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PubMed1995

Stapled intestinal anastomosis in neonates and infants: use of the endoscopic intestinal stapler.

Stapled anastomoses of the gastrointestinal tract, commonplace in adults and older children, are rarely performed in newborns because of the size of the instruments. The development of smaller stapling devices for laparoscopic and thoracoscopic procedures presented an opportunity to evaluate the efficacy of such anastomoses in neonates and infants. Over an 11-month period, seven newborn or young infants underwent stapled functional end-to-end small or large intestinal anastomoses using the Endo-GIA 30. The male:female ratio was 3:4, and the mean age was 72d (range, 1 to 134 days). The mean weight at the time of the stapled anastomosis was 3.7 kg (range, 1.88 to 6.6 kg). The clinical setting requiring the intestinal anastomoses included ileostomy closure after perforated necrotizing enterocolitis (3), intestinal atresia (1), distal ileal volvulus (1), left colon mesenteric cyst (1), and biliary atresia (1). There were no deaths or anastomotic leaks. Nasogastric decompression was discontinued at a mean of 6 days (range, 3 to 11 days), and oral feedings were begun at a mean of 7.0 days (range, 4 to 12 days). The patients were discharged from the hospital 7 to 117 days after the operation (mean, 33 days). The endoscopic stapling instrument is safe and effective in performing small and large intestinal anastomoses in newborns and young infants.

Age Factors↗
PubMed1987

Vibrio cholerae metalloproteinase degrades intestinal mucin and facilitates enterotoxin-induced secretion from rat intestine.

Mucin secretion in situ from rat intestinal loops was promoted more effectively by dialysed crude cholera filtrate than by an equivalent amount of purified enterotoxin. The filtrate could be rendered inactive by incubation with mixed gangliosides or passage through a GM1-affinity column, which indicated that the secretory action of the filtrate depended upon its enterotoxin component. In an effort to explain the greater potency of the filtrate, we established the presence of a metalloproteinase in the filtrate and demonstrated that this enzyme was capable of degrading purified rat intestinal mucin. Sufficient degradation occurred to cause a substantial decrease in viscosity (57% in 120 min). Biochemical analysis of the mucin before and after exposure to filtrate revealed a rise in the combined percentage of serine, threonine and proline (53-58%), suggesting that poorly glycosylated areas (which are less abundant in these amino acids) were being partly removed from the mucin. The carbohydrate composition was essentially unaltered. Inhibition of the filtrate metalloproteinase by Zincov and alpha 2-macroglobulin significantly (P less than 0.005) reduced the ability of cholera filtrate to degrade mucin or to stimulate mucin secretion from rat intestinal slices in vitro. Purified cholera enterotoxin added to enterotoxin-depleted filtrate was a more potent secretagogue (secretory stimulant) in intestinal loops than an equivalent amount of enterotoxin alone. We therefore propose that mucin secretion induced by cholera filtrate is caused by cholera enterotoxin, but that degradation of the protective epithelial mucus layer by a constituent metalloproteinase may assist the toxin by allowing increased access to mucosal GM1 receptor sites.

Amino Acids↗
PubMed1985

Somatostatin binding sites in cytosolic fraction of rabbit intestinal mucosa: distribution throughout the intestinal tract.

Specific binding sites for somatostatin have been identified in cytosolic fraction of both small and large intestinal mucosa. The stoichiometric data suggested the presence of two classes of binding sites in each part of the intestine. The binding capacity varied depending on the segment considered (rectum greater than duodenum = jejunum greater than ileum, caecum and colon). However, the affinities of the binding sites were similar throughout the whole intestinal mucosa, with the exception of rectum which showed higher Kd values. The binding sites were shown to be highly specific for somatostatin since neuropeptides such as vasoactive intestinal peptide, neurotensin, substance P and Leu-enkephalin did not show any effect upon somatostatin binding.

Animals↗
PubMed2005

Intestinal-fatty acid binding protein and lipid transport in human intestinal epithelial cells.

Intestinal-fatty acid binding protein (I-FABP) is a 14-15 kDa cytoplasmic molecule highly expressed in the enterocyte. Although different functions have been proposed for various FABP family members, the specific function of I-FABP in human intestine remains unclear. Here, we studied the role of I-FABP in molecularly modified normal human intestinal epithelial cells (HIEC-6). cDNA transfection resulted in 90-fold I-FABP overexpression compared to cells treated with empty pQCXIP vector. The high-resolution immunogold technique revealed labeling mainly in the cytosol and confirmed the marked phenotype abundance of I-FABP in cDNA transfected cells. I-FABP overexpression was not associated with alterations in cell proliferation and viability. Studies using these transfected cells cultured with [14C]oleic acid did not reveal higher efficiency in de novo synthesis or secretion of triglycerides, phospholipids, and cholesteryl esters compared to cells treated with empty pQCXIP vector only. Similarly, the incubation with [35S]methionine did not disclose a superiority in the biogenesis of apolipoproteins (apo) A-I, A-IV, B-48, and B-100. Finally, cells transfected with I-FABP did not exhibit an increased production of chylomicrons, VLDL, LDL, and HDL. Our observations establish that I-FABP overexpression in normal HIEC-6 is not related to cell proliferation, lipid esterification, apo synthesis, and lipoprotein assembly, and, therefore, exclude its role in intestinal fat transport.

Apolipoproteins↗
PubMed2004

Induced reactivity of intestinal CD4(+) T cells with an epithelial cell lectin, galectin-4, contributes to exacerbation of intestinal inflammation.

Inflammatory bowel disease is an immune-mediated intestinal inflammatory condition that is associated with an increase in autoantibodies that bind to epithelial cells. However, it is unknown whether the epithelial cell-derived products that are recognized by such autoantibodies are involved in the pathogenic process. Through a combined antigen-screening approach utilizing humoral and cellular immune responses, we identify herein an epithelial lectin, galectin-4, that specifically stimulates IL-6 production by CD4(+) T cells. Interestingly, the reactivity of CD4(+) T cells to galectin-4 is precisely elicited under intestinal inflammatory conditions. The galectin-4-mediated production of IL-6 is MHC class II independent and induced by PKCtheta-associated pathway through the immunological synapse. The galectin-4-mediated stimulation of CD4(+) T cells is shown to exacerbate chronic colitis and delay the recovery from acute intestinal injury. These studies identify the presence of an immunogenic, endogenous lectin in the intestine and dissect the biological role of lectin/CD4(+) T cell interactions under inflammatory conditions.

Animals↗
PubMed2003

Prevalence of liver complications in pediatric patients on home parenteral nutrition: indications for intestinal or combined liver-intestinal transplantation.

Parenteral nutrition (PN) is the only treatment for patients affected by chronic intestinal failure (CIF). Home parenteral nutrition (HPN) programs are started when patients need prolonged PN. Unfortunately, many patients on prolonged PN develop liver disease (LD). The aim of our study was to assess the prevalence of LD in our series of patients on HPN. We reviewed our records of patients discharged from the hospital on HPN for CIF. HPN was started when one parent was fully trained in the use of this treatment and if the social and familial home environment was reliable. All patients received total PN by a central venous catheter. All patients with abnormal AST, ALT, ALK, gammaGT, and bilirubin values for more than 3 months were considered affected by PN-related LD. Thirty-six patients (23 of whom were boys and 13 girls) were discharged on HPN. During the study period, for CIF, 16 were affected by short bowel syndrome (SBS), of whom 6 had ultra-short bowel; 16 with functional intestinal failure, and 4 with chronic intestinal pseudobstruction (CIPO). Mean duration of HPN was 2.1 years/patient. Nine of 36 patients (25%) on HPN for CIF showed LD. Seven of the 16 patients (43%) with LD were affected by SBS and 2 (12.5%) patients by functional intestinal failure. No patients with CIPO developed LD. In patients affected by SBS, the onset of LD was very earlier than in patients with ID.

Adult↗
PubMed2004

Intestinal graft versus native liver cytokine expression in a rat model of intestinal transplantation: effect of donor-specific cell augmentation.

INTRODUCTION: Immunomodulation by portal vein delivery of donor antigen reduces intestinal graft rejection. We investigated the impact of portal venous donor-specific cell augmentation (blood versus bone marrow) on cytokine expression in intestinal grafts versus native livers. METHODS: Ten groups of intestinal transplants (brown Norway male to Lewis female rats) varied by (1). the type of donor-specific cell augmentation and (2). the use and dose of tacrolimus-based immunosuppression. Tissue samples for histologic analysis and cytokine mRNA analysis were obtained at designated time points. RESULTS: Without immunosuppression, no type of cell augmentation reduced the rate of rejection. With immunosuppression, outcome was significantly better after portal donor-specific blood transfusion (versus bone marrow infusion). Irrespective of the type of cell augmentation, severe rejection caused strong intragraft expression of IL-1alpha, IL-1beta, IFN-gamma, and TNF-alpha; liver expression mainly involved TNF-alpha. Of note, nonimmunosuppressed, cell-augmented rats showed hardly any differences in cytokine expression in their grafts versus significant increases in their native livers. With immunosuppression, bone marrow infusion (versus blood transfusion) increased intragraft cytokine expression of IL-1alpha, IL-1beta, IFN-gamma, as well as TNF-alpha, and liver expression of IL-1beta. CONCLUSIONS: (1). Rejection and donor-specific cell augmentation independently caused differences in intragraft versus native liver cytokine expression after intestinal transplants. (2). Portal donor-specific blood transfusion (versus bone marrow infusion) lowered the incidence of rejection and diminished intragraft cytokine up-regulation. (3). In our study, TNF-alpha appeared to be the cytokine most strongly associated with rejection.

Animals↗
PubMed1998

Oleic acid distribution in small intestinal epithelial cells expressing intestinal-fatty acid binding protein.

Intestinal-fatty acid binding protein (I-FABP) has been proposed to target long chain fatty acids (LCFA) to triglyceride synthesis pathways in the intestinal epithelium. In the present studies hBRIE 380i cells, which endogenously express I-FABP only when fully differentiated, were used to investigate the role of I-FABP in LCFA incorporation and targeting by examining the relative distribution of [3H]-oleic acid in cellular lipids in these cells. [3H]-oleic acid incorporation into triglyceride was significantly higher in hBRIE 380i cells expressing I-FABP than in cells not expressing I-FABP. After 15 min, 1 and 4 h of incubation, cells expressing I-FABP incorporated 24.0%, 34.0% and 43.9% of [3H]-oleic acid into triglyceride, while newly confluent cells (no I-FABP expression) incorporated 15.6%, 18.3% and 31.9%. An I-FABP negative cell line, hBRIE 380i-neg cells, was stably transfected to investigate the effect of adding I-FABP to small intestinal epithelial cell lines. No measurable differences in [3H]-oleic acid incorporation into triglyceride was detected in these transfectants. Additionally I-FABP expression had no effect on [3H]-oleic acid incorporation or distribution within phospholipid subclasses in hBRIE 380i or transfected hBRIE 380i-neg fabpi cells. Our data from hBRIE 380i cells suggest that I-FABP can target LCFA to triglyceride synthesis pathway. However, endogenous I-FABP expression was also correlated to cellular differentiation and therefore raises the possibility that other differentiation-dependent factors may have a role in LCFA targeting. Because no effects of I-FABP were detected in the transfected hBRIE 380i-neg fabpi cells, it is concluded that factors in addition to I-FABP play a major role in determining the metabolic fate of LCFA in small intestinal epithelial cells. (c) 1998 Elsevier Science B.V.

Animals↗
PubMed2003

Intestinal myofibroblasts in innate immune responses of the intestine.

BACKGROUND & AIMS: Intestinal myofibroblasts are known to respond to inflammatory signals and may play a role in Crohn's disease-associated fibrosis. However, putative involvement by myofibroblasts in innate immune responses as part of intestinal host defense has not been characterized. We therefore analyzed expression and regulation of toll-like receptors (TLRs) in colonic human myofibroblasts (CCD-18) and primary human colonic myofibroblasts in comparison with human lung myofibroblasts (CCD-37). METHODS: Expression of TLRs (1-10) and NOD 1 and 2 was assessed before and after stimulation with either lipopolysaccharide (LPS) or lipoteichoic acid (LTA) by using a custom microarray, reverse-transcription polymerase chain reaction, Northern blot and Western blot analysis, and immunohistochemistry. Activation of signaling pathways, translocation of p65, and secretion of interleukin (IL)-8 were determined. RESULTS: Messenger RNAs encoding for TLR1-9, as well as NOD1 and NOD2, were amplified from cultured and primary human intestinal myofibroblasts. After stimulation with LPS or LTA, a 1.5-4.2-fold up-regulation of TLRs (2, 3, 4, 6, 7) and elements of the signaling cascade (MyD88, TIR domain-containing adapter protein [TIRAP]) was observed. CCD-18 and CCD-37 cells expressed TLR 2 and 4 protein, which were located primarily on the cell membrane. Stimulation with LTA or LPS resulted in activation of the mitogen-activated protein kinases pathway, nuclear translocation of p65, and significantly increased IL-8 secretion. CONCLUSIONS: Bacterial components directly activate intestinal myofibroblasts expressing TLRs. These cells may therefore participate in innate immune responses by sensing and responding to bacterial products that have penetrated into the subepithelial compartment.

Cells, Cultured↗
PubMedDate not supplied

Effect of intestinal helminthiasis on intestinal permeability of early primary schoolchildren.

Intestinal permeability of 246 early primary schoolchildren at 2 schools (106 of whom were infected with intestinal helminths) was assessed by using the lactulose/mannitol differential absorption test. The ratio of the urinary recoveries of lactulose and mannitol was determined after oral administration of a standard solution of the 2 sugars. Assessment of intestinal permeability was repeated on 100 infected children after treatment and on a cohort of 68 uninfected children. Infected and uninfected groups were compared with respect to baseline lactulose/mannitol ratio (L/M1) and change in lactulose/mannitol ratio between assessments (delta L/M). The correlations between baseline intensity of infection and L/M1, and between fall in intensity and delta L/M, were evaluated. Based on a crude index of socioeconomic status, each child was assigned to one of 3 socioeconomic groups; all but 3 children belonged to either groups 2 or 3. Trichuris trichiura and Ascaris lumbricoides were the 2 predominant infections; the hookworm infection rate was relatively low. The results suggested that helminthiasis exerted only a marginal effect on intestinal permeability, the impact of which in children from lower socioeconomic backgrounds was negligible in comparison with the cumulative effects of other factors.

Albendazole↗
PubMedDate not supplied

An unique CD4+CD8+ intestinal intraepithelial lymphocyte specific for DnaK (Escherichia coli HSP70) may be selected by intestinal microflora of rats.

We have previously shown an age-associated increase in unique CD4+CD8+ intestinal intraepithelial lymphocytes (i-IEL) in rats. To elucidate the potential causes of the increase in CD4+CD8+ i-IEL with age, we analyzed the specificity of the CD4+CD8+ i-IEL and influence of intestinal microflora on the increase in this subset in aged rats. The purified CD4+CD8+ i-IEL proliferated in response to DnaK [Escherichia coli (E. coli) HSP70] in the presence of mitomycin-c (MMC)-treated syngeneic spleen cells. The proportion of CD4+CD8+ T cells in whole i-IEL were significantly increased in aged rats fed commercial (CL-2) diet but not in those fed home-made (purified) diet under conventional condition. No CD4+CD8+ i-IEL were detected in aged rats under germfree condition, irrespective of diet feeding. A larger number of Enterobacteriaceae, especially E. coli, were detected in the intestinal contents and feces from aged rats with CD4+CD8+ i-IEL compared with those from aged rats fed without CD4+CD8+ i-IEL. The unique CD4+CD8+ i-IEL population specific for E. coli HSP may be associated with long term exposure to intestinal E. coli in aged rats.

Aging↗
PubMed1992

The effects of S(-) and R(+) sulpiride, metoclopramide, cisapride and domperidone on the small intestine suggest DA2-receptors are involved in the control of small intestinal transit time in rats.

To study the effect of intraperitoneal S(-)sulpiride (1-15 mg/kg), R(+)sulpiride (5-10 mg/kg), metoclopramide (1-15 mg/kg), cisapride (10 mg/kg) and domperidone (5-10 mg/kg) on intestinal progression, rats were given the test drug followed by oral lactulose. Their hydrogen excretion was used to calculate the small bowel transit time (SBTT) and maximum peak time (MPT). Metoclopramide (7.5 mg/kg) had the greatest effect on SBTT (-25%), followed by S(-)sulpiride and domperidone. S(-)sulpiride (10 mg/kg) had the greatest activity on the MPT (-35.2%) followed by metoclopramide. R(+)sulpiride and cisapride did not modify SBTT and MPT. In conclusion S(-)sulpiride is the isomer active on intestinal transit and DA2-receptors seem important targets in the modulation of intestinal progression, since S(-)sulpiride, metoclopramide and domperidone are DA2-receptor antagonists, and R(+)sulpiride and cisapride are not. The H2 breath test proved a valid method for measuring the effect of drugs on the small intestine in animals.

Animals↗
PubMed2003

Turkey intestine as a commercial source of heparin? Comparative structural studies of intestinal avian and mammalian glycosaminoglycans.

Heparin is a glycosaminoglycan (GAG) that is extracted primarily from porcine intestinal tissues and is widely used as a clinical anticoagulant. It is biosynthesized as a proteoglycan and stored exclusively in mast cells and is partially degraded to peptidoglycan and GAG on immunologically activated mast cell degranulation. In contrast, the structurally related heparan sulfate, is the polysaccharide portion of a ubiquitous proteoglycan, localized on cell surface and in the extracellular matrix of all animal tissues. Heparin and heparan sulfate are made in the Golgi through a similar biosynthetic pathway. The current study was undertaken in a search for alternative, non-mammalian, sources of anticoagulant heparin. The heparin/heparan sulfate family of GAGs, prepared and purified from turkey intestine, were assayed for anticoagulant activity and structurally characterized. The resulting GAGs displayed a very low anticoagulant activity when compared to those obtained from porcine intestine using an identical procedure. Structural characterization studies clearly demonstrate that heparan sulfate is the major GAG in the turkey intestine. This observation is rationalized based on differences in the mammalian and avian coagulation and immune systems.

Animals↗
PubMed2000

Intestinal fatty acid binding protein may favor differential apical fatty acid binding in the intestine.

The intestinal mucosa metabolizes fatty acids differently when presented to the lumenal or basolateral membrane. Expression of both liver and intestinal fatty acid binding proteins (L- and I-FABPs) uniquely in the enterocyte offers a possible explanation of this phenomenon. An organ explant system was used to analyze the relative binding of fatty acids to each protein. More fatty acid was bound to L-FABP than to I-FABPs (28% vs. 6% of cytosolic radioactivity), no matter on which side the fatty acid was added. However, a 2-3-fold increase in fatty acid binding to the intestinal paralog was noted after apical addition of palmitic or oleic acid in mucosa from chow fed rats. When oleic acid was added apically, a 1.4-fold increase in binding to I-FABP was observed in mucosa derived from chronically fat fed rats, consistent with the previously observed 50% increase in the content of that protein. Immunocytochemical localization of both FABPs in vivo demonstrated an apical cytoplasmic localization in the fasting state, and redistribution to the entire cytoplasm after fat feeding. These data are consistent with the hypothesis that I-FABP may contribute to the metabolic compartmentalization of apically presented fatty acids in the intestine.

Animals↗
PubMed1967

Enzymic hydrolysis of the carbon-fluorine bond of alpha-D-glucosyl fluoride by rat intestinal mucosa. Localization of intestinal maltase.

1. alpha-d-Glucosyl fluoride was hydrolysed by an extract of rat intestinal mucosa. The pH optimum was 6.6 and the K(m) 0.4mm at 20 degrees . Activity was assayed by release of either glucose or fluoride. 2. The alpha-d-glucosyl fluoride-hydrolase activity of the extract was associated with both mutarotase and alpha-d-glucosidase activities. 3. Tris (5mm) inhibited both the alpha-d-glucosidase and alpha-d-glucosyl fluoride-hydrolase activities by 55% but did not inhibit mutarotase. The K(i) of tris for both enzyme activities was 2mm. 4. The extract did not hydrolyse melibiose and lactose. Mutarotase used both alpha-d-glucose and beta-l-arabinose as substrates but the glucosyl fluoride-hydrolase activity did not extend to beta-l-arabinosyl fluoride. 5. The thermal stability of alpha-d-glucosidase and alpha-d-glucosyl fluoride hydrolase was identical. Mutarotase was more thermolabile. 6. A preparation of the brush border of intestinal epithelial cells contained both alpha-d-glucosyl fluoride-hydrolase and alpha-d-glucosidase activities. In each precipitate and washing the ratio of the two activities was the same. All the mutarotase activity was in the first supernatant. 7. Agidex, a fungal amyloglucosidase, cleaved glucosyl fluoride in addition to maltose. Tris inhibited both activities and in each case the K(i) was 3mm. 8. The probable identity of alpha-d-glucosyl fluoride hydrolase with alpha-d-glucosidase is discussed and a possible mechanism for the reaction suggested. 9. Incubation of intestinal slices with alpha-d-glucosyl fluoride led to complete hydrolysis in 30min. The glucose rapidly entered the cell and was metabolized, leaving the fluoride in the incubation medium. This constitutes a further proof that the intestinal alpha-d-glucosidase, although on the brush border, is located outside the site of active transport of sugars.

Animals↗
PubMed2000

Comparison of clinical, endoscopic and functional findings in patients with intestinal metaplasia at the cardia, carditis and short-segment columnar epithelium of the distal esophagus with and without intestinal metaplasia.

In recent years, the diagnosis of short segments of intestinal metaplasia lining the distal esophagus has increased. The aim of the present study was to determine the clinical, endoscopic, histologic and functional results in patients with intestinal metaplasia at the cardia (IMC), carditis and short-segment columnar epithelium (CE) lining the distal esophagus with and without intestinal metaplasia. Four groups were studied: 48 patients with carditis, 105 patients with IMC, 78 patients with short-segment CE (SSCE) without IM and 69 patients with short-segment CE with IM. All had clinical questionnaire, endoscopic and histological evaluation, manometric studies and measurements of acid and bilirubin exposition of the distal esophagus over 24 h. Patients without IM were found to be younger than those with IM. Erosive esophagitis was observed in similar proportions, but hiatal hernia was present in patients with SSCE with or without IM. Patients without IM had mainly cardial mucosa more than fundic mucosa. However, patients with IM had almost exclusively cardial mucosa. Low-grade dysplasia was observed only in patients with IM. Manometric evaluation demonstrated a structural defective lower esophageal sphincter in all groups. Acid and duodenal exposures of the distal esophagus over 24 h were significantly greater in patients with SSCE with IM. In the presence of pathologic gastroesophageal reflux (GER), there are several histological changes at the mucosa distal to the squamous columnar junction. The first metaplastic change is one from fundic to cardial mucosa and, when duodenal reflux occurs, a second metaplastic change to intestinal metaplasia from cardial mucosa occurs. Therefore, in all patients with symptoms of GER, biopsies specimens distal to the squamous columnar junction should be taken routinely.

Cardia↗
PubMed2002

Disruption of hedgehog signaling reveals a novel role in intestinal morphogenesis and intestinal-specific lipid metabolism in mice.

BACKGROUND & AIMS: The hedgehog (hh) signaling pathway has been shown to play crucial roles in the development of embryonic gut. However, its role in intestinal development and function beyond the embryonic stage is still undefined. METHODS: Expression of hh and its receptor, Patched, were examined by Western blot and X-gal staining. An anti-hh monoclonal antibody was administered into developing embryos or postnatal mice and histologic analyses were performed. Effects on lipid metabolism were examined by Oil Red O and Sudan III stainings, messenger RNA (mRNA) analysis, and electron microscopy. Serum apolipoprotein IV level, a marker for lipid absorption, was quantified by Western blot. RESULTS: Mice receiving anti-hh monoclonal antibody in utero or after birth exhibited progressive runting and died before weaning. Histology revealed hyperproliferation of intestinal crypt epithelial cells and disorganization of the villi with prominent vacuolation and accumulation of neutral lipid. Fecal fat microscopy revealed numerous large fat droplets. Intestinal mRNA abundance of 2 candidate genes involved in lipid transport, mtp and apob, was unchanged, although serum levels of apolipoprotein A-IV were reduced. CONCLUSIONS: Abnormal villus structure, lipid-filled enterocytes, and fatty stools in anti-hh monoclonal antibody-treated mice indicate a novel role for hh signaling in intestinal morphogenesis and lipid transport in postnatal mice.

Age Factors↗
PubMed2006

Intestinal replacement therapy: timing and indications for referral of patients to an intestinal rehabilitation and transplant program.

Current treatment options for patients suffering from intestinal insufficiency include all forms of intestinal replacement therapy (IRT). Parenteral nutrition has achieved extended success for the majority of patients requiring interval treatment, however, complications leading to failure of this treatment increases with the duration of therapy. There is currently no consensus as to the appropriate timing for transplantation of the intestine or the timing of referral for evaluation at a center experienced with this therapy. Certain patient characteristics warrant evaluation. Those patients with no jejunoileum who have guaranteed lifelong parenteral dependence, both adult and pediatric, should be immediately referred to a transplant center due to the high likelihood of the development of liver disease. Patients with metastatic infectious complications from catheter sepsis, patients with cholestasis seen intermittently with sepsis episodes, patients who are not successfully weaning and who demonstrate progressive thrombocytopenia, and patients with motility disorder experiencing deterioration should also warrant early referral to an intestinal rehabilitation and transplant program. The objective of evaluation is to maximize the opportunities for rehabilitation while not missing the critical window of opportunity for successful transplantation when needed. We favor an aggressive directed approach to rehabilitation, coupled with psychological preparation for both transplantations and other options. Early referral requires trust between the patient, referring physician, and the transplant team to assure that a rush to judgment will not lead to a premature transplant. The current wait list mortality is high, mandating early referral and listing with an approach aimed at maximizing both the success of gastrointestinal support, as well as of transplantation when necessary.

Adult↗