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| 1 | Hematopoietic cell transplantation for Crohn’s disease;is it time?显示文摘AIM: To review all studies in the literature that have assessed Hematopoietic cell transplantation (HCT) and Crohn’s disease (CD) with the ultimate aims of determining if this is a viable treatment option for those with CD. A secondary aim was to review the above literature and determine if the studies shed further light on the mechanisms involved in the pathogenesis of CD. METHODS: An extensive Medline search was performed on all articles from 1970 to 2005 using the ; bone marrow transplant, stem cell, hematopoietic cell, Crohn’s disease and inflammatory bowel disease. RESULTS: We identified one case in which a patient developed CD following an allogeneic HCT from a sibling suffering with CD. Evidence for transfer of the genetic predisposition to develop CD was also identified with report of a patient that developed severe CD following an allogeneic HCT. Following HCT it was found that the donor (that had no signs or symptoms of CD) and the recipient had several haplotype mismatches in HLA class Ⅲ genes in the IBD3 locus including a polymorphism of NOD2/CARD15 that has been associated with CD. Thirty three published cases of patients with CD who underwent either autologous or allogeneic HCT were identified. At the time of publication 29 of these 33 patients were considered to be in remission. The median follow-up time was seven years, and twenty months for allogeneic and autologous HCT respectively.For patients who underwent HCT primarily for treatment of their CD there have been no mortalities related to transplant complications. CONCLUSION: Overall these preliminary data suggest that both allogeneic and autologous HCT may be effective in inducing remission in refractory CD. Thissupports the hypothesis that the hematolymphatic cells play a key role in CD and that resetting of the immune system may be a critical approach in the management or cure of CD. | Y Leung M Geddes J Storek R Panaccione PL Beck | 2006 | World Journal of Gastroenterology2006，12，41： | 5 |
| 2 | Gut hormones, and short bowel syndrome: The enigmatic role of glucagon-like peptide-2 in the regulation of intestinal adaptation显示文摘Short bowel syndrome (SBS) refers to the malabsorption of nutrients, water, and essential vitamins as a result of disease or surgical removal of parts of the small intestine. The most common reasons for removing part of the small intestine are due to surgical intervention for the treatment of either Crohn's disease or necrotizing enterocolitis. Intestinal adaptation following resection may take weeks to months to be achieved, thus nutritional support requires a variety of therapeutic measures, which include parenterai nutrition. Improper nutrition management can leave the SBS patient malnourished and/or dehydrated, which can be life threatening. The development of therapeutic strategies that reduce both the complications and medical costs associated with SBS/long-term parenterai nutrition while enhancing the intestinal adaptive response would be valuable. Currently, therapeutic options available for the treatment of SBS are limited. There are many potential stimulators of intestinal adaptation including peptide hormones, growth factors, and neuronally-derived components. Glucagon-like peptide-2 (GLP-2) is one potential treatment for gastrointestinal disorders associated with insufficient mucosal function. A significant body of evidence demonstrates that GLP-2 is a trophic hormone that plays an important role in controlling intestinal adaptation. Recent data from clinical trials demonstrate that GLP-2 is safe, well-tolerated, and promotes intestinal growth in SBS patients. However, the mechanism of action and the localization of the glucagon-like peptide-2 receptor (GLP-2R) remains an enigma. This review summarizes the role of a number of mucosal-derived factors that might be involved with intestinal adaptation processes; however, this discussion primarily examines the physiology, mechanism of action, and utility of GLP-2 in the regulation of intestinal mucosal growth. | GR Martin PL Beck DL Sigalet | 2006 | World Journal of Gastroenterology2006，12，26： | 3 |
| 3 | Hapten-induced model of chronic inflammation and ulceration in the rat colon显示文摘 | Morris GP Beck PL Herridge MS Depew WT Szewczuk MR Wallace JL | 1989 | Gastroenterology1989，96，3： | 1 |
| 4 | Hapten-induced model of chronic inflammation and ulceration in the rat colon显示文摘 | Morris GP Beck PL Herridge MS | 1989 | Gastroenterology1989，96，3： | 1 |
| 5 | Chemotherapy- and radiotherapy- induced intestinal damage is regulated by intestinal trefoil factor显示文摘 | Beck PL Wong JF Li Y | 2004 | Gastroenterology2004，126，3： | 1 |
| 6 | Hapten-induced model of chronic inflammation and ulceration in the rat colon 显示文摘 | Morris GP Beck PL Herridge MS | 1989 | Gastroenterology1989，96，： | 1 |
| 7 | Hapten-induced model of chronic inflammation and ulceration in the rat colon显示文摘 | Beck PL Herridge MS | 1989 | Gastroenterology1989，96，3： | 1 |
| 8 | Gallbladder polyps:Epidemiology,natural history and management显示文摘 | Myers RP Shaffer EA Beck PL | 2003 | Can J Gustroenterol2003，16，3： | 1 |
| 9 | Chemotherapy - and radiotherapy - induced inteslinaldarnage is regulated by intestinal trefoil factor 显示文摘 | Beck PL Wong JF Li Y | 2004 | Gastroenterology2004，126，3： | 1 |
| 10 | Prostaglandin modulation of the gastric vasculature and mucosal integrity in cirrhotic rats显示文摘 | McKnight W Lee SS | 1993 | Am J Physiol1993，265，31： | 1 |
| 11 | Hapten-induced chronic colitis in the rat: alternatives to trinitrobenzene sulfonic acid显示文摘 | Le T Carter L Appleyard CB Beck PL | 1995 | J Pharmacol Toxicol Methods1995，33，4： | 1 |
| 12 | Hapten-induced model of chronic inflammation and ulceration in the rat colon显示文摘 | Morris GP Beck PL Herridge MS | 1989 | Gastroenterology1989，96，3： | 1 |
| 13 | Hapten-induced model of chronic inflammation and ulceration in the rat color 显示文摘 | Morris GP BECK PL DEPEW WT | 1989 | Gastroenterology1989，96，3： | 1 |
| 14 | Chemotherapy-and radiotherapy-induced intestinal damage is regulated by intestinal trefoil factor显示文摘 | Wong JF Li Y | 2004 | Gastroenterology2004，126，3： | 1 |
| 15 | Hapten-induced model of chronic inflammation and ulceration in the rat colon显示文摘 | Morris GP Beck PL Herridge MS | 1989 | Gastroenterology1989，96，： | 1 |
| 16 | Hapten-induced model of chronic inflammation and ulceration in the rat colon 显示文摘 | Morris GP Beck PL Herridge MS | 1989 | Gastroenterology1989，96，3： | 1 |
| 17 | Microscopic colitis-a com- mon cause of diarrhoea in older adults 显示文摘 | Williams JJ Beck PL Andrews CN | 2010 | Age Ageing2010，39，2： | 1 |
| 18 | Gallbladder polyps:epide-miology,natural history and management显示文摘 | Myers RP Shaffer EA Beck PL | 2002 | Can J Gastro-enterol2002，16，： | 1 |
| 19 | Hapten-indueed model of chronic inflammation and ulceration in the rat colon显示文摘 | Morris GP Beck PL Erridge MS | 1989 | Gastro- enterology1989，，3： | 1 |
| 20 | Hapten - induced model of chronic inflammation and ulceration in the rat colon显示文摘 | Morris GP Beck PL Herridge MS | 1989 | Gastroenterology1989，96，3： | 1 |
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