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)

Histological features of endothelial and vascular changes seen in cell mediated immune reactions were evaluated in skin biopsies from 44 HLA matched and mismatched recipients of bone marrow transplantation. The mismatched group (n = 24) was further subdivided into 'D-mismatched' (n = 14) and 'AB-mismatched' (n = 10). All patients had clinical grade III and histological grade II graft-versus-host disease (GVHD). Comparison groups consisted of skin biopsies from 10 non-GVHD cases. Histological evidence of endothelial damage including perivascular factor VIII related antigen deposition was assessed and compared between the groups. The results showed that all patients post-transplant had evidence of a non-specific vascular response consisting mainly of a perivascular lymphocytic infiltrate, perivascular oedema and factor VIII related antigen extravasation. However, a significant difference between matched and mismatched patients who developed GVHD was the more frequent observation of perivascular nuclear dust in the HLA mismatched group (p less than 0.01) suggesting a greater degree of endothelial cell damage in these patients.
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PMID:Endothelial changes in cutaneous graft-versus-host disease: a comparison between HLA matched and mismatched recipients of bone marrow transplantation. 204 75

The presence of an erythematous skin rash and hemorrhagic complications in acute graft-versus-host disease (GVHD) suggest that the vasculature may be involved in the immunopathologic process. We reviewed endothelial and vascular histopathologic changes on light microscopy and on immunoperoxidase stained sections of skin biopsies obtained from 41 HLA-identical allogeneic marrow transplant recipients with at least grade 2 GVHD. Biopsies taken from 14 allogeneic HLA-identical bone marrow transplant recipients who never developed GVHD were used as controls. Sections were evaluated for evidence of immunologic vascular injury using the rank file analysis of histologic features, expression of HLA-DR antigen, and the distribution of fibrin and factor VIII-related antigen (F VIII RAg). Patients with acute GVHD had significantly greater intimal lymphocytic infiltrates, perivascular nuclear dust deposition, perivascular F VIII Rag extravasation and deposition and vascular proliferation than controls. We find significantly greater endothelial injury in GVHD patients, which may represent primary immunologic injury to the vasculature. The clinical findings in acute GVHD probably result from cumulative endothelial as well as epithelial injury.
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PMID:Endothelial-cell injury in cutaneous acute graft-versus-host disease. 259 72

A 57-year-old female with recurrent AML underwent a T cell-depleted (TCD) bone marrow (BM) plus TCD and CD34-selected peripheral blood stem cell (PBSC) transplant. Eleven weeks post transplantation, the patient developed acute graft-versus-host disease (GVHD) manifested by rash and elevated liver enzymes. Concurrently, the patient presented with a bleeding diathesis and a left forearm hematoma due to the development of a spontaneous factor VIII inhibitor. She was treated with human recombinant factor VIII and intravenous methylprednisolone. Subsequently she was managed with a prednisone taper leading to resolution of the GVHD, as well as the spontaneous factor VIII inhibitor. Bone marrow transplant-related spontaneous factor VIII inhibitor has previously been reported in association with one patient with chronic GVHD. To our knowledge this is the first report of spontaneous factor VIII inhibitor associated with acute GVHD.
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PMID:Development of spontaneous factor VIII inhibitor in association with acute graft-versus-host disease. 1147 49

Previous clinical attempts to correct genetic deficiencies such as hemophilia or Gaucher disease by transplantation of allogeneic spleen were associated with aggressive graft versus host disease, mediated by mature T cells derived from the donor spleen. We show that a fetal pig spleen harvested at the embryonic day 42 stage, before the appearance of T cells, exhibited optimal growth potential upon transplantation into SCID mice, and the growing tissue expressed factor VIII. Transplantation of embryonic day 42 spleen tissue into hemophilic SCID mice led to complete alleviation of hemophilia within 2-3 months after transplant, as demonstrated by tail bleeding and by assays for factor VIII blood levels. These results provide a proof of principle to the concept that transplantation of a fetal spleen, obtained from a developmental stage before the appearance of T cells, could provide a novel treatment modality for genetic deficiencies of an enzyme or a factor that can be replaced by the growing spleen tissue.
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PMID:Correction of hemophilia as a proof of concept for treatment of monogenic diseases by fetal spleen transplantation. 1714 7

A 65-year-old woman who had suffered from chronic graft-versus-host disease (GVHD) presented with extensive purpura and was diagnosed with acquired hemophilia A. Because she was refractory to corticosteroids and her condition was complicated with diabetes mellitus, glaucoma, and hypoglobulinemia, she was treated with tocilizumab. Tocilizumab treatment increased the activity of factor VIII in a rapid and sustained manner, leading to a reduction of the prednisolone dose. Tocilizumab may thus be an optional treatment modality for acquired hemophilia A.
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PMID:Successful treatment of acquired hemophilia A, complicated by chronic GVHD, with tocilizumab. 2124 Jun 17

Human umbilical cord blood cell (HUCBC) has low immunity. In the present study we investigated intestinal graft-versus-host disease (GVHD) induced by HUCBC transplantation in a myocardial infarction (MI) rat model. MI was established by using left anterior descending coronary artery (LAD) ligation. HUCBCs were injected into the animals 5 days post MI. Four weeks after the HUCBC transplantation, histology changes in small intestine were observed under an optical microscope. In addition, cardiac functions were tested. Further, factor VIII, vascular endothelial growth factor (VEGF) in the myocardium and small intestine were assayed. The HUCBC transplantation significantly induced intestinal GVHD in the MI rats. The HUCBC implantation remarkably improved ejection fraction (EF), fractional shortening (FS), and dp/dtmax in the MI rats (P<0.05). In the myocardium, the capillary density was larger in the small intestine of the HUCBC-transplanted rats compared to the controls. Real-time PCR and western blotting revealed that VEGF mRNA and protein levels in the myocardium and the small intestine dramatically significantly upregulated in the HUCBC-transplanted rats (P<0.05). The HUCBC transplantation significantly improves aggravated cardiac function of MI rats, but it induces intestinal GVHD.
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PMID:Human umbilical cord blood cell transplantation improves cardiac function in a myoardial infarction rat model but induces intestinal graft versus host disease. 2492 7