Document Detail


Intestinal graft-versus-host disease: mechanisms and management.
MedLine Citation:
PMID:  12487619     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Allogeneic haematopoietic stem cell transplantation remains the treatment of choice for a number of malignancies. However, graft-versus-host disease (GVHD) has long been regarded as a serious complication of this procedure. Although GVHD may affect any organ, intestinal GVHD is particularly important because of its frequency, severity and impact on the general condition of the patient. Recent studies have led to progressive elucidation of the mechanism of GVHD. Donor T cells are critical for the induction of GVHD, because depletion of T cells from bone marrow grafts effectively prevents GVHD but also results in an increase of leukaemia relapse. It has been shown that the gastrointestinal tract plays a major role in the amplification of systemic disease because gastrointestinal damage increases the translocation of endotoxins, which promotes further inflammation and additional gastrointestinal damage. Consequently, the management of intestinal GVHD (and the intestine itself) is a subject that should be highlighted. In this article, approaches to the prevention of intestinal GVHD are discussed after being classified into three categories: regimens in common clinical use, regimens under investigation and original regimens used at our hospital. The standard regimen that is used most widely for prevention of GVHD is cyclosporin plus short-term methotrexate. Corticosteroids can be added to this regimen but careful consideration of the adverse effects of these hormones should be considered. Tacrolimus is a newer, more potent alternative to cyclosporin. T-cell depletion (TCD) after transplantation has been shown to prevent acute GVHD, however, the survival benefit of TCD has not been as great as expected. Mycophenolate mofetil can be useful for the treatment of acute GVHD as part of combination therapy. Regimens currently under investigation in animal experiments include suppression of inflammatory cytokines and inhibition of T-cell activation, and, specifically at our institution, hepatocyte growth factor gene therapy. The evidence-based therapy used at our institution includes systemic antibacterial therapy (including eradication of intestinal bacteria) to prevent the intestinal translocation of lipopolysaccharide and avoid the subsequent increase of various inflammatory cytokines. In addition, because of the similarities between intestinal GVHD and ulcerative colitis, sulfasalazine, betamethasone enemas and eicosapentaenoic acid have been used to treat intestinal GVHD in some patients.
Authors:
Hiroyuki Takatsuka; Tsuyoshi Iwasaki; Takahiro Okamoto; Eizo Kakishita
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Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  Drugs     Volume:  63     ISSN:  0012-6667     ISO Abbreviation:  Drugs     Publication Date:  2003  
Date Detail:
Created Date:  2002-12-18     Completed Date:  2003-04-29     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  7600076     Medline TA:  Drugs     Country:  New Zealand    
Other Details:
Languages:  eng     Pagination:  1-15     Citation Subset:  IM    
Affiliation:
Second Department of Internal Medicine, Hyogo College of Medicine, Hyogo, Japan. hematol@hyo-med.ac.jp
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MeSH Terms
Descriptor/Qualifier:
Adrenal Cortex Hormones / therapeutic use
Animals
Anti-Inflammatory Agents, Non-Steroidal / therapeutic use
Clinical Trials as Topic
Cytokines / antagonists & inhibitors
Diagnosis, Differential
Digestive System / immunology*,  pathology
Drug Therapy, Combination
Fatty Acids, Unsaturated / therapeutic use
Gene Therapy
Graft vs Host Disease / etiology,  immunology,  therapy*
Hematopoietic Stem Cell Transplantation / adverse effects
Hepatocyte Growth Factor / genetics
Humans
Immunosuppressive Agents / therapeutic use
Sulfasalazine / therapeutic use
T-Lymphocytes / immunology,  pathology
Chemical
Reg. No./Substance:
0/Adrenal Cortex Hormones; 0/Anti-Inflammatory Agents, Non-Steroidal; 0/Cytokines; 0/Fatty Acids, Unsaturated; 0/Immunosuppressive Agents; 0/eicosapentanoic acid; 599-79-1/Sulfasalazine; 67256-21-7/Hepatocyte Growth Factor

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