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)

The development of airflow obstruction, most often due to bronchiolitis, is a significant cause of morbidity and mortality in recipients of allogeneic BMT. Current consensus holds that this airways disease is the result of chronic GVHD and/or CMV infection. However, recent studies of idiopathic forms of BRO have demonstrated a striking influx of neutrophils into the lungs of affected individuals. Reasoning that the immune cell populations involved in tissue injury associated with either CGVHD or CMV infection would consist predominantly of lymphocytes, we tested this hypothesis by performing BAL in 12 adults with minimal or absent smoking histories who developed significant airflow obstruction (FEV1/FVC = 80.7 +/- 1 percent preBMT and 56.8 +/- 2.4 percent postBMT; p less than 0.001) following allogeneic BMT. Eleven of 12 patients had evidence of chronic, stable GVHD at the time of the study. In contrast to non-BMT patients with BRO, BAL defined two distinct patterns of lung inflammation in the BMT patients with airflow obstruction: (a) neutrophil predominance (five patients; neutrophil percentage = 20.2 +/- 6.6 percent); and (b) lymphocyte predominance (three patients; lymphocyte percentage = 35.9 +/- 12.1 percent). These data suggest that the pattern of inflammation in the lungs of BMT patients with BRO is not uniform and is not associated with active microbial infection. From these results, it is inferred that the airways injury in BMT patients may reflect diverse pathogenetic mechanisms initiated in the context of CGVHD and cytotoxic drug therapy.
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PMID:Analysis of airflow obstruction by bronchoalveolar lavage following bone marrow transplantation. Implications for pathogenesis and treatment. 239 38

Considering the merit and demerit of GVHD in leukemia patients following allogeneic BMT, our strategies for GVHD are as follows; (1) a mild prevention, (2) a treatment to control the severity, if occurred, and (3) an induction of GVHD in recipients who did not develop GVHD. We reported the results of recent trials in prevention, treatment and induction of GVHD. For the prevention, T cells were depleted from bone marrow cells in 11 recipients with the results of graft failure in 5 and death in 9. The data from IBMTR were similar to our data. For the treatment, new drugs, 15-Deoxyspergualin. Mizoribine and anti-human lymphocyte globulin were introduced with compromising outcomes and mild adverse effects. For the induction, Ubenimex, an immunostimulator, was administered to recipients who did not develop GVHD until 30 days after BMT. The interim data suggests that Ubenimex may induce chronic GVHD and suppress the relapse of leukemia. We experienced the sudden onset of GVHD during the tapering of immunosuppressants in two recipients, who were found to have arbitrarily discontinued them. The interruption of drugs for the prevention of GVHD may cause the induction of GVHD.
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PMID:[Control of graft-vs-host disease]. 239 9

Serum IgA levels were monitored at 3, 6, 12, and 24 months after BMT in 131 allogeneic and 3 syngeneic bone marrow transplant recipients. In general, IgA levels were low during the first 6 months and did not return to normal levels until 1-2 years after transplantation. Children (less than 15 years) had lower IgA levels at 3 and 6 months post-BMT compared to the adults (P less than 0.05), but donor age had no influence on the recipient IgA levels after BMT. Patients receiving either methotrexate or cyclosporine alone for GVHD prophylaxis had markedly lower IgA levels compared to those given a combination of these two drugs or patients transplanted with T-cell-depleted marrow (P less than 0.001). Mean IgA levels in patients without or with grade I acute GVHD were within the normal range at 3, 6, 12, and 24 months after BMT (greater than 0.3 g/L), although approximately 20% of the patients in each group showed low IgA levels (less than or equal to 0.3 g/L) early after transplantation. Patients with grade II or III acute GVHD had significantly lower values from 3 months up to 2 years after transplantation (P less than 0.01). Patients with chronic GVHD had significantly lower IgA levels 1 and 2 years after BMT compared to patients without chronic GVHD (P less than 0.005). Severe acute GVHD, particularly when followed by chronic GVHD, seems to be the main reason for low IgA levels, while other factors such as CMV infection or donor status may also contribute to the development of IgA deficiency after BMT.
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PMID:Development of IgA deficiency after bone marrow transplantation. The influence of acute and chronic graft-versus-host disease. 240 90

The feasibility and toxicity of six-week continuous intravenous 3 mg/kg/day cyclosporine (CsA) treatment in conjunction with a short course of methotrexate (MTX) was studied in 69 consecutive patients after HLA genotypically identical bone marrow transplantation. In light of the uncertain efficacy of prolonged oral CsA immunoprophylaxis in preventing de novo chronic graft-versus-host disease (GVHD). CsA treatment was terminated three months after BMT. Sixty-one (88%) patients received the full intravenous regimen and no patient exclusions were necessary due to intolerable adverse effects. Weekly median blood CsA concentrations ranged between 820 ng/ml in the first and 648 ng/ml in the sixth week of treatment. No significant correlation existed between blood CsA concentrations and CsA dosages. Major adverse effects of the regimen included hypertension in 36%, acute nephrotoxicity in 36%, acute hepatotoxicity in 41%, and central nervous system toxicity in 4% of the patients. Since hepatotoxicity occurred predominantly in the early posttransplant period (median onset day 9), the relatively high incidence of this untoward effect might have been additionally caused by MTX and/or the preparative regimen. Blood CsA concentrations and CsA dosages did not significantly correlate with serum creatinine or total and conjugated bilirubin levels. In addition, blood CsA and serum creatinine levels did not differ between hypertensive and normotensive patients. Acute GVHD developed in 16% of the patients. Median CsA doses and blood CsA concentrations were identical for each week after BMT for patients contracting acute GVHD as compared with those without acute GVHD. In 55 patients surviving without acute or secondary chronic GVHD, the cumulative probability of de novo chronic GVHD after termination of CsA treatment was 13%. In conclusion, this regimen was tolerable and provided constant blood CsA concentrations for six posttransplant weeks that were not adversely influenced by the development of acute GVHD. Restriction of CsA treatment to the first three months after BMT appeared not to increase the risk of de novo chronic GVHD, which challenges regimens employing oral CsA immunoprophylaxis for 6-12 months after BMT.
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PMID:Six weeks of continuous intravenous cyclosporine and short-course methotrexate as prophylaxis for acute graft-versus-host disease after allogeneic bone marrow transplantation. 240 91

HLA-DR expression by keratinocytes and enterocytes was studied in 23 patients undergoing BMT (12 autologous; 11 allogeneic). Two monoclonal antibodies were used to detect the HLA-DR antigen. Only in two patients before transplant and in one following autologous BMT was HLA-DR expressed on keratinocytes. Of 11 allogeneic recipients, 7 developed clinical GVHD, and HLA-DR-positive keratinocytes were seen in 6 of these. HLA-DR was expressed by enterocytes in 5 patients with GVHD and 4 of these also showed HLA-DR expression by keratinocytes. HLA-DR expression by keratinocytes correlated well with clinical GVHD. Expression of this antigen by enterocytes was associated with characteristic histological appearances of GVHD, even in the absence of intestinal symptoms. A combination of traditional and immunocytochemical techniques offers a sensitive and accurate method of confirming GVHD before it becomes florid.
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PMID:Class II antigen expression by keratinocytes and enterocytes--an early feature of graft-versus-host-disease. 245 41

Results from phase I/II studies of Granulocyte-colony stimulating factor (G-CSF) for bone marrow transplantation were reported. G-CSF in 200-800 micrograms/m2 was administered from day 3 or 5 daily for 14 days. A very rapid recovery of granulocytes was observed in most cases. Stem cell exhaustion was considered not serious. Stimulation on myeloid leukemic cells was observed in vitro tests, but relapse was observed in only 2 out of 17 myeloid leukemia patients. There was no marked difference in the grade and incidence of GVHD from historical control patients. As side effects, 3 cases of bone pain and 2 of skin rash were observed. All these symptoms were slight, reversible and tolerated for further administration. As a whole, courses of BMT with G-CSF seemed very smooth and uneventful with very rapid and steady recovery of granulocytes. G-CSF seemed promising for bone marrow transplantation in which the severe granulocytopenic stage is inevitable and normal stem cells without contact with cytostatic agents are procured.
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PMID:[Granulocyte colony stimulating factor for bone marrow transplantation]. 247 38

8 patients with severe and 4 with non-severe aplastic anaemia, aged 7 to 46 years, whose suppressor lymphocyte activity was in most cases elevated and who had no histocompatible sibling donor, underwent 1-2 courses of ALG/ATG treatment. 6 patients got CR and 1 PR and during 1-4 years they live with sustaining haemopoiesis, independent of blood transfusion (except one in PR). Among these seven responders increased suppressor lymphocyte activity normalized in 6. The adverse effects of the treatment were granulocyto- and thrombocytopenia, subfebrile states, hepatotoxicity, serum sickness and skin allergy. Five patients died because of early or late complications of the treatment or it's failure. Our results, similar to other authors', are like after BMT and supports the immunological mechanism of A.A. Immunosuppressive treatment with ALG/ATG has many advantages: no need to have identical bone marrow donor, no GVHD, possibility of treatment of patients over 30, even pretreated with blood transfusions, and finally much lower costs and efforts.
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PMID:ALG/ATG treatment--a useful alternative for BMT in selected aplastic anaemia patients. 248 Feb 77

In acute leukaemias there was a stable plateau in the survival curve at 45% after two years if grafted in first complete remission (n = 20) but only 13% of the patients are disease-free alive if grafted in a more advanced stage of the disease (n = 8). In 16 patients transplanted for chronic myeloid leukaemia the overall survival is 40%, in cases with graft-versus-host disease (GVHD) prevention by cyclosporine survival rate could be improved. Only 8 patients with severe aplastic anaemia, partially in low performance status were able to be transplanted; three died of infections, another by acute GVHD. The fatal complications in our study characterize the international well-known major problems in BMT: GVHD, interstitial pneumonitis, infections, graft failure in aplastic anaemia and recurrence of leukaemia, especially in more advanced leukaemia stage.
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PMID:Allogeneic bone marrow transplantation for leukaemia and aplastic anaemia. Results of the Leipzig BMT Group. 248 Feb 78

Of 25 HLA-identical, MLC negative transplants 10 patients had acute lymphoblastic leukaemia (ALL), 8 acute nonlymphoblastic leukaemia (ANLL), 3 severe aplastic anaemia, 2 malignant histiocytosis, 1 patients neuroblastoma and 1 Fanconi anaemia. 3 HLA nonidentical, MLC positive transplants were performed, two children had malignant infantile osteopetrosis and 1 child had a severe combined immunodeficiency disease. Patients with ALL and ANLL received cyclophosphamide and single dose total body irradiation. 3 patients received fractionated TBI. The results for the allogeneic group overall indicate that the actuarial disease free survival rate is 0.62. 16 of 25 patients are in continuous complete remission (CCR) periods of 3-78 months posttransplant. All three transplanted children with severe aplastic anaemia alive disease-free for periods of 21-81 months. 10 patients with ALL were transplanted (2 in first remission for high risk ALL, 8 in second remission). 7 of 10 patients are alive and disease-free (CCR rate 0.67). 8 patients underwent BMT for ANNL while in first remission in 7 patients and in third partial remission in 1 patient. 4 of 8 patients are alive and disease-free for periods of 25-56 months (CCR rate 0.50). 1 patient with neuroblastoma stage IV survives 24 months, 1 child with Fanconi anemia died on day +25 of GVHD and septicaemia. 1 of the 2 patients transplanted for malignant histiocytosis relapsed 3 months posttransplant, 1 patient is alive and disease-free 5 months posttransplant. In none of the HLA-nonidentical and MLC positive transplantations T-cell depleted marrow engrafted.
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PMID:Status of allogeneic bone marrow transplantation in childhood in the GDR. 248 Feb 79

Possible donors may be recommended by the following order: 1. HLA-identical twins (syngeneic) 2. HLA-identical siblings 3. HLA-haploidentical related donors The increased number of additional HLA-incompatibilities (HLA-A, -B, -DR) increases the risk of GVHD. 4. HLA-phenoidentical and MLC-negative unrelated donors The DRS for BMT includes the early HLA typing of the patient and of all related potential donors, covering all known antigens. Evidence on the basis of MLC should be available for cellular non-reactivity between donor and recipient cells, although this will be rarely possible with haploidentical related donors. Donor-specific HLA antibodies must not be detectable in the recipient. No generally accepted method has so far become available for consideration of minor histocompatibility antigens in the context of DRS for BMT.
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PMID:Histocompatibility and bone marrow transplantation (BMT). 248 Feb 87


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