes can be used for enteral nutrition. Patients who receive bolus or continuous feedings should also be encouraged to eat orally. Patients should be engaged in oral motor stimulation therapy if needed. Early referral to occupational and speech therapists is important, especially given the difficulty in treating feeding aversion in SBS patients.10 Patients may initially require PN support until they tolerate goal enteral nutrition. Enteral feedings should be advanced steadily as clinical status permits. Parenteral calories are simultaneously decreased by rate or number of hours to ensure nutrition status and fluid balance. It is not uncommon to have some GI intolerance as feedings are advanced. Typically, however, fecal samples should have reducing substances <1% and a fecal pH above 5.5.5 Severe carbohydrate malabsorption is identified if fecal reducing substances are >1% and fecal pH is <5.5.5
Transition to Enteral Nutrition: Factors for Consideration
Dietary Modifications Although protein provides little osmotic load, simple carbohydrates, such as sucrose and fructose, can lead to osmotic diarrhea. GI bacteria break down these simple sugars in osmotically active acids that increase the osmotic load.5 In contradistinction, complex carbohydrates found in pasta, potatoes, and breads are well tolerated and, if possible, should comprise the majority of energy intake (eg, 50%–60%).21 Fat can be a significant source of energy intake for IF patients. Unfortunately, fat is not well tolerated due to bile salt malabsorption, which leads to decreased micelle formation and fat digestion. Medium-chain triglycerides (MCTs) compared with long-chain triglycerides (LCTs) do not require micelles for absorption and thus are better tolerated in patients with bile acid or pancreatic insufficiency. MCTs, however, also increase the osmotic load in the intestine and provide fewer calories than LCTs. In addition, LCTs may stimulate intestinal adaptation after intestinal resection.7 In SBS patients with a colon in continuity, it has been shown that a mixture of an MCT and LCT diet can improve energy and fat absorption.22 The addition of fiber to the diet can decrease overall intestinal transit time. In patients with a colon in continuity, the metabolism of fiber can serve as an energy source,23 as well as lead to the production of short-chain fatty acids (SCFAs). SCFAs, such as butyrate, are considered a fuel source for colonocytes24 and also enhance sodium and water absorption, thereby reducing stool output and sodium losses.25 Of the formulas available, Alimentum (Ross, Columbus, OH), Pregestimil, and Nutramigen (Mead Johnson, Evansville, IN) are "semielemental" hypoallergenic formulas with hydrolyzed casein as the protein source, not amino acids. Nutramigen is the most nutritious choice for babies with moderate protein allergies. The most elemental formulas are Elecare (Ross) and Neocate (SHS, Gaithersburg, MD). Both have amino acids as a protein source. Elecare has 33% MCT and Neocate has only about 5% MCT as a fat source. Babies with severe protein allergies or multiple food allergies should be given Elecare or Neocate. In babies with severe fat malabsorption and SBS, Elecare may be preferable.
Patients with SBS often require unique therapies to assist in bowel adaptation (Table 2). Depending on the patient, they may require prokinetic agents or antidiarrheal agents or a combination of both. Other therapies such as the use of IV fish oil have been used to treat PN-associated liver injury in these patients.6 Due to the complexities of SBS, dosage recommendations are often quite different from established norms.
Antimotility Agents
Prokinetic Agents Cisapride, a 5-HT3 agonist, is associated with serious cardiac arrhythmias and sudden death, limiting its usefulness. Cisapride has been part of an FDA-mandated limited-access protocol in the United States since May 2000 due to concerns of adverse cardiac events. The prescribing physician participating in the limited-access program must be board eligible or certified in 1 or more of the following areas: internal medicine (including gastroenterology and cardiology), family practice, pediatrics (including neonatology), or surgery. As part of this program, institutional review board (IRB) approval completion of a Form FDA 1572 and signed informed consent are required.30 Tegaserod (Zelnorm; Novartis, East Hanover, NJ), a selective 5-HT4 receptor agonist, stimulates peristalsis and accelerates colonictransit.29,31 Originally approved for irritable bowel syndrome (constipation type) in women, doses of up to 12 mg/d have been used to accelerate small bowel and colonic transit. It modulates both normal and altered motility throughout the GI tract. Evidence supporting its use is limited to case series in critically ill adults to advance enteral feedings in the presence of impaired gastric motility.32 Because its main metabolic pathway is presystemic, no clinically relevant drug-drug interactions have been identified. It does not cross the blood-brain barrier, nor does it have cardiac repolarization effects or QTc-interval prolongation.33 In March 2007, however, tegaserod was withdrawn from the market over concerns of increased risks of cardiovascular events, such as heart attacks and strokes.
Antisecretory Drugs In patients with ileal resection and loose, watery stools, the bile acid binder cholestyramine may be useful in reducing secretory diarrhea. In patients with fat malabsorption due to bile salt insufficiency, however, it may actually worsen diarrhea and increase the risk of deficiency of fat-soluble vitamins.36
Antimicrobials (Table 3)
Short courses of oral antimicrobials are the main-stay of therapy in the management of bacterial overgrowth.39 Most protocols include metronidazole with or without trimethoprim/sulfamethoxazole, aminoglycosides, extended-spectrum penicillins/cephalosporins, or vancomycin. Some centers also include a week of antifungals such as amphotericin B. Due to product design limitations, oral administration of injectable products may be necessary. Typically, antimicrobials are given for 1 week per month, although some patients may require continuous administration. Concerns about the development of resistance may require rotating the agents in the protocol. In addition to antimicrobials, other therapies have been used to reduce bacterial overgrowth. Periodic flushes with oral polyethylene glycol electrolyte solutions or other cathartics have been used.40 Probiotics, such as Lactobacillus rhamnosus GG, have been used, although additional studies are needed.41,42
Mineral Supplementation
Vitamin Deficiencies
Similarly, low vitamin A concentrations are present in children with cholestatic liver disease receiving routine vitamin supplementation.46 Altered hepatic synthetic function, however, may also decrease retinol binding protein synthesis, suggesting that unbound vitamin A concentrations could actually be elevated in liver failure. Interestingly, vitamin E levels remain normal in this population, although unsupplemented infants and children continue to demonstrate deficiencies.46
Nutritional Supplements: Growth Hormone and Glutamine To date, there is insufficient evidence to support the use of GH, glutamine, or a combination of the 2 as standard therapy in IF patients. There have been several small studies that evaluated the use of GH, or a combination of GH and glutamine, that have demonstrated an improved nutrient absorption and ability to wean off PN.51–53 Increased lean body mass was shown in 2 studies, using GH and glutamine.54,55 Other studies, however, have failed to demonstrate clinical improvement in fecal volume or intestinal absorption.56–58 None of these studies, including those with positive findings, have shown statistically significant increases in fat absorption.
Other Considerations
Emerging Therapies Pharmaceutical care of the patient with SBS is complex and ever changing as intestinal function improves or complications develop. Pharmacologic therapy is directed at controlling gut motility, enhancing intestinal adaptation, minimizing small bowel overgrowth, and preventing nutrient deficiencies and hepatic complications. No single approach is effective for all patients with SBS, and care must be directed toward specific patient conditions, using an integrated team approach.
In addition to medical and pharmacologic treatments for IF, some patients may require surgical management. Surgical indications for IF can be divided into 2 categories: (1) procedures aimed at correcting the etiology of IF, and (2) procedures addressing the numerous complications from IF. Initial surgeries focus on the correction of anatomic or mechanical abnormalities that threaten the patient's bowel or life. Diseases such as necrotizing enterocolitis, gastroschisis, volvulus, and intestinal atresias all can result in the resection of a large percentage of small and large bowel. The major principles of management are bowel conservation (especially small intestine) and the prompt reestablishment of bowel continuity.8 Surgical management of IF should not be viewed as a last resort but rather an integral aspect of intestinal rehabilitation. Although not fully understood, the small intestine undergoes an adaptation process that may consist of histologic and enzymatic changes, enhancing nutrient absorption and improving bowel motility. Surgeons have used various techniques to manage the symptoms of IF. In 1980, a method of longitudinal intestinal lengthening and tailoring (LILT) was developed.66 This method takes advantage of the 2 leaves of the mesenteric blood supply to the intestines by dividing the bowel longitudinally, at the 12 o'clock position (with the mesentery at the 6 o'clock position). Next, these hemiloops are anastomosed isoperistaltically, resulting in bowel that is smaller in diameter and longer in length. Isolated bowel segments, in which there is an imported blood supply to the antimesenteric border of a dilated bowel loop by attachment to the abdominal wall, have also been attempted.67 A useful adjunct to bowel-lengthening procedures is the creation of a nipple valve.68 This valve, tailored to cause proximal bowel dilation without obstruction, can facilitate a bowel-lengthening operation.
Outcomes With LILT Reported survival after LILT ranges from 30% to 100%.69,70 Survivors that were successfully weaned off PN ranged from 28% to 100%.69,70 The wide disparity in mortality and reduction of PN dependence can likely be attributed to multiple variables among institutions, including preoperative bowel length and degree of liver failure. Furthermore, many of the reported series have been limited by small sample sizes, with the largest including 49 patients.70 Bowel necrosis with LILT has also been reported.70
Serial Transverse Enteroplasty A salient advantage of the STEP procedure is that it is simple to perform. Because of the adaptation process, there can be redilation of the bowel after a LILT operation. Further, bowel segments of variable dilation can be lengthened with the maintenance of a uniform channel. Multiple STEP procedures are feasible by repeating the operation after the process of adaptation and dilation has occurred.73,74 The STEP procedure is also suitable for patients with neonatal atresias and limited bowel length, as well as patients with refractory D-lactic acidosis.71,75–77 Initial studies demonstrated that after the STEP procedure, there are improvements in enteral tolerance, nutrition indices, and ability to wean off PN.74,78,79
Outcomes With STEP
Transplantation Historically, intestinal transplantation was complicated by significant morbidity and mortality. With recent advances in immunosuppression, specifically the use of tacrolimus, outcomes such as mortality, cost-effectiveness, and quality of life have improved over the last decade.81 Currently, patients undergoing intestinal transplants experience 1-year graft survivals of 80% and survival of 80%.82 Three different types of transplants can be offered to patients depending on the nature and extent of their IF: isolated intestinal, liver-intestinal, and multivisceral (eg, stomach, duodenum, pancreas, intestine, and liver). Recent data show that of pediatric intestinal transplantations, 50% are liver-intestinal, 37% are isolated, and 13% are multivisceral.82 The decision regarding the type of transplantation should be based on each patient's specific disease and condition.
Intestinal rehabilitation for pediatric patients with IF is best approached in a multidisciplinary fashion. With specialized nutritionists, pharmacists, gastroenterologists, nurses, and surgeons, patients can be provided with complex medical care tailored to their specific needs. The overriding goal remains the use of the GI tract for oral/enteral nutrition. 1 Btaiche IF, Khalidi N. Parenteral nutrition-associated liver complications in children. Pharmacotherapy.2002; 22:188 –211.[CrossRef][Web of Science][Medline] [Order article via Infotrieve] 2 Javid PJ, Greene AK, Garza J, et al. The route of lipid administration affects parenteral nutrition-induced hepatic steatosis in a mouse model. J Pediatr Surg.2005; 40:1446 –1453.[CrossRef][Web of Science][Medline] [Order article via Infotrieve] 3 Ferezou J, Bach AC. Structure and metabolic fate of triacylglycerol- and phospholipid-rich particles of commercial parenteral fat emulsions. Nutrition.1999; 15:44 –50.[CrossRef][Web of Science][Medline] [Order article via Infotrieve] 4 Mayer K, Fegbeutel C, Hattar K, et al. Omega-3 vs. omega-6 lipid emulsions exert differential influence on neutrophils in septic shock patients: impact on plasma fatty acids and lipid mediator generation. Intensive Care Med.2003; 29:1472 –1481.[CrossRef][Web of Science][Medline] [Order article via Infotrieve] 5 Utter S, Duggan C. Short bowel syndrome. In: Hendricks KM, Duggan C, eds. Manual of Pediatric Nutrition. 4th ed. Hamilton, Ontario, Canada: BC Decker; 2005:718 –735. 6 Gura KM, Duggan CP, Collier SB, et al. Reversal of parenteral
nutrition-associated liver disease in two infants with short bowel syndrome
using parenteral fish oil: implications for future management.
Pediatrics.2006; 118:e197
–e201. 7 Kollman KA, Lien EL, Vanderhoof JA. Dietary lipids influence intestinal adaptation after massive bowel resection. J Pediatr Gastroenterol Nutr. 1999;28:41 –45.[CrossRef][Web of Science][Medline] [Order article via Infotrieve] 8 Andorsky DJ, Lund DP, Lillehei CW, et al. Nutritional and other postoperative management of neonates with short bowel syndrome correlates with clinical outcomes. J Pediatr.2001; 139:27 –33.[CrossRef][Web of Science][Medline] [Order article via Infotrieve] 9 Parker P, Stroop S, Greene H. A controlled comparison of continuous versus intermittent feeding in the treatment of infants with intestinal disease. J Pediatr.1981; 99:360 –364.[CrossRef][Web of Science][Medline] [Order article via Infotrieve] 10 Wessel JJ, Kocoshis SA. Nutritional management of infants with short bowel syndrome. Semin Perinatol.2007; 31:104 –111.[CrossRef][Web of Science][Medline] [Order article via Infotrieve] 11 Sundaram A, Koutkia P, Apovian CM. Nutritional management of short bowel syndrome in adults. J Clin Gastroenterol.2002; 34:207 –220.[CrossRef][Web of Science][Medline] [Order article via Infotrieve] 12 Nordgaard I, Hansen BS, Mortensen PB. Colon as a digestive organ in patients with short bowel. Lancet.1994; 343:373 –376.[CrossRef][Web of Science][Medline] [Order article via Infotrieve] 13 Ovesen L, Chu R, Howard L. The influence of dietary fat on
jejunostomy output in patients with severe short bowel syndrome. Am
J Clin Nutr. 1983;38:270
–277. 14 Woolf GM, Miller C, Kurian R, Jeejeebhoy KN. Diet for patients with a short bowel: high fat or high carbohydrate? Gastroenterology.1983; 84:823 –828.[Medline] [Order article via Infotrieve] 15 Cosnes J, Evard D, Beaugerie L, Gendre JP, Le Quintrec Y. Improvement in protein absorption with a small-peptide-based diet in patients with high jejunostomy. Nutrition.1992; 8:406 –411.[Web of Science][Medline] [Order article via Infotrieve] 16 Levy E, Frileux P, Sandrucci S, et al. Continuous enteral nutrition during the early adaptive stage of the short bowel syndrome. Br J Surg. 1988;75:549 –553.[CrossRef][Web of Science][Medline] [Order article via Infotrieve] 17 McIntyre PB, Fitchew M, Lennard-Jones JE. Patients with a high jejunostomy do not need a special diet. Gastroenterology.1986; 91:25 –33.[Medline] [Order article via Infotrieve] 18 Ksiazyk J, Piena M, Kierkus J, Lyszkowska M. Hydrolyzed versus nonhydrolyzed protein diet in short bowel syndrome in children. J Pediatr Gastroenterol Nutr.2002; 35:615 –618.[CrossRef][Web of Science][Medline] [Order article via Infotrieve] 19 Vanderhoof JA. New and emerging therapies for short bowel syndrome in children. J Pediatr Gastroenterol Nutr.2004; 39 (Suppl 3):S769 –S771.[CrossRef][Web of Science][Medline] [Order article via Infotrieve] 20 Bines J, Francis D, Hill D. Reducing parenteral requirement in children with short bowel syndrome: impact of an amino acid-based complete infant formula. J Pediatr Gastroenterol Nutr.1998; 26:123 –128.[CrossRef][Web of Science][Medline] [Order article via Infotrieve] 21 Matarese LE, O'Keefe SJ, Kandil HM, Bond G, Costa G, AbuElmagd K.
Short bowel syndrome: clinical guidelines for nutrition management.
Nutr Clin Pract.2005; 20:493
–502. 22 Jeppesen PB, Mortensen PB. The influence of a preserved colon on
the absorption of medium chain fat in patients with small bowel resection.
Gut. 1998;43:478
–483. 23 Nightingale JM, Lennard-Jones JE, Gertner DJ, Wood SR, Bartram CI.
Colonic preservation reduces need for parenteral therapy, increases incidence
of renal stones, but does not change high prevalence of gall stones in
patients with a short bowel. Gut.1992; 33:1493
–1497. 24 Bond JH, Currier BE, Buchwald H, Levitt MD. Colonic conservation of malabsorbed carbohydrate. Gastroenterology.1980; 78:444 –447.[Medline] [Order article via Infotrieve] 25 Goulet O, Ruemmele F, Lacaille F, Colomb V. Irreversible intestinal failure. J Pediatr Gastroenterol Nutr.2004; 38:250 –269.[Web of Science][Medline] [Order article via Infotrieve] 26 Lennard-Jones JE. Review article: practical management of the short bowel. Aliment Pharmacol Ther.1994; 8:563 –577.[Web of Science][Medline] [Order article via Infotrieve] 27 Heel RC, Brogden RN, Speight TM, Avery GS. Loperamide: a review of its pharmacological properties and therapeutic efficacy in diarrhoea. Drugs. 1978;15:33 –52.[Web of Science][Medline] [Order article via Infotrieve] 28 Remington M, Malagelada JR, Zinsmeister A, Fleming CR. Abnormalities in gastrointestinal motor activity in patients with short bowels: effect of a synthetic opiate. Gastroenterology. 1983;85 : 629–636.[Medline] [Order article via Infotrieve] 29 Karamanolis G, Tack J. Promotility medications: now and in the future. Dig Dis.2006; 24:297 –307.[CrossRef][Web of Science][Medline] [Order article via Infotrieve] 30 Jones MP. Access options for withdrawn motility-modifying agents. Am J Gastroenterol.2002; 97:2184 –2188.[CrossRef][Web of Science][Medline] [Order article via Infotrieve] 31 Scarpignato C, Pelosini I. Management of irritable bowel syndrome: novel approaches to the pharmacology of gut motility. Can J Gastroenterol.1999; 13(Suppl A):50A –65A.[Medline] [Order article via Infotrieve] 32 Banh HL, MacLean C, Topp T, Hall R. The use of tegaserod in critically ill patients with impaired gastric motility. Clin Pharmacol Ther. 2005;77:583 –586.[CrossRef][Web of Science][Medline] [Order article via Infotrieve] 33 Muller-Lissner SA, Fumagalli I, Bardhan KD, et al. Tegaserod, a 5-HT(4) receptor partial agonist, relieves symptoms in irritable bowel syndrome patients with abdominal pain, bloating and constipation. Aliment Pharmacol Ther.2001; 15:1655 –1666.[CrossRef][Web of Science][Medline] [Order article via Infotrieve] 34 Lamberts SW, van der Lely AJ, de Herder WW, Hofland LJ. Octreotide.
N Engl J Med.1996; 334:246
–254. 35 Nehra V, Camilleri M, Burton D, Oenning L, Kelly DG. An open trial of octreotide long-acting release in the management of short bowel syndrome. Am J Gastroenterol.2001; 96:1494 –1498.[CrossRef][Web of Science][Medline] [Order article via Infotrieve] 36 Sinha L, Liston R, Testa HJ, Moriarty KJ. Idiopathic bile acid malabsorption: qualitative and quantitative clinical features and response to cholestyramine. Aliment Pharmacol Ther.1998; 12:839 –844.[CrossRef][Web of Science][Medline] [Order article via Infotrieve] 37 Kaufman SS, Loseke CA, Lupo JV, et al. Influence of bacterial overgrowth and intestinal inflammation on duration of parenteral nutrition in children with short bowel syndrome. J Pediatr.1997; 131:356 –361.[Web of Science][Medline] [Order article via Infotrieve] 38 Puwanant M, Mo-Suwan L, Patrapinyokul S. Recurrent D-lactic acidosis in a child with short bowel syndrome. Asia Pac J Clin Nutr. 2005;14:195 –198.[Web of Science][Medline] [Order article via Infotrieve] 39 Dibaise JK, Young RJ, Vanderhoof JA. Enteric microbial flora, bacterial overgrowth, and short-bowel syndrome. Clin Gastroenterol Hepatol. 2006;4:11 –20.[CrossRef][Web of Science][Medline] [Order article via Infotrieve] 40 Demirogullari B, Poyraz A, Cirak MY, et al. Effects of hyperosmolar agents—lactulose, lactitol, sodium phosphate and polyethylene glycol—on cecal coliform bacteria during traditional bowel cleansing: an experimental study in rats. Eur Surg Res.2004; 36:159 –164.[CrossRef][Web of Science][Medline] [Order article via Infotrieve] 41 Vanderhoof JA, Young RJ, Murray N, Kaufman SS. Treatment strategies for small bowel bacterial overgrowth in short bowel syndrome. J Pediatr Gastroenterol Nutr.1998; 27:155 –160.[CrossRef][Web of Science][Medline] [Order article via Infotrieve] 42 Marteau PR, de Vrese M, Cellier CJ, Schrezenmeir J. Protection from
gastrointestinal diseases with the use of probiotics. Am J Clin
Nutr. 2001;73(2
Suppl): 430S–436S. 43 Richette P, Ayoub G, Bardin T, Bouvet S, Orcel P, Badran AM.
Hypomagnesemia and chondrocalcinosis in short bowel syndrome. J
Rheumatol. 2005;32:2434
–2436. 44 Howard Payne J, De Wing LT, Commons RR. Metabolic observations in patients with jejunocolic shunts: 1963. Nutr Hosp.2006; 21:209 –221.[Medline] [Order article via Infotrieve] 45 Mager DR, McGee PL, Furuya KN, Roberts EA. Prevalence of vitamin K deficiency in children with mild to moderate chronic liver disease. J Pediatr Gastroenterol Nutr.2006; 42:71 –76.[CrossRef][Web of Science][Medline] [Order article via Infotrieve] 46 Alvarez F, Cresteil D, Lemonnier F, Lemonnier A, Alagille D. Plasma vitamin E levels in children with cholestasis. J Pediatr Gastroenterol Nutr. 1984;3:390 –393.[Web of Science][Medline] [Order article via Infotrieve] 47 Peterson CA, Ney DM, Hinton PS, Carey HV. Beneficial effects of insulin-like growth factor I on epithelial structure and function in parenterally fed rat jejunum. Gastroenterology.1996; 111:1501 –1508.[CrossRef][Web of Science][Medline] [Order article via Infotrieve] 48 Gu Y, Wu ZH, Xie JX, Jin DY, Zhuo HC. Effects of growth hormone (rhGH) and glutamine supplemented parenteral nutrition on intestinal adaptation in short bowel rats. Clin Nutr.2001; 20:159 –166.[CrossRef][Web of Science][Medline] [Order article via Infotrieve] 49 Ziegler TR, Mantell MP, Chow JC, Rombeau JL, Smith RJ. Gut adaptation and the insulin-like growth factor system: regulation by glutamine and IGF-I administration. Am J Physiol.1996; 271(5 Pt 1):G866 –G875.[Web of Science][Medline] [Order article via Infotrieve] 50 Wu G, Knabe DA, Yan W, Flynn NE. Glutamine and glucose metabolism in enterocytes of the neonatal pig. Am J Physiol.1995; 268(2 Pt 2):R334 –R342.[Web of Science][Medline] [Order article via Infotrieve] 51 Seguy D, Vahedi K, Kapel N, Souberbielle JC, Messing B. Low-dose growth hormone in adult home parenteral nutrition-dependent short bowel syndrome patients: a positive study. Gastroenterology.2003; 124:293 –302.[CrossRef][Web of Science][Medline] [Order article via Infotrieve] 52 Byrne TA, Morrissey TB, Nattakom TV, Ziegler TR, Wilmore DW. Growth
hormone, glutamine, and a modified diet enhance nutrient absorption in
patients with severe short bowel syndrome. JPEN J Parenter Enteral
Nutr. 1995;19:296
–302. 53 Byrne TA, Wilmore DW, Iyer K, et al. Growth hormone, glutamine, and an optimal diet reduces parenteral nutrition in patients with short bowel syndrome: a prospective, randomized, placebo-controlled, double-blind clinical trial. Ann Surg. 2005;242 :655 –661.[CrossRef][Web of Science][Medline] [Order article via Infotrieve] 54 Scolapio JS. Effect of growth hormone, glutamine, and diet on body
composition in short bowel syndrome: a randomized, controlled study.
JPEN J Parenter Enteral Nutr.1999; 23:309
–313. 55 Jeppesen PB, Szkudlarek J, Hoy CE, Mortensen PB. Effect of high-dose growth hormone and glutamine on body composition, urine creatinine excretion, fatty acid absorption, and essential fatty acids status in short bowel patients: a randomized, double-blind, crossover, placebo-controlled study. Scand J Gastroenterol.2001; 36:48 –54.[Web of Science][Medline] [Order article via Infotrieve] 56 Scolapio JS, Camilleri M, Fleming CR, et al. Effect of growth hormone, glutamine, and diet on adaptation in short-bowel syndrome: a randomized, controlled study. Gastroenterology.1997; 113:1074 –1081.[CrossRef][Web of Science][Medline] [Order article via Infotrieve] 57 Ellegard L, Bosaeus I, Nordgren S, Bengtsson BA. Low-dose recombinant human growth hormone increases body weight and lean body mass in patients with short bowel syndrome. Ann Surg.1997; 225:88 –96.[CrossRef][Web of Science][Medline] [Order article via Infotrieve] 58 Szkudlarek J, Jeppesen PB, Mortensen PB. Effect of high dose growth
hormone with glutamine and no change in diet on intestinal absorption in short
bowel patients: a randomised, double blind, crossover, placebo controlled
study. Gut.2000; 47:199
–205. 59 Severijnen R, Bayat N, Bakker H, Tolboom J, Bongaerts G. Enteral drug absorption in patients with short small bowel: a review. Clin Pharmacokinet. 2004;43:951 –962.[CrossRef][Web of Science][Medline] [Order article via Infotrieve] 60 Drucker DJ, Erlich P, Asa SL, Brubaker PL. Induction of intestinal
epithelial proliferation by glucagon-like peptide 2. Proc Natl Acad
SciUSA. 1996;93:7911
–7916. 61 Scott RB, Kirk D, MacNaughton WK, Meddings JB. GLP-2 augments the adaptive response to massive intestinal resection in rat. Am J Physiol. 1998;275(5 Pt 1): G911–G921.[Web of Science][Medline] [Order article via Infotrieve] 62 Wojdemann M, Wettergren A, Hartmann B, Holst JJ. Glucagon-like peptide-2 inhibits centrally induced antral motility in pigs. Scand J Gastroenterol. 1998;33:828 –832.[CrossRef][Web of Science][Medline] [Order article via Infotrieve] 63 Wojdemann M, Wettergren A, Hartmann B, Hilsted L, Holst JJ.
Inhibition of sham feeding-stimulated human gastric acid secretion by
glucagon-like peptide-2. J Clin Endocrinol Metab.1999; 84:2513
–2517. 64 Jeppesen PB, Hartmann B, Thulesen J, et al. Glucagon-like peptide 2 improves nutrient absorption and nutritional status in short-bowel patients with no colon. Gastroenterology.2001; 120:806 –815.[CrossRef][Web of Science][Medline] [Order article via Infotrieve] 65 Jeppesen PB, Sanguinetti EL, Buchman A, et al. Teduglutide
(ALX-0600), a dipeptidyl peptidase IV resistant glucagon-like peptide 2
analogue, improves intestinal function in short bowel syndrome patients.
Gut. 2005;54:1224
–1231. 66 Bianchi A. Intestinal loop lengthening: a technique for increasing small intestinal length. J Pediatr Surg.1980; 15:145 –151.[CrossRef][Web of Science][Medline] [Order article via Infotrieve] 67 Ienaga T, Kimura K, Hashimoto K, Lee SC, Brakstad M, Soper RT. Isolated bowel segment (Iowa model 1): technique and histological studies. J Pediatr Surg.1990; 25:902 –904.[CrossRef][Web of Science][Medline] [Order article via Infotrieve] 68 Georgeson K, Halpin D, Figueroa R, Vincente Y, Hardin W Jr. Sequential intestinal lengthening procedures for refractory short bowel syndrome. J Pediatr Surg.1994; 29:316 –321.[Web of Science][Medline] [Order article via Infotrieve] 69 Bianchi A. From the cradle to enteral autonomy: the role of autologous gastrointestinal reconstruction. Gastroenterology.2006; 130(2 Suppl 1):S138 –S146.[Medline] [Order article via Infotrieve] 70 Hosie S, Loff S, Wirth H, Rapp HJ, von Buch C, Waag KL. Experience of 49 longitudinal intestinal lengthening procedures for short bowel syndrome. Eur J Pediatr Surg.2006; 16:171 –175.[CrossRef][Web of Science][Medline] [Order article via Infotrieve] 71 Kim HB, Fauza D, Garza J, Oh JT, Nurko S, Jaksic T. Serial transverse enteroplasty (STEP): a novel bowel lengthening procedure. J Pediatr Surg.2003; 38:425 –429.[CrossRef][Web of Science][Medline] [Order article via Infotrieve] 72 Kim HB, Lee PW, Garza J, Duggan C, Fauza D, Jaksic T. Serial transverse enteroplasty for short bowel syndrome: a case report. J Pediatr Surg. 2003;38:881 –885.[CrossRef][Web of Science][Medline] [Order article via Infotrieve] 73 Piper H, Modi BP, Kim HB, Fauza D, Glickman J, Jaksic T. The second STEP: the feasibility of repeat serial transverse enteroplasty. J Pediatr Surg. 2006;41:1951 –1956.[CrossRef][Web of Science][Medline] [Order article via Infotrieve] 74 Modi BP, Javid PJ, Jaksic T, et al. First report of the International Serial Transverse Enteroplasty Data Registry: indications, efficacy, and complications. J Am Coll Surg.2007; 204:365 –371.[CrossRef][Web of Science][Medline] [Order article via Infotrieve] 75 Modi BP, Langer M, Duggan C, Kim HB, Jaksic T. Serial transverse enteroplasty for management of refractory D-lactic acidosis in short-bowel syndrome. J Pediatr Gastroenterol Nutr.2006; 43:395 –397.[CrossRef][Web of Science][Medline] [Order article via Infotrieve] 76 Wales PW, Dutta S. Serial transverse enteroplasty as primary therapy for neonates with proximal jejunal atresia. J Pediatr Surg. 2005;40:E31 –E34.[Web of Science][Medline] [Order article via Infotrieve] 77 Ismail A, Alkadhi A, Alnagaar O, Khirate A. Serial transverse enteroplasty in intestinal atresia management. J Pediatr Surg. 2005;40:E5 –E6.[Web of Science][Medline] [Order article via Infotrieve] 78 Chang RW, Javid PJ, Oh JT, et al. Serial transverse enteroplasty enhances intestinal function in a model of short bowel syndrome. Ann Surg.2006; 243:223 –228.[CrossRef][Web of Science][Medline] [Order article via Infotrieve] 79 O'Keefe SJ, Buchman AL, Fishbein TM, Jeejeebhoy KN, Jeppesen PB, Shaffer J. Short bowel syndrome and intestinal failure: consensus definitions and overview. Clin Gastroenterol Hepatol.2006; 4:6 –10.[CrossRef][Web of Science][Medline] [Order article via Infotrieve] 80 Barksdale EM, Stanford A. The surgical management of short bowel syndrome. Curr Gastroenterol Rep.2002; 4:229 –237.[CrossRef][Medline] [Order article via Infotrieve] 81 Sudan D. Cost and quality of life after intestinal transplantation. Gastroenterology.2006; 130(2 Suppl 1):S158 –S162.[Medline] [Order article via Infotrieve] 82 The Intestinal Transplant Registry. Available at: http://www.intestinaltransplant.org. Accessed June 30, 2007.
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-6 fatty acids and triglycerides, but are devoid of
cholesterol or
protein.