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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. [ABSTRACT FROM AUTHOR]

Study Objective: Respiratory disturbance caused by ARDS has been reported during administration of granulocyte-colony stimulating factor. The clinical features of such respiratory distress were investigated in this study.Design: Retrospective case review.Setting: A 1,100-bed university teaching hospital.Patients: Five patients who had dyspnea caused by ARDS develop after chemotherapy or bone marrow transplantation (BMT) at our hospital.Interventions: None.Measurements and Results: Levels of cytokines, human leukocyte antigen (HLA) typing, and the clinical course were analyzed to clarify common features. All five patients possessed HLA-B51 or HLA-B52, and all had fever and an enhanced inflammatory response at the time of the WBC nadir. The tumor necrosis factor (TNF)-alpha and interleukin (IL)-8 levels increased when respiratory distress syndrome occurred.Conclusions: If patients with HLA-B51 or HLA-B52 have infection develop at the time of WBC nadir after chemotherapy or BMT, ARDS may occur in association with elevation of TNF-alpha and IL-8 during WBC recovery. [ABSTRACT FROM AUTHOR]