Gene/Protein Disease Symptom Drug Enzyme Compound
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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)

Perinatal C57BL/1 mice given injections of (SJL/J X C57BL/1)F1 spleen cells developed a highly lethal runting syndrome, designated host-versus-graft disease (HVGD). The mortality was related to the dosage of F1 cells. Acute pathologic changes resembled those occurring in parent leads to F1 graft-versus-host disease (GVHD), except for more pronounced plasmacytosis. Mice suffering from HVGD recovered clinically with no sequelae except for a slight increase in the incidence of lymphomas over control mice. Such mice were hyperreactive to F1 cells utilized to initiate the original HVGD syndrome. Most of the tumors developed in those animals receiving the initial injection of F1 spleen cells within 24 hours of birth. Tumor incidence was unrelated to the clinical severity of HVGD. By contrast, GVHD in the same strain combination resulted in a much higher incidence of lymphomas in a much shorter time. Parental strain cells were detectable in the F1 hosts up to the time of tumor development. HVGD has a low tumor induction potential; GVHD has a high tumor induction potential.
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PMID:Tumor induction in host-versus-graft disease. I. Clinical and pathologic features. 2 43

Host versus graft (HVG) syndrome may be induced in parental strain mice by perinatal inoculations of F1 hybrid spleen cells. The principal manifestations of the disease include thrombocytopaenia, intravascular fibrin deposits, intestinal haemorrhage, hepatic infarcts, lymphosplenomegaly and renal disease. Immune complexes have been shown to be the cause of the renal lesions, and have been implicated as the triggers for disseminated intravascular coagulation. In the present studies of RFM mice perinatally inoculated with (T6 x RFM)F1 spleen cells (RFM/(T6 x RFM)F1 mice), quantitative determinations of serum immunoglobulins (Ig) revealed marked elevations of IgG1, IgG2, IgA and IgM. Electrophoretic analyses revealed the polyclonal pattern which typically follows chronic antigenic stimulation. However, IgG1 levels which reached 29 to 72 times control values suggested disruption of homeostatic mechanisms which control circulating Ig levels. Because antibody responses to histocompatibility antigens were present only occasionally, and then in low titre, it seemed unlikely these antigens were the principal causes of hypergammaglobulinaemia and plasmacytosis. Morphological studies indicated that the elevated levels of Ig seen in end-stage HVG syndrome correlated well with marked plasmacytosis, the third morphological finding in a sequence that included the precocious development of germinal centres and subsequent depletion of thymic-dependent (T) lymphocytes. The fact that spleen cells from RFM/(T6 x RFM)F1 mice were severely impaired in their capacity to cause graft versus host disease in related (T6 x RFM)F1 and unrelated C3H mice provided strong evidence that the HVG reaction resulted in T-cell depletion, rather than specific immunoincompetence.
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PMID:Hyperimmunoglobulinaemia, T-cell deficiency and plasmacytosis in RFM mice with host versus graft disease induced by the perinatal inoculations (T6XRFM)F1 spleen cells. 108 3

This study of chronic graft-versus-host disease (GVHD) describes the clinical, pathologic and laboratory features, and the causes of morbidity and mortality in 20 patients who received allogeneic marrow transplants from HLA identical sibling donors. Chronic GVHD is a pleiotrophic syndrome with variability in the time of onset, organ systems involved and rate of progression. The clinical-pathologic features resemble an overlap of several collagen vascular diseases with frequent involvement of the skin, liver, eyes, mouth, upper respiratory tract, esophagus and less frequent involvement of the serosal surfaces, lower gastrointestinal tract and skeletal muscles. Major causes of morbidity are scleroderma with contractures and ulceration, dry eyes and mouth, pulmonary insufficiency and wasting. Chronic GVHD has features of immune dysregulation with elevated levels of eosinophils, circulating autoantibodies, hypergammaglobulinemia and plasmacytosis of viscera and lymph nodes. In this study, three patients had limited chronic GVHD with relatively favorable prognosis characterized by localized skin involvement and/or hepatic disease without chronic aggressive histology. Most patients, however, had extensive disease with a progressive course. Survival was largely determined by the presence or absence of serious recurrent bacterial infections. The over-all severity of disease was best assessed by using the Karnofsky performance rating.
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PMID:Chronic graft-versus-host syndrome in man. A long-term clinicopathologic study of 20 Seattle patients. 699 81

Adoptive immunotherapy with donor leukocytes has emerged as a promising strategy for the treatment of myeloma recurrence after allogeneic transplantation. 2.9 x 10(8)/kg donor mononuclear cells containing 1.4% CD34+ and 37% CD3+ cells were administered to a 48-year-old patient with non-secretory plasmablastic myeloma relapsing 9 months after a blood stem cell transplant from his HLA-identical sibling. In view of the extensive marrow infiltration and the aggressive behaviour of the disease, the donor cells were preceded by a course of EDAP chemotherapy. There was rapid clinical improvement, and CR was achieved on day 30 post infusion. However, three subcutaneous plasmacytomas showing anaplastic features developed within a few days. These failed to respond to interferon-alpha and continued to grow for 5 weeks in the absence of marrow plasmacytosis or other evidence of systemic disease. Grade 3 acute liver GVHD developed on day 79 which was controlled with immunosuppression. Overt systemic relapse occurred on day 90 as the GVHD came under control. The course of our case suggests highly proliferative malignant cells may escape the graft-versus-tumour effect of immunocompetent allogeneic cells in extramedullary sites subsequently resulting in overt systemic relapse if left untreated. New approaches are needed to deal with the problem of extramedullary disease recurrence.
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PMID:Graft-versus-myeloma after donor leukocyte infusion: maintenance of marrow remission but extramedullary relapse with plasmacytomas. 964 83

Post-transplant lymphoproliferative disorder (PTLD) is uncommonly of T cell origin, especially following BMT. We describe a 13-year-old boy with severe aplastic anemia (SAA) and no evidence of Fanconi's anemia who underwent BMT at 11 years of age using CY 10 mg/kg once daily i.v. on days -5, -4, antilymphocyte globulin (ALG) 30 mg/kg once daily i.v. on days -5 approximately -3 and CsA from day -1 as conditioning. The BMT failed and he received a further peripheral blood stem cell transplant (PBSCT) 240 days after BMT. Conditioning was with CY 50 mg/kg once daily i.v. on days -5 approximately -2, and ALG 15 mg/kg once daily i.v. on days -4 approximately -2. GVHD prophylaxis included CsA and MTX. Engraftment was later confirmed by cytogenetic studies. Desquamation and ulcers of the oral mucosa and mouth angle developed in the 13th month post PBSCT. A buccal mucosa biopsy on day +524 revealed only plasmacytosis. Immunosuppressants were discontinued at that point. Generalized lymphadenopathy, prolonged fever (waxing and waning) and facial swelling developed in the 18th month post PBSCT. A neck lymph node biopsy on day +601 showed T cell lymphoma of diffuse large cell type with monoclonal TCR gamma-chain gene rearrangement. A FISH study showed that the malignant T cells were of recipient origin. EBV in situ hybridization was negative. He did not receive further treatment apart from discontinuation of immunosuppressants. He was followed up in our out-patient clinic and showed good performance 1170 days post PBSCT. We speculate that a different mechanism was operating in the pathogenesis of T cell lymphoma in this case. Risk factors include SAA and two transplants, conditioned with CY and ALG, long term use of CsA and treatment with azathioprine.
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PMID:T cell lymphoproliferative disorder following bone marrow transplantation for severe aplastic anemia. 1108 91