Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0018133 (graft-versus-host disease)
 18,032 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To determine the graft-versus-leukemia effect after hematopoietic stem cell transplantation (HSCT), we studied 199 patients with acute lymphoblastic leukemia who underwent transplantation at Huddinge University Hospital between 1981 and 2001. Seventy-four patients were in first complete remission (CR1), and 125 were in later stages of the disease. Most patients had an HLA-identical sibling donor. Conditioning consisted mainly of total body irradiation and cyclophosphamide, and graft-versus-host disease (GVHD) prophylaxis consisted of cyclosporine and methotrexate. Acute GVHD developed in 143 patients and chronic GVHD in 67. The 5-year probability of relapse and relapse-free survival (RFS) were 32% and 49%, respectively, in patients in CR1, as compared with 53% and 33% in those with more advanced disease. In the multivariate risk factor analysis of relapse, we found that the absence of chronic GVHD (P<.001), absence of herpes simplex virus infection after HSCT (P=.003), combination prophylaxis with methotrexate and cyclosporine (P=.01), and >6 weeks from the diagnosis to CR (P=.025) were independent risk factors for relapse after HSCT. Factors associated with a better relapse-free survival were chronic GVHD (P<.001), ABO blood group mismatch (P=.006), younger patient age (P=.01), and an HLA-matched donor (P=.01). The association between herpes simplex virus infection and a low frequency of relapse is a new observation and may indicate that viral antigens play a role in the induction of an antileukemic effect.
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PMID:Graft-versus-host disease is associated with a lower relapse incidence after hematopoietic stem cell transplantation in patients with acute lymphoblastic leukemia. 1499 85

A 31-year-old woman with acute myeloblastic leukemia (AML) underwent allogeneic peripheral blood stem cell transplant (PBSCT). On day +274 following transplantation, the patient had severe chest pain, high-grade fever, and general fatigue. Electrocardiographic examination revealed ST segment elevation, and echocardiographic examination revealed an obvious pericardial. The diagnosis of pericarditis was made. We could not exclude the possibility of a combination of chronic GVHD involving the liver, because biochemistry examination revealed altered liver dysfunction, but liver biopsy was not performed. The patient underwent empirical treatment for bacterial or viral infection, and was given prednisolone for chronic GVHD. Retrospective serologic examination revealed that EBV reactivation had occurred at this time. This is the first reported case of pericarditis associated with EBV reactivation after allogeneic-stem cell transplantation (allo-SCT).
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PMID:Pericarditis associated with Epstein-Barr virus reactivation in a patient following allogeneic peripheral blood stem cell transplantation from an HLA genotypic 1-locus mismatched sibling donor. 1510 30

Complementarity-determining region (CDR3) size spectratyping has often been used to analyze the clonal expansion of T-cells. CDR3 size spectratyping has been useful in the analysis of the oligoclonal expansion of T-cells in virus infection, graft-versus-leukemia effect (GVL), graft-versus-host disease (GVHD), and immune reconstitution of T-cells after allogeneic stem cell transplantation (allo-SCT). We analyzed 26 T cell receptor (TCR)-beta-chain subfamilies (VB) in 25 patients who underwent allo-SCT. Fifteen of these patients developed acute GVHD (aGVHD). Many TCR-VB were skewed in the early stage. In these TCR-VB subfamilies, VB6 was most often skewed at the time of skin aGVHD. We then analyzed the average score of the complexity of 26 TCR-VB spectratypings in patients with or without cGVHD. The patients who developed chronic GVHD (cGVHD) had a lower average score of TCR-VB complexity than that of patients without cGVHD (P = 0.010). In particular. the patients who developed the quiescent type and de novo type of cGVHD from 4 months after allo- SCT had a lower average score of TCR-VB complexity at 3 months than that of the patients who had no cGVHD (P = 0.0055). These results suggest that we might be able to consider a possible development of cGVHD by analyzing TCR-VB spectratyping after allo-SCT.
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PMID:Molecular analysis of T-cell repertoire in patients with graft-versus-host disease after allogeneic stem cell transplantation. 1516 Sep 9

This report describes the first allogeneic hematopoietic stem cell transplantation (HSCT) performed for the indication of rheumatoid arthritis (RA). We used nonmyeloablative allogeneic HSCT to treat a 52-year-old woman who had treatment-refractory RA and a poor prognosis (24 swollen and 38 involved joints). She was treated with fludarabine, cyclophosphamide, CAMPATH-1H, and CD34-selected HSCT (8 million CD34+ donor cells/kg); the donor was the patient's HLA-matched, rheumatoid factor-negative sister. One year post-HSCT, the patient has had no infection except dermatomal varicella-zoster virus infection and no acute or chronic graft-versus-host disease (GVHD). Her RA has remained in remission with no immunosuppressive or immunomodulatory medications. The patient is a mixed chimera, with 55% donor T (CD3+) cells and 70% donor myeloid (CD33+) cells. This is the first published report of allogeneic HSCT performed for the indication of RA. Mixed chimerism has resulted in marked amelioration of RA, without GVHD.
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PMID:Induction of remission of severe and refractory rheumatoid arthritis by allogeneic mixed chimerism. 1533 49

Graft-versus-host disease (GVHD) and graft-versus leukemia (GVL) effects are closely related to each other after allogeneic stem cell transplantation. This association exists because of the extensive and complicated interaction between cellular donor components and recipient components concomitant with cytokine storms. It has been demonstrated that part of this interaction may be related to the induction of a variety of regulatory cells, such as regulatory T-cells and natural killer T (NKT) cells. A lower number of NKT cells may be found in patients with autoimmune diseases, cancer, viral infection, and severe GVHD. When activated, NKT cells rapidly release suppressive cytokines, such as interleukin 4 (IL-4), IL-10, and IL-13, as well as inflammatory cytokines, such as interferon gamma and tumor necrosis factor alpha. NKT cells therefore act as a double-edged sword in their progressive or suppressive effects on diseases. Such contradictory phenomena may be related to the function or types of antigen-presenting cells (APCs) in response to their ligand. A single-dose injection of a ligand for NKT cells, alpha-galactosylceramide (alpha-GalCer), can induce immunity through fully mature dendritic cells in an antigen-specific manner. By contrast, multiple injections of alpha-GalCer would induce tolerance, which may be caused by immature APCs. This response suggests that the function of NKT cells can be determined by alpha-GalCer for controlling the immune response. Furthermore, activation of NKT cells followed by activation of APCs and IL-12 production may lead to activation of NK cells and suppress GVHD in mismatched major histocompatibility complex combinations or may induce GVL effects. Control and modification of NKT cell function may play an important role in regulating GVHD/GVL effects.
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PMID:Application of natural killer T-cells to posttransplantation immunotherapy. 1571 80

Haemopoietic stem cell transplants (HSCT) cure increasing numbers of primary immunodeficiencies (PID): residual recipient T-cell function increases risk of incomplete or decreasing immune reconstitution, which may resolve following a second, unconditioned, infusion from the same donor (boost infusion). We assessed the outcome of 20 boost infusions in 19/139 patients transplanted for PID patients at our centre since 1987. Boost infusion was given 64-1226 days after the original HSCT. Follow-up was 4-124 months. In all, 12 of 19 patients cleared viral infection (6), or showed sustained increase in donor chimerism, T- and B-cell numbers and function, or other markers (6). In 7/12 patients, immunoglobulin replacement has been discontinued. Four were partially successful with stable low-level chimerism (two patients) or improved T-cell function, but not B cell function (two patients). Four failed with no change in donor chimerism or cell number. No significant association with donor source, T-cell depletion, conditioning regimen, boost infusion stem cell dose or time from original HSCT to boost was found. One patient developed grade III acute graft-versus-host disease despite cyclosporine, and one developed severe pneumonitis; both have recovered. Boost infusion was successful or partially successful in 84% of patients. The risk of adverse effects is low.
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PMID:Outcome of boost haemopoietic stem cell transplant for decreased donor chimerism or graft dysfunction in primary immunodeficiency. 1572 84

Allogenic hematopoietic stem cell transplantation (HSCT), a procedure that is widely used in the treatment of a large number of malignant and non-malignant hematological diseases, is still associated with a wide range of complications, one of the most important of which is graft versus host disease (GVHD). The patients undergoing allogenic HSCT are also at high risk of developing secondary neoplasms, particularly leukemias and lymphomas. Solid tumors are less frequent, and the incidence appears to increase over time; the most frequent solid tumors are squamous cell carcinomas. We found that almost all studies of solid cancers occurring after transplantation are based on relatively small numbers of cases which have been monitored for short periods, and little information is available on individual cancers. In particular, reports of oral cancers in HSCT are very few. Potential risk factors associated with the development of secondary solid cancers after HSCT have been well described. They include graft versus host disease (GVHD), preoperative regimens, with either radio-chemotherapy or chemotherapy alone, conditioning regimes, immunosuppressive GVHD prophylaxis, viral infection and chronic stimulation as a result of viral antigens, antigenic stimulation from histocompatibility differences between recipient and donor, primary diagnosis, interaction of any of these factors with genetic predisposition, and other factors such as sex and age. All patients treated with HSCT should therefore be closely followed over the long term with the aim of identifying the onset of secondary tumors as early as possible.
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PMID:Oral malignancies following HSCT: graft versus host disease and other risk factors. 1608 55

This study was to analyze the infectious complications after hematopoietic stem cell transplantation (HSCT) according to the recent changes of HSCT. Medical records of 379 adult patients who underwent HSCT consecutively at Catholic HSCT Center from January 2001 to December 2002 were reviewed retrospectively. Allogeneic HSCT accounted for 75.7% (287/379) and autologous HSCT for 24.3% (92/379). During pre-engraftment period, bacterial infection was predominant, and E. coli was still the most common organism. After engraftment, viral infection was predominant. The incidence of invasive fungal infection showed bimodal distribution with peak correlated with neutropenia and graft-versus-host disease (GVHD). The overall mortality and infection-related mortality rates according to 3 periods were as follows; during pre-engraftment, 3.16% (12/379) and 1.8% (7/379); during midrecovery period, 7.9% (29/367) and 4.1% (15/367); during late-recovery period, 26.9% (91/338), and 15.9% (54/338). Risk factors for infection-related mortality were as follows; during pre-engraftment period, fungal infection and septic shock; during the mid-recovery period, hemorrhagic cystitis and delayed engraftment; during the late-recovery period, fungal infection, chronic GVHD, and relapse. In conclusion, infection was still one of the main complications after HSCT and highly contributes to mortality. The early diagnosis and the effective vaccination strategy are needed for control of infections.
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PMID:Current trends of infectious complications following hematopoietic stem cell transplantation in a single center. 1661 1

Human cytomegalovirus (HCMV) infections are the major viral complications associated with the post-transplant period in haematopoietic stem cell and solid organ transplant recipients. HCMV infection may be systemic (high viral load in blood associated with fever, leucopenia and thrombocytopenia) or local (clinical symptoms of viral infection within a single organ [e.g. lungs] or apparatus [gastrointestinal tract]). Both infection types can be associated with each other. Systemic HCMV infections are diagnosed by performing antigenaemia or DNAemia assay (polymerase chain reaction [PCR]) on blood samples: both assays are quantitative. Local infections are diagnosed by virus isolation from tissue biopsies or secretions, or by PCR. To prevent HCMV disease, a prophylactic approach is usual in the USA, while a pre-emptive (presymptomatic) approach, which is more common in Europe, involves administering antivirals when a predetermined viral load is reached in blood. Simultaneous virological and immunological follow-up is the best approach to efficient monitoring of HCMV infections in transplant recipients. Lack of immune reconstitution entails repeated episodes of recurrent infection with multiple courses of antiviral treatment, whereas reconstitution of both arms of the HCMV-specific T-cell mediated immune response controls HCMV infection. The exception is for cases of graft rejection or graft versus host disease treated with steroids or antilymphocyte globulin, which require virological monitoring and (in some cases) antiviral treatment until resolution of the adverse event.
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PMID:Monitoring transplant patients for human cytomegalovirus: Diagnostic update. 1673 95

Major histocompatibility complex class II deficiency, a rare autosomal recessive primary immunodeficiency, is caused by the defective expression of human leucocyte antigen (HLA) class II molecules due to mutated trans-acting elements of any one of four regulatory genes (CIITA, RFXANK, RFX5, RFXAP). The impaired CD4 T-cell differentiation and antigen presentation in the periphery results in a severe defect of cellular and humoral response consistent with severe recurrent infections, leading to a poor prognosis. Currently, allogeneic haematopoietic stem cell transplantation (HSCT) is the only curative approach, but the overall cure rate is lower than in other immunodeficiencies. We report a single centre experience of 17 HSCTs with 15 HLA-identical donors between 1981 and 2004. Eight patients survived, while the occurrence of acute graft-versus-host disease (GVHD) was 50%. This study aimed to identify potential risk factors for GVHD and outcome within pre-HSCT complications related to the immunodeficiency. Five of seven patients with pre-existing viral infections developed acute GVHD > or = grade II, of whom four died. Two of seven patients without detectable pre-existing viral infection developed GVHD > or = grade II, and one died. The difference was significant (P < 0.05). A plausible link with other factors potentially associated with the development of GVHD could not be found. We suggest that the reduced survival after HLA-identical HSCT may be caused by the high incidence of pre-existing viral infections and associated with the onset of severe acute GVHD.
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PMID:Human leucocyte antigen-identical haematopoietic stem cell transplantation in major histocompatiblity complex class II immunodeficiency: reduced survival correlates with an increased incidence of acute graft-versus-host disease and pre-existing viral infections. 1684 95


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