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)

Twenty-nine patients with severe aplastic anaemia (SAA) were submitted to bone marrow transplantation (BMT) and their immunological recovery analysed. Total lymphocyte counts, estimation of B lymphocytes, T lymphocytes and their subsets, natural-killer (NK) activity were performed. Cells with the CD8+ phenotype and NK activity were the first signs of immunological recovery, whereas the CD4+ subset recovered later in patients who suffered from acute graft versus host disease (GvHD) and infections. Acute and chronic GvHD, cirrhosis, rejection and HIV viral infection contributed to the persistence of the profound immunodeficiency status observed after BMT. Our results did not differ greatly from the others and confirmed that BMT may be performed in underdeveloped countries despite the difficulties it might pose.
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PMID:Immunological recovery after bone marrow transplantation for severe aplastic anaemia: a Brazilian experience. 792 58

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

Concurrent infection with MCMV has been observed to result in the marked exacerbation of a P-->F1 GVHR across a class I MHC only donor-recipient disparity. We have previously determined that MCMV induces several alterations characteristic of severe GvHR/D which are not observed during GvHR or MCMV infection alone. Most notable of these alterations is the enhanced development of donor anti-host cytotoxic T cell activity. The present studies were performed to examine the requirement of specific donor and host cell populations. Only depletion of donor CD8+ T cells (not NK1.1+ or CD4+) prevented development of severe GVHR/D. By in vivo antibody treatments, depletion of host CD4+ but not CD8+ T cells also abrogated the development of severe GVHR/D. These findings therefore support the hypothesis that MCMV-activated CD4+ T cells enhance the production of a donor anti-host class I CD8+ response. Thus, the present findings support hypotheses attributing the association of viral infection and GVHD development with pathogen-induced immune responses.
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PMID:CD8+ and CD4+ T cells contribute to the exacerbation of class I MHC disparate graft-vs-host reaction by concurrent murine cytomegalovirus infection. 809 96

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

A 33-year-old woman with AML (M4) resistant to chemotherapy received syngeneic marrow graft from her identical twin following high dose busulfan and etoposide. However, the relapse was confirmed on the 60th day after the procedure. Since she failed to achieve remission despite intensive chemotherapy, a second BMT from the same donor was performed following total body irradiation and high dose etoposide on the 126th day after the initial BMT. At this time, cyclosporine (1 mg/kg/day) was administered to induce graft-versus-host disease (GVHD). Skin rash appeared on the 18th day after the 2nd BMT, and biopsy from the rash on the 23rd day showed a typical picture of cutaneous GVHD (grade 2) and there was no evidence of viral infection. On the 36th day after the 2nd BMT, the patient died of veno-occlusive disease. Although graft-versus-leukemia effect in this patient could not be evaluated because of early death, the induction of GVHD with cyclosporine might be effective to reduce the relapse rate after syngeneic or autologous BMT. Further studies are required to confirm this effect.
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PMID:[Cyclosporine-induced graft-versus-host disease in a syngeneic bone marrow transplantation]. 845 Jun 5

Chronic cutaneous graft-versus-host disease may appear clinically as a lichenoid eruption. We describe a 26-year-old man who developed a unilateral linear lichenoid eruption 7 months after allogeneic bone marrow transplantation. We believe this represents an unusual form of localized, chronic graft-versus-host disease. The possible relationship to viral infection or cellular mosaicism and the clinical, histologic, and immunologic similarities to idiopathic lichen planus are discussed.
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PMID:Unilateral linear lichenoid eruption after bone marrow transplantation: an unmasking of tolerance to an abnormal keratinocyte clone? 849 88

The recovery of gamma delta T lymphocytes was studied in 31 recipients of T cell-depleted allogeneic bone marrow (BMT) to determine if the dynamics of reconstitution could be related to graft-versus-host disease (GVHD) or other complications of marrow transplantation. Two distinct patterns of regeneration were apparent. In 12 patients, there was a progressive rise in both the percentage and the absolute number of peripheral blood gamma delta T cells over the first year post-transplantation, but these increases never breached levels found in 14 healthy donors. Each of the 19 remaining patients had abnormally high proportions and numbers of gamma delta T cells on at least two occasions following transplantation. The clinical factor that best explained these observations was the frequency of intercurrent infections. Of 19 patients with abnormally increased percentages and numbers of gamma delta T lymphocytes, 18 had one or more episodes of confirmed viral or fungal infection, contrasted with only two of 12 in the comparison group (P < 0.001). There was no significant association of gamma delta T cell recovery patterns with the presence of GVHD (P = 0.33). We conclude that the recovery of gamma delta T lymphocytes after marrow transplantation may vary. Supranormal levels of this T cell subset are associated with infection and may contribute significantly to cellular immune defenses against fungal or viral disease.
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PMID:Gamma delta T lymphocyte regeneration after T lymphocyte-depleted bone marrow transplantation from mismatched family members or matched unrelated donors. 864 Jan 74

Hepatic dysfunction is common in patients who receive intensive chemotherapy and it is important to determine the etiology in order to institute appropriate therapy. The role of laparoscopic liver biopsy in patients with neutropenia, thrombocytopenia, or both was evaluated as a mean of making treatment decisions and as a determinant of clinical outcome. Laparoscopic liver biopsy was performed in 29 subjects who were receiving intensive cytotoxic therapy with or without bone marrow transplantation. One to three direct-vision laparoscopic liver biopsies were performed in each patient using a Tru-cut needle during general anesthesia. Platelet concentrate transfusions were usually given before, during, and immediately after biopsy. Bleeding was controlled with spatula electrocautery. Thirty-two biopsies were obtained in 29 patients. At the time of liver biopsy, white blood cell and platelet counts ranged from 0 to 14,300/microliters (median: 2500/microliters), and 1000 to 47,000/microliters (median: 20,000/microliters), respectively. Bleeding at the liver biopsy site was readily controlled during the procedure without clinical evidence of significant bleeding; no procedure-related complications were noted and no patients required re-exploration. All biopsies were informative and the lesions observed in 32 biopsies revealed graft-versus-host disease (n = 5), hepatic candidiasis (n =1), hepatic veno-occlusive disease (n = 3), cholestasis (n = 19), hemosiderosis (n = 26), toxic injury (n = 8), hepatic steatosis (n = 4), granuloma (n = 1), viral infection (n =1), and malignancy (n = 1). Laparoscopic liver biopsy has been proven to be an effective means of assessing the cause of liver dysfunction in patients who were thrombocytopenic and immunosuppressed. The diagnosis obtained at laparoscopic liver biopsy altered therapy in nine of 29 (31%) patients.
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PMID:Laparoscopic liver biopsy to evaluate hepatic dysfunction in patients with hematologic malignancies: a useful tool to effect changes in management. 872 71

To investigate the presence of nondiagnosed viral lung infections in patients who developed acute respiratory failure and diffuse pulmonary infiltrates after bone marrow transplantation (BMT), we studied necropsy-obtained lung specimens with features of diffuse alveolar damage (DAD) where no other specific histological diagnosis could be established, by using in situ hybridization and immunohistochemistry. Lung tissue samples obtained at necropsy from 19 patients (12 males and 7 females; 31 +/- 11 yrs mean +/- SD age) who died 56 +/- 36 days after BMT (12 allogeneic and 7 autologous), were studied retrospectively using specific deoxyribonucleic acid (DNA) probes to detect cytomegalovirus (CMV), herpes simplex virus (HSV), Epstein-Barr virus (EBV), and adenovirus genomes. Tissue samples were additionally processed with antibodies to CMV and HSV antigens. Cells infected by CMV were detected by in situ hybridization in five cases, and by immunohistochemistry in four cases. Combining the results of both procedures, a previously undiagnosed CMV infection was found in six patients. All of them had received an allogeneic BMT and had developed graft-versus-host disease (GVHD). No evidence of cells infected by HSV, EBV, or adenovirus was found in any case. No viral infection was detected either in recipients of autologous marrow or in recipients of allogeneic BMT without GVHD. These results indicate that pulmonary cytomegalovirus infection not detected by conventional histological examinations may be present in patients with diffuse alveolar damage associated with bone marrow transplantation, especially in recipients of allogeneic marrow who develop graft-versus-host disease. Furthermore, the use of in situ hybridization and/or immunohistochemistry on pulmonary histology might improve the diagnosis of viral lung infections in patients receiving bone marrow transplantation.
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PMID:Undetected viral infection in diffuse alveolar damage associated with bone marrow transplantation. 880 24

Cytomegalovirus (CMV) infection has been associated with graft rejection in solid organ transplantation and with graft-versus-host disease in marrow transplantation. We hypothesized that CMV-infected endothelial cells play an important role in the rejection process, because of their strategic localization at the interface with the host immune system and their ability to modulate T cell function. To study the effect of CMV infection on cell-mediated cytotoxicity against endothelial cells, peripheral blood mononuclear cells (MNC) were incubated with CMV-infected umbilical vein endothelial cells (CMV-UVEC) or mock-infected controls (M-UVEC) and lysis measured by [3H]leucine release. MNC lysed only CMV-UVEC to a maximum of 23% at E:T 20:1. Lysis was not affected by CD3+ cell depletion, but was abolished by CD16+ cell depletion, indicating that NK cells were the effectors. The kinetics of the NK-mediated lysis of CMV-UVEC paralleled the time course of CMV antigen expression. Furthermore, ganciclovir treatment of CMV-UVEC cultures decreased both specific antigen synthesis and NK-mediated lysis. This indicated that NK might recognize either a viral antigen or a cellular antigen modulated by CMV infection. Treatment of CMV-UVEC with F(ab)2 fragments of human polyclonal anti-CMV antibodies failed to inhibit NK cytotoxicity. In contrast, F(ab)2 fragments of MB40.5, a murine MAb reactive with a conserved epitope on the human MHC class I, significantly decreased lysis, proving that NK lysis of CMV-UVEC is an MHC class I-dependent function. To determine whether CMV-UVEC lysis was dependent solely on upregulation of MHC class I, MNC were incubated with CMV-UVEC mixed with uninfected UVEC. There was no competition for NK-target recognition sites, indicating that NK lysis required an interaction with an MHC class I antigen modified by viral infection. Antibodies against IFN-alpha or -beta did not block NK cytotoxicity against CMV-UVEC. Our findings provide a working frame for further evaluation of cellular immune responses to CMV infection.
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PMID:NK recognition of cytomegalovirus-infected endothelial cells depends on viral replication and MHC class I expression. 882 29


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