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 possibility that antigenically active protein macromolecules affect the risk of developing acute graft-versus-host disease (aGVHD) was investigated in a cohort of patients who underwent allogeneic marrow transplantation for hematologic malignancy (n = 575). Daily records of food intake from transplant through discharge or death were evaluated for grams of total protein and summed over consecutive 4-day intervals. The day of onset of aGVHD was partitioned into 4-day time intervals such that assessments of food intake preceded onset of aGVHD by 3-6 days. Acute GVHD developed in 308 (54%) patients. The cumulative incidence of aGVHD among patients eating any amount of protein was lower (4-13%) than that of patients not eating protein (8-19%) for each of the time intervals through day 21 post-transplant; the relative risk associated with protein intake, adjusted for patient and transplant characteristics that are correlated with the occurrence of aGVHD, ranged from 0.23 (95% confidence interval (CI) 0.09, 0.63) to 0.83 (CI 0.46, 1.51). A proportional hazards regression analysis, using protein intake as a time-dependent covariate, confirmed these results. The findings of this study provide no support for the hypothesis that intake of protein-containing foods during the first 3 weeks after marrow transplantation increases the risk of aGVHD.
Bone Marrow Transplant 1991 Sep
PMID:Oral protein intake and the risk of acute graft-versus-host disease after allogeneic marrow transplantation. 195

Patients transplanted with marrow from an HLA-phenotypically identical unrelated donor have a much higher risk of acute graft-versus-host disease (GVHD) than patients transplanted from an HLA-genotypically identical sibling. Much of this increased risk may be due to disparity for antigens encoded by genes within the MHC. Although the development of molecular genetic methods for HLA-typing may enable better matching between unrelated donor/recipient pairs, the extent to which GVHD risk might be decreased remains uncertain because disparity for minor histocompatibility antigens encoded by genes outside the MHC also causes GVHD. By application of fundamental population genetics, it can be demonstrated that the disparity for minor histocompatibility antigens is substantially greater between unrelated individuals than between family members. These findings imply that even with improved HLA-matching, unrelated marrow transplantation will carry more risk of GVHD than transplantation from a related donor.
Bone Marrow Transplant 1991 Sep
PMID:Increased disparity for minor histocompatibility antigens as a potential cause of increased GVHD risk in marrow transplantation from unrelated donors compared with related donors. 195 2

An acute pulmonary syndrome possibly representing acute graft-versus-host disease (GVHD) involving lung interstitium occurred in a patient given an allogeneic bone marrow transplant for haematological malignancy. He presented at day 34 with acute GVHD of skin and bowel, and this was associated with cough, dyspnoea and an asymmetrical change on chest X-ray. Lung biopsy demonstrated an interstitial and peribronchial lymphocytic infiltrate and acute bronchial epithelial degeneration. He responded symptomatically to high dose intravenous methylprednisolone. The radiological change resolved completely. This case, thought to represent GVHD involving lung interstitium, emphasizes the need for tissue procurement in the management of non-bacterial lung disease after marrow transplantation.
Bone Marrow Transplant 1991 Sep
PMID:An acute pulmonary syndrome possibly representing acute graft-versus-host disease involving the lung interstitium. 195 5

In DA rats grafted with PVG hearts a short course of cyclosporine induces a state of specific unresponsiveness. In animals with grafts surviving greater than 75 days, the W3/25+ (CD4+) subset loses its capacity to mediate rejection of PVG but not third-party heart grafts when transferred into irradiated DA hosts. In this study we examined whether there was an associated change in the capacity of peripheral lymphoid T cell subsets from unresponsive animals to induce graft versus host (GVH) reactivity. First we demonstrated that there is synergy between naive CD4+ and CD8+ cells in the popliteal lymph node PLN assay, but that alone, only CD4+ and not CD8+ cells proliferate. Unfractionated and CD4+ cells from unresponsive animals produced similar PLN enlargement in both donor-specific (DAxPVG)F1 hosts and third-party (W/FxDA)F1 hosts. This enlargement was comparable to that produced cells from naive and specifically sensitized hosts. MRC OX8+ cells from both unresponsive and naive hosts did not produce PLN enlargement unless large numbers were injected; small numbers of sensitized MRC OX8+ cells produced specific PLN enlargement CD4+ cells from CsA-treated DA did not respond to DA anti-PVG idiotype in an in vivo assay adapted from the host versus graft (HVG) PLN assay. As the PLN assay does not test cells capacity to effect tissue damage, cells from CsA-treated DA rats were tested in a lethal GVHD assay. These cells had the same capacity to induce lethal GVH in irradiated (DAxPVG)F1 and (DAxW/F)F1 hosts. The normal response of cells from unresponsive animals in both proliferative and effector GVH assays shows that cells with the potential to respond to PVG alloantigen and mediate tissue damage are present in unresponsive animals but are prevented from mediating rejection, possibly due to the relatively weak immune stimulus of an organ graft.
Transplantation 1990 Sep
PMID:Specific unresponsiveness in rats with prolonged cardiac allograft survival after treatment with cyclosporine. IV. Examination of T cell subsets in graft-versus-host assays. 197 83

The development of methods of avoiding graft-versus-host disease (GVHD) while retaining the alloengraftment-promoting and anti-leukemic effects of allogeneic T cells is a major goal of research in bone marrow transplantation (BMT). We have recently obtained evidence suggesting that natural suppressor (NS) cells derived from T cell-depleted (TCD) syngeneic marrow can protect against GVHD while permitting alloengraftment. We have now attempted to enrich and then propagate NS cells in vitro, with the goal of obtaining an enhanced anti-GVHD effect by adoptive transfer in vivo. Two long-term cell lines were generated culturing BMC depleted of Mac1-positive cells and of Mac1-positive plus Thy1-positive cells in high concentrations of IL-2. Both cell lines showed anti-GVHD effects when administered along with a GVHD-producing inoculum, while permitting complete allogeneic reconstitution. A clone derived from Mac1-depleted BMC protected completely against a more chronic pattern of GVHD. These cell lines demonstrated suppressive activity in vitro, cytolytic activity against a broad range of natural killer (NK)-sensitive and NK-resistant targets, and a novel cell surface phenotype, with characteristics of both alpha beta-TcR-bearing T cells and of NK cells. In some respects, these cells resemble LAK cells and differ from fresh NS cells, and from the cloned NS cells derived from spleens of total lymphoid irradiation (TLI)-treated mice and neonatal mice. To our knowledge, this is the first detailed phenotypic analysis of cell lines with in vivo anti-GVHD activity. If applicability can be demonstrated in large animal models, the ability to use bone marrow as a source of such protective cell lines might also have potential utility in clinical BMT.
Cell Immunol 1990 Sep
PMID:In vitro and in vivo analysis of bone marrow-derived CD3+, CD4-, CD8-, NK1.1+ cell lines. 214 39

The induction of a chronic graft-versus-host (cGVH) disease in (Balb/c x A/J)F1 mice by the intravenous injection of either Balb/c or A/J parental lymphoid cells led to the development of two different models of disease. In this paper we compared the clinical aspects and the antigen specificities which recognized the autoantibodies developed by the animals of these two models of cGVH disease. Renal disease, alopecia, and purpura lesions were common in both models, although their frequency and intensity varied between groups. The models were differentiated by two main characteristics. When donor cells were of Balb/c origin, a joint disease similar to rheumatoid arthritis developed in 50% of the animals, and when donor cells were of A/J origin, 25% of the animals developed edema of the front feet, occasionally with loss of the nails, similar to that of scleroderma. Differences among the autoantibodies found in the sera of these two groups of mice were also observed. After the injection of Balb/c lymphoid cells, rheumatoid factors reactive with human and murine IgG were characteristically present (69 and 75%, respectively) and a statistically significant correlation was found between high titers of rheumatoid factor and arthritis (P less than 0.001). Antinuclear antibodies (ANAs) were present in all animals. Anti-dsDNA and anti-histones were positive in 50 and 25%, respectively. Anti-snRNP were detected at a low titer in 35% of the animals. When donor cells were of A/J origin, ANAs were also present in all mice. Anti-dsDNA, anti-histones, and anti-snRNPs antibodies were present in 90, 15, and 65%, respectively. The most outstanding characteristics among anti-snRNPs were the high titers of anti-U1 and anti-U3 detected in 50 and 30%, respectively. Rheumatoid factors reactive with human and murine IgG were positive in 15 and 42% of animals, respectively, but no significant correlation was found between these factors and disease. Our results indicate that the graft-versus-host disease induced in the same F1 strain of mice can be manifested in different forms of connective tissue disease, depending on whether the cells come from one or the other of the parental strains. Furthermore, in this paper the occurrence of rheumatoid factors in mice with cGVH is described for the first time.
Clin Immunol Immunopathol 1990 Sep
PMID:Different strains of donor parental lymphoid cells induce different models of chronic graft-versus-host disease in murine (Balb/c x A/J)F1 hybrid hosts. 214 68

"Postoperative erythroderma", the pathogenesis of this disease have solved as graft-versus-host disease (GVHD) due to blood transfusion, is fatal and impossible to cure for the time being. Therefore the prevention against the disease is very important. One woman and three men who underwent an operation and blood transfusion at our department died of this disease. They fell into high fever on 11-13 days, erythroderma on 12-16 days, liver dysfunction on 14 days, and leukocytopenia on 17-19 days, after surgery and transfusion. Eventually, they all suffered from thrombocytopenia, diarrhea, renal dysfunction, and sepsis which led to death. The clinical course, macroscopic and microscopic findings of them coincided with those of GVHD. Since 1989, we have tried following methods for prevention of postoperative erythroderma: Reducing blood transfusion, especially fresh blood and fresh thrombocyte plasma, by using predeposited autologous blood, autologous washed erythrocytes collected from the operative area before and after extracorporeal circulation (ECC), concentrated residual blood from the ECC using a hemoconcentrater, and 1,500 rad of cobalt-irradiation of fresh blood, fresh thrombocyte plasma, and blood collected within 7 days prior to the transfusion. Postoperative erythroderma has not been experienced by introduction of these methods since 1989.
Kyobu Geka 1990 Sep
PMID:[Studies on so-called "postoperative erythroderma": report of four cases]. 214 58

We report a patient who had abrupt onset of pure red cell aplasia (PRCA) induced by B19 parvovirus during allogeneic bone marrow transplantation (BMT). A 14-year-old girl with APL in complete remission was admitted in February 1988, for the purpose of BMT. She was received marrow from HLA identical sister on March 17, 1988 (day 0). She received 120 mg/kg cyclophosphamide and 12 Gy total body irradiation for conditioning of BMT. For graft-versus-host disease (GVHD) prophylaxis she was given cyclosporine and short term methotrexate. She did not develop acute GVHD after BMT, but on the day 28 a bone-marrow aspirate revealed findings of PRCA. During this course the number of white blood cell and platelet favorably recovered. B 19 parvovirus DNA was detected in the serum of the day 30 and day 42. Antihuman B 19 parvovirus (HPV) antibody titers were increased: the values of anti-HPV IgM were suddenly elevated and those of anti-HPV IgG were elevated. Serum on the day 42 inhibited erythroid progenitors (CFU-E, BFU-E) but not inhibited myeloid progenitors (CFU-C). A reticulocyte count recovered on the day 50. As the patient was HPV-IgG negative prior to BMT and the donor was HPV-IgG seronegative, the source of infection may be platelet transfusion (day 7 through 14).
Rinsho Ketsueki 1990 Sep
PMID:[Pure red cell aplasia induced by B19 parvovirus during allogeneic bone marrow transplantation]. 217 87

One hundred forty-seven consecutive patients with leukemia, myelodysplastic syndrome, or aplastic anemia were treated by marrow grafts from genotypically HLA-identical siblings (n = 122) or HLA-haploidentical family members (n = 25). Haploidentical recipients differed from their donors for no more than one HLA locus on the nonshared haplotype. All were given postgrafting immunosuppression with a combination of methotrexate and cyclosporine. In a randomized study we explored whether prednisone administered from day 0 through 35 along with methotrexate/cyclosporine could improve prevention of acute graft-versus-host disease (GVHD). The GVHD incidence in patients not given prednisone was comparable with that previously reported with methotrexate/cyclosporine. Unexpectedly, significant increases in acute and also chronic GVHD were seen in HLA-identical recipients administered prednisone, but not in the small number of patients administered HLA-nonidentical grafts. However, the resultant increase in transplant-related mortality in patients administered prednisone was offset by an increase in leukemic relapse in patients not administered prednisone, presumably related to the absence of a graft-versus-leukemia effect. Therefore, overall disease-free survival of the two groups of patients was comparable, with slightly more than 50% of the patients being alive at more than 2 years after transplantation. We speculated that prednisone adversely affected GVHD prophylaxis, interfering with methotrexate's cell cycle-dependent suppression of donor lymphocyte proliferation in response to host antigens. In a pilot study we explored whether beginning prednisone on day 15, after completion of methotrexate administration, would avoid this adverse effect. The GVHD incidence in patients administered methotrexate/cyclosporine along with "late" prednisone was comparable with that in patients not administered prednisone. We conclude that methotrexate/cyclosporine is effective in decreasing the incidence of grade II through IV GVHD, and that the addition of prednisone to this regimen is not beneficial in recipients of HLA-identical marrow grafts.
Blood 1990 Sep 01
PMID:What role for prednisone in prevention of acute graft-versus-host disease in patients undergoing marrow transplants? 220 81

Tumor necrosis factor is one of the recently cloned cytokines with pleiotropic effects on normal and malignant cells. Our knowledge about the scope of cells producing or responding to this cytokine has enormously expanded. In critically ill patients with acute hepatic failure, acute graft-versus-host disease, or septic shock, circulating tumor necrosis factor can be measured and useful prognostic correlations do exist. Despite promising in vitro results, early clinical trials with tumor necrosis factor for the treatment of cancer have failed thus far to reveal major antineoplastic activity in cancer patients. However, more clinical trials are necessary, since different routes of administration and combinations with other cytokines may lead to favorable results.
Klin Wochenschr 1990 Sep 03
PMID:Tumor necrosis factor: an update on basic research and clinical applications. 221 7


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