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)

Fourteen patients with T-cell-derived leukemia and lymphoma underwent high-dose chemoradiotherapy and anti-T-cell monoclonal antibody-treated autologous bone marrow transplantation (ABMT). All patients were either in sensitive relapse or had adverse prognostic features, and five patients had a history of bone marrow involvement with disease. Patients received a median of 2 (1 to 3) prior chemotherapy regimens; 10 patients received local radiotherapy. After high-dose ablative therapy, greater than 500/mm3 granulocytes and greater than 20,000 untransfused platelets/mm3 were noted at a median of 23 (13 to 48) and 26 (15 to 43) days post-ABMT, respectively. Natural killer (NK) cells, T cells (predominantly T8+), and monocytes were noted within the first 1 to 2 months post-AMBT, as seen in other series. Disease-free survival was a median of 10.1 months, 5.9 months for patients with T acute lymphoblastic leukemia or lymphoblastic lymphoma and 25.6 months for patients with T non-Hodgkin's lymphoma (NHL). Toxicities were common and severe. Thirty-six percent of patients developed bacteremias early post-BMT. Late complications included a skin rash consistent with graft versus host disease; infections with Herpes zoster, hepatitis, and Pneumocystis carinii; and the development of Epstein-Barr virus associated lymphoproliferative syndrome. Our findings suggest that patients who have undergone T-depleted ABMT have a profound immunodeficiency not reflected in the phenotypic reconstitution of the T and NK cells. Characterization of the functional deficiency may facilitate the development of methods to reduce the long-term toxicity of AMBT in these patients.
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PMID:T-cell-depleted autologous bone marrow transplantation therapy: analysis of immune deficiency and late complications. 219 91

A 12-year-old boy with Philadelphia chromosome positive acute lymphoblastic leukemia received bone marrow transplantation (BMT) from an HLA identical sibling during the second remission. The diagnosis was made at the age of nine. Laboratory examination on admission revealed remarkable leukocytosis (92,000/microliters) with 93% lymphoblasts in the peripheral blood. Blastic cells were FAB L1 common ALL. Chromosomal study on both peripheral blood and bone marrow cells showed that lymphoblasts had an abnormal karyotype of 47, XY, inv (9), t(9; 22), +17. One month later he achieved remission by induction therapy consisting of vincristine, L-asparaginase, doxorubicin, and prednisolone. He was given intrathecal injection of methotrexate and cranial irradiation of 24 Gy for CNS prophylaxis. The cells with Philadelphia chromosome disappeared during remission. Hematological relapse occurred twenty one months later after first remission on April, 1986. He received re-induction therapy including L-Asp VDP, and high-doses of cyclophosphamide, methotrexate and araC. He obtained karyotypic remission on October 1986. Subsequently, bone marrow transplantation was performed following high-dose araC, CY and TBI as preconditioning on December 18, 1986. Methotrexate and cyclosporin A were given intravenously to prevent GVHD. On day 14, karyotypic conversion was detected, suggesting the successful bone marrow grafting. Acute GVHD appeared on day 25, and was treated with prednisolone and cyclosporin A. Prednisolone was tapered by day 80. On day 91, cyclosporin A was discontinued because herpes zoster occurred. Acyclovir was effective, but skin GVHD reappeared. With low-dose prednisolone, skin GVHD improved. Sicca syndrome soon appeared and was followed by chronic GVHD.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Allogeneic bone marrow transplantation in a case of acute lymphoblastic leukemia with positive Philadelphia chromosome]. 279 82

Forty-two patients undergoing bone marrow transplantation were included in a randomised, double-blind and placebo controlled trial of prolonged acyclovir prophylaxis against infections with viruses of the herpes group. Twenty patients were allocated to receive acyclovir and 22 to receive placebo. Acyclovir or placebo was administered i.v. at a dose of 250 mg/m2 twice daily, starting 5 days before transplantation. At 5 weeks after transplantation, administration was changed to tablets, 400 mg three times daily (children less than 6 years, 200 mg three times daily) and continued until 6 months after transplantation. In the placebo group, 10 acute herpes simplex virus (HSV) infections occurred in 7 patients (5 HSV-1 and 2 HSV-2), and another patient repeatedly shed HSV in throat washings. Five patients developed herpes zoster. Among patients receiving acyclovir only one episode of HSV infection occurred and no herpes zoster. The difference in the number of infection episodes and the number of infected patients was strongly significant (p = 0.0002 and 0.0017, respectively). The only acyclovir patient who reactivated HSV was terminally ill, and it is highly likely that she did not absorb a sufficient amount of the orally administered drug to control infection. All HSV and varicella zoster virus (VZV) infections were reactivations, and 9 of 10 patients who developed HSV infections or shed virus had a pre-transplantation HSV IgG titer of greater than 10 000 (ELISA). Acyclovir had no effect on cytomegalovirus (CMV), time of engraftment, or graft versus host disease (GVHD). Apart from a possible allergic reaction (skin rash) to acyclovir tablets, no adverse reactions were seen during this long prophylaxis with acyclovir.
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PMID:Acyclovir prophylaxis in bone marrow transplant recipients. 300 28

BMT has become an important therapy for many hematologic disorders. Following BMT, the recipient may develop GVHD when it appears that immunocompetent donor lymphocytes react to host antigens. Acute and chronic GVHD represent two distinct syndromes. Acute GVHD has not been associated with primary neurologic involvement. Polymyositis has been reported in 12 patients with chronic GVHD, with the most common underlying illness being aplastic anemia. The clinical, serologic, and muscle biopsy features of the myositis in GVHD have been similar to those observed in idiopathic polymyositis. Weakness was moderate to severe and responded to prednisone, sometimes with the addition of azathioprine. Prognosis depended upon the underlying disease and not on the severity of the myositis. MG occurs rarely in chronic GVHD. Most patients with MG and GVHD have had aplastic anemia; those with aplastic anemia are more likely to have anti-AchR prior to BMT. The clinical manifestations of GVHD MG have not differed from classic autoimmune MG; each patient had elevated antiacetylcholine receptor antibodies titers. All patients have responded well to cholinesterase inhibitors but have received other immunosuppressants. These observations suggest that aplastic anemia is an important host factor in the development of the autoimmune disorders seen with chronic GVHD, certainly of myositis and MG. Herpes zoster peripheral nerve infections have occurred in patients with chronic GVHD. One patient had mononeuritis multiplex. In both acute and chronic GVHD, CNS impairment is usually caused by metabolic encephalopathy or infection. Primary CNS involvement has not been recognized.
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PMID:Neurologic complications of graft-versus-host disease. 304 48

We report three cases of haemolytic-uraemic syndrome following bone marrow transplantation in young males. None of them was treated with cyclosporin A. All died in renal failure. Renal histology showed the typical appearances of haemolytic-uraemic syndrome. Immunoperoxidase examination of renal biopsies showed IgM and complement in blood vessels and glomeruli of all three cases. Cytomegalovirus infection was present in two cases and probable in the third. Two cases had been infected with herpes zoster. All had episodes of graft-versus-host disease. Possible pathogenetic mechanisms are discussed.
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PMID:Haemolytic-uraemic syndrome in recipients of bone marrow transplants not treated with cyclosporin A. 353 15

Nearly one-half of marrow transplant recipients who survive at least 6 months develop varicella-zoster virus (VZV) infection. Of 92 cases studied, 82 occurred within the first 12 months after transplant. Only one patient had recurrent infection. Seventy-seven patients had herpes zoster, 22 with subsequent cutaneous dissemination, and 15 had varicella. The overall mortality rate was 8%, and all deaths occurred within 9 months of transplant. Twenty-six of 32 patients studied had significant rises in VZV antibody during recovery. Among patients with acute leukemia, those with syngeneic transplants had a significantly lower incidence of VZV infection than those with allogeneic transplants. Incidence was slightly, but not significantly, decreased among patients with aplastic anemia. In contrast to other infections, the incidence of VZV infection was not influenced by graft-versus-host disease or predicted by the results of dinitrochlorobenzene skin testing.
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PMID:Varicella-zoster virus infection after marrow transplantation for aplastic anemia or leukemia. 624 86

A retrospective study was carried out in 161 patients who underwent allogeneic or autologous hemopoietic stem cell transplants. The aim was to determine the frequency, outcome and risk-factors associated with varicella zoster virus (VZV) infection. Post-transplant VZV infection occurred in 29 patients. The median onset of infection was 6.5 months post-transplant, with 82% of cases occurring within the first year. Localized herpes zoster was seen in 27 patients, one patient had varicella, and one patient had simultaneous presentation of both herpes zoster and varicella. No cutaneous or visceral dissemination was noted in the series. Each patient was treated with intravenous acyclovir. Mild complications with postherpetic neuralgia were reported by three patients. There were no deaths from VZV infection. Two risk factors noted to be associated with VZV infection were the presence of graft-versus-host disease in allogeneic transplants and leukemia as the underlying disease in autologous transplants. The overall incidence of post-transplant VZV infection in the present series was relatively low compared with that of other reports involving either allogeneic or autologous bone marrow transplantation.
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PMID:Varicella zoster virus infection after allogeneic or autologous hemopoietic stem cell transplantation. 754 49

Herpes zoster (HZ) has been often observed after bone marrow transplantation (BMT) in childhood. The occurrence of HZ was reviewed in children who received BMT. The clinical features of HZ were reviewed in 44 children who underwent BMT at Kyushu Cancer Center. Among the 35 recipients with a history of varicella before BMT, several factors associated with BMT and the lymphocyte subsets were compared between the patients who developed HZ (HZ+ group) and those who did not (HZ- group). Twenty-two recipients (50%) developed HZ; in two-thirds of these cases (15/22: 68%), HZ occurred between 80 and 120 days after BMT (median 101 days). The recipients treated with busulfan had a higher occurrence of HZ than those treated without it. The patients with Grade II-IV acute graft-versus-host disease (GVHD) developed HZ more frequently. In the HZ+ group, the absolute number of lymphocytes, CD3+, CD4+ or CD8+ cells at 3 months was significantly lower than that observed at 12 months after BMT and the CD4/CD8 ratio was significantly lower at 1 month than after 3 months of BMT. In conclusion, recipients were susceptible to HZ at around 100 days after BMT. The development of HZ may be associated with unbalanced T lymphocytes at that time.
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PMID:Herpes zoster in children with bone marrow transplantation: Report from a single institution. 764 77

A 31-year-old man with refractory anaemia of excess blasts, which had karyotypic abnormalities, received an allogeneic bone marrow transplant (BMT). At time of relapse, 3 months after BMT, he was treated with donor leucocyte transfusion (DLT). Grade III acute GVHD (graft-versus-host disease) occurred 35 d after DLT which was fully reversed with cyclosporin and prednisolone. His condition was complicated by a herpes zoster infection. 2 months after DLT, neutrophil and platelet count were increased and karyotypic abnormalities disappeared. This observation demonstrates that DLT is an effective treatment for relapse of myelodysplastic syndrome (MDS) after BMT.
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PMID:Donor leucocyte transfusions for relapse in myelodyplastic syndrome after allogeneic bone marrow transplantation. 863 32

Localized cutaneous graft-versus-host disease (GVHD) following a dermatomal distribution or in a pattern of Blaschko's lines. Some authors have postulated that dermatomal GVHD is triggered by a varicella-zoster virus infection, although in reported cases, there was no history of a preceding herpes zoster. We describe a case of GVHD localized to the exact dermatome of a culture-proven varicella-zoster virus infection. PCR analysis failed to detect persistence of viral genome in the affected skin.
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PMID:Dermatomal lichenoid chronic graft-vs-host disease following varicella-zoster infection despite absence of viral genome. 900 91


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