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Query: UMLS:C0018133 (graft-versus-host disease)
18,032 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Review of autopsies of 28 children with severe combined immunodeficiency (SCID) or combined immunodeficiency (CID) and three with DiGeorge syndrome showed a high incidence of acute graft-versus-host disease (GVHD) in the pancreas. Acute GVHD (seven cases: four SCID, two CID, and one DiGeorge syndrome) was characterized by lymphocytes around large to medium ducts, damage to ductal epithelium (focal necrosis, reactive nuclear changes, inspissated secretions in duct lumens), and periductal edema. Changes were judged indeterminate but suspicious for GVHD when ductal damage was slight (six cases: three SCID, two CID, and one DiGeorge syndrome). All patients with pancreatic GVHD had received allogeneic bone marrow, fetal liver or thymus transplant, or nonirradiated blood products and had evidence of GVHD in other organs. Immunoperoxidase stain for HLA-DR showed strong-to-moderate staining of duct epithelium in two of four GVHD cases for which blocks were available. This change was nonspecific; weaker staining for HLA-DR was seen in cases with nonspecific abnormalities and in viral pancreatitis. Four cases had histological evidence of viral infection: two had cytomegalovirus pancreatitis, one had patchy parenchymal necrosis caused by adenovirus, and one had giant cell pancreatitis caused by parainfluenza virus. Mild nonspecific changes, such as focal fat necrosis or acinar dilatation, were seen in seven cases. One case had unexplained marked pancreatic atrophy and fibrosis. Acute pancreatic GVHD is not uncommon in autopsies of children with congenital immune deficiencies with GVHD of other organs; however, this finding may not have strong clinical implications in this group of patients. Careful attention to pancreatic ducts is necessary for diagnosis. Unusual viral pancreatitis may also be seen in this group, as well as nonspecific abnormalities.
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PMID:Pathology of the pancreas in severe combined immunodeficiency and DiGeorge syndrome: acute graft-versus-host disease and unusual viral infections. 808 66

Bone marrow transplantation (BMT) has evolved over the last decade from a controversial research procedure to a standard therapeutic modality, becoming an important innovative treatment for hematological malignancies, solid tumors, immunodeficiency diseases and metabolic disorders. Historically in research and clinical literature, the BMT procedure is divided into several stages, each accompanied by particular emotional tones and psychological issues. In providing care for transplant recipients, donors, and families, caregivers must be familiar with the psychological stages of the procedure, the psychological themes such as body image, and the patient's mechanisms of coping with the stress of such protocols. BMT's complex regimens of high-dose chemotherapy and total-body irradiation, germ-free environments, graft-versus-host disease, and total parenteral nutrition can precipitate significant psychological sequelae in some patients with acute and long-term consequences. In response to their illness, transplant patients may also develop emotional disturbances of anxiety, depression, agitation, and non-compliance. This paper will address the psychological care of the patient, donor and family from pre-BMT consultation, through informed consent, hospitalization and convalescence. Various psychotherapeutic, pharmacological and behavioral interventions will be briefly described. Finally, areas of research in quality of life after BMT and factors that may predict BMT adjustment and outcome will be explored. We hope this brief paper will familiarize the reader with this psychologically intriguing field and will provide a departure point for future reading, study, research, and patient/family care.
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PMID:Bone marrow transplantation: support of the patient and his/her family. 815 56

Allogenic diseases induced in rodents by the inoculation of foreign lymphocytes represent useful models to investigate the mechanisms governing the activation of autoreactive B cells in systemic lupus erythematosus and related autoimmune disorders. The role of CD4+ helper T cells recognizing foreign class II MHC molecules has been particularly well established in murine chronic graft-versus-host disease and host-versus-graft disease. The T cells involved in these models essentially produce interleukin-4 and interleukin-10, which corresponds to the phenotype of Th2 cells. The association between autoimmunity and cellular immunodeficiency in experimental allogenic diseases could therefore be directly related to the hyperactivity of Th2 cells. Similar mechanisms might be operative in human systemic autoimmune diseases as well as in other clinical settings such as graft-versus-host disease after bone marrow transplantation or the acquired immunodeficiency syndrome.
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PMID:[Allogenic reaction, a model of autoimmunity]. 817 59

Patients undergoing BMT have a long-lasting defect of B cell-mediated immunity, especially if chronic GVHD ensues. It has been postulated that the post-transplant B cell abnormalities can be explained by the recapitulation of B cell ontogeny. To test this hypothesis, we studied the quantitative and phenotypic reconstitution of circulating B cells in 24 transplant recipients and compared it with normal ontogeny. The results confirm that a second round of ontogeny occurs in transplant recipients without chronic GVHD. This was evidenced by the pattern of quantitative B cell reconstitution (low-->high-->normal B cell counts), large B cell size and a high proportion of B cells overexpressing CD38, membrane IgM (mIgM) and membrane IgD (mIgD). The recapitulation of ontogeny was blunted in most patients with chronic GVHD, as evidenced by the absence of the overshoot of total B cells and by the relative lack of CD38high, mIgMhigh and mIgDhigh B cells. We conclude the post-transplant B cell development in patients without chronic GVHD parallels ontogeny. The limited ability of patients with chronic GVHD to re-enact B cell ontogeny may contribute to their longer-lasting and more severe humoral immunodeficiency.
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PMID:B cell reconstitution after human bone marrow transplantation: recapitulation of ontogeny? 827 39

The role of TNF in the expression of GVHD and GVHD-related immunodeficiency was studied in a well-established murine GVHD model of bone marrow transplantation across minor histocompatibility barriers (B10.BR-->GBA/J) both in vitro and in vivo. Splenocytes from animals with GVHD profoundly inhibited the proliferation of normal spleen cells in response to a wide range of stimuli in an MHC-nonrestricted fashion. Neutralizing mAbs to TNF reversed the ability of splenocytes from animals with GVHD to suppress the proliferation of normal splenocytes stimulated by the mitogen concanavalin A. Addition of rTNF enhanced the degree of suppression. This reversal was similar to that previously reported for IFN gamma and leucine methyl ester treatment of the GVHD populations. All three components are necessary for suppression to occur because addition of rTNF to cultures in which suppression had been reversed by anti-IFN gamma or leucine methyl ester treatment did not reconstitute suppression. Neutralization of endogenous TNF production in vivo resulted in an amelioration of clinical GVHD, but neutralization of endogenous IFN gamma resulted in a more severe course. However, in vivo neutralization of either TNF or IFN gamma post-BMT resulted in a decreased ability of splenocytes from animals with GVHD to suppress mitogen responses but did not affect the generation of the suppressor cell population. These findings support multiple roles for TNF and IFN gamma in the pathophysiology of GVHD, including terminal cellular differentiation and/or regulation of effector cell function.
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PMID:The role of tumor necrosis factor and interferon gamma in graft-versus-host disease and related immunodeficiency. 831 May 20

We describe an infant with multiple segmental areas of atresia of the small and large bowel, with histologic features characteristic of the hereditary form of the disease. Posttransfusion graft-versus-host disease developed first, and then immunodeficiency was found. This report confirms the association between hereditary multiple intestinal atresia and immunodeficiency. We recommend irradiation of blood products in patients with multiple intestinal atresia pending evaluation of immune system status.
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PMID:Multiple areas of intestinal atresia associated with immunodeficiency and posttransfusion graft-versus-host disease. 832 Jun 33

While half of all patients receiving bone marrow transplantation (BMT) for malignancies and related diseases may achieve prolonged disease-free survival, 2-10% of patients undergoing allogeneic transplantation develop bronchiolitis obliterans (BrOb). We have hypothesized that total body irradiation (TBI) which has been used for pretreatment may influence the subsequent development of BrOb in patients undergoing allogeneic BMT. Since 1976, we have treated 104 patients undergoing allogeneic BMT with non-TBI preconditioning. Of 60 patients that survived and were evaluable for chronic graft versus host disease (GVHD) 26 developed chronic GVHD (43%). Four of 104 patients (3.9%) developed BrOb by clinical and/or pathologic findings. Four of 4 patients (100%) with BrOb had chronic GVHD. Two of these 4 patients (50%) were alive at the end of 2 years. These data demonstrate that chronic GVHD is a risk factor for BrOb in patients receiving non-TBI preconditioning regimens. The similar incidence of BrOb in this population compared to other studies using TBI suggest that the preconditioning regimen is not a factor in the development of BrOb. Further study is needed to confirm these findings. Allogeneic bone marrow transplantation (BMT) has revolutionized the therapeutic approach toward acute and chronic leukemias, aplastic anemia and rare immunodeficiency disorders. Half of all patients that undergo BMT achieve long-term disease-free survival but a similar number develop significant complications [1].(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Bronchiolitis obliterans after bone marrow transplantation: the effect of preconditioning. 834 52

Bone marrow transplantation is currently used in the treatment of a variety of neoplastic and nonneoplastic diseases. However, significant obstacles still limit the efficacy of this procedure. These include the occurrence of graft-versus-host disease, the failure of the marrow to engraft, the susceptibility of patients to opportunistic infections during the period of immunodeficiency after transplantation before full recovery of immune function, and finally, the recurrence of the cancer. Natural killer (NK) cells are lymphoid cells responsible for mediating a variety of immunologic and homeostatic functions. Initially described almost 20 years ago, the full range of functions carried out by these enigmatic cells continues to unfold. NK cells may be both beneficial and deleterious in bone marrow transplantation, depending on their genotype and activation status. Resting host-derived NK cells appear capable of mediating resistance to both autologous and allogeneic bone marrow cell grafts. At the other end of the spectrum, the transfer of activated NK cells of donor type appears to produce multiple beneficial effects during both syngeneic and allogeneic bone marrow transplantation. Here, we review and attempt to reconcile the literature concerning the basic biology of NK cells and their effects on hematopoiesis, both in vitro and in vivo. We also discuss the current issues in bone marrow transplantation and the potential role NK cells may play in determining the outcome of the marrow graft, the occurrence of graft-versus-host disease, and the generation of a graft-versus-tumor response when bone marrow transplantation is used for the treatment of cancer.
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PMID:Natural killer cells and bone marrow transplantation. 836 Sep 30

Review of liver biopsy or autopsy material from 33 patients with severe combined immunodeficiency or combined immunodeficiency and four patients with DiGeorge syndrome revealed a wide range of hepatic pathology. The most common abnormality was graft-versus-host disease (16 patients), followed by viral infection (4 patients had adenovirus hepatitis, 3 had cytomegalovirus hepatitis). Centrilobular fibrosis with or without veno-occlusive disease was seen in five patients. Three patients had nonspecific hepatitis, four had changes attributed to total parenteral nutrition, and two had lymphoproliferative disorders involving the liver. Both patients with lymphoproliferative disorders had received transplants. Two patients had resolving necrosis probably secondary to non-A, non-B hepatitis. One had atypical mycobacterial infection. Hemosiderosis was a common nonspecific abnormality, seen in nine patients. All patients with hepatic graft-versus-host disease had received transplants or nonirradiated blood products. Hepatic graft-versus-host disease varied in severity from hepatic necrosis with destruction of both large and small bile ducts in a transfusion-associated case to subtle damage to interlobular bile ducts. Even minimal bile duct changes correlated with the clinical impression of graft-versus-host disease in these patients. Late chronic graft-versus-host disease was not seen in any patient, although acute graft-versus-host disease sometimes occurred late after transplant.
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PMID:Pathology of the liver in severe combined immunodeficiency and DiGeorge syndrome. 837 33

Several transfusion-related complications have particular relevance to the transplant setting. Transfusions reportedly improve solid organ graft survival, especially when the donor and recipient share at least one HLA-DR antigen. Whereas the mechanism for this effect is unclear, less favorable "immunomodulating" effects of transfusion may increase postoperative infections and shorten survival time and disease-free intervals in patients with a variety of malignancies who are undergoing surgery. The contribution of the different components of the blood transfusion to these outcomes remains speculative. Directed donations, especially from relatives and in the setting of a recipient who is immunosuppressed, may give rise to a severe but under-appreciated immunologic consequence of transfusion: graft-versus-host disease. Although still rarely reported, transfusional graft-versus-host disease is almost invariably fatal. This complication is entirely avoidable if the transfused blood product is appropriately gamma-irradiated. Infectious complications remain the most feared consequence of transfusion; the cytomegalovirus, the human immunodeficiency virus, and hepatitis B and C may run a more fulminant course in transplant patients who are immunosuppressed. Red cell substitutes, hematopoietic growth factors, and autologous transfusion are among the strategies for preventing complications of blood transfusion. With the advent of cyclosporine and more potent and specific immunosuppressive therapies, the desirability of preoperative transfusion for organ grafts warrants reevaluation.
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PMID:Transfusion in transplant patients: the good, the bad, and the ugly. 844 86


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