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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)

Cold blood cardioplegia followed by terminal cardioplegia was employed as a method of myocardial protection for acquired valvular disease. Postoperative clinical results of both cardiac iso-enzyme and cardiac function were discussed from the effect of the myocardial protection. In operative procedures of 62 cases, 30 cases underwent mitral valve replacement and other mitral repair, 17 cases aortic valve replacement, 10 cases double valve replacement and 5 cases modified Bentall operation. Iso-enzymes of Creatine-Kinase (CK) and Lactate-Dehydrogenase (LDH) were measured by the constant time-interval. Cardiac function was estimated in acute postoperative phase and late phase. Hospital mortality was 1.5%. The cause of death was thought to be postoperative Graft Versus Host Disease with skin rash and pancytopenia. Cardiac function during acute phase well recovered in 62 cases of which two cases were controlled with intra-aortic balloon pumping. The values of CK-MB were measured during aortic cross-clamp, 30 min, 3 hours, 6 hours and 24 hours after cross-clamp release. Peak CK-MB value was detected 3 hours or 6 hours in almost cases. In contrast, peak LDH-1 value was detected 24 hours after cross-clamp release. Perioperative myocardial infarction was occurred in one case with modified Bentall operation whose CK-MB value was elevated over 150 IU/L at 3rd hour and 24th hour. However, the cardiac radio-isotope data of this case revealed good cardiac function with left ventricular ejection fraction (LVEF) 76% by cardiac pool imaging in spite of small postero-lateral perfusion defect by Thallium 201 scintigram.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Operative results of acquired valvular disease with blood cardioplegia followed by terminal cardioplegia]. 318 95

This is a retrospective analysis of marrow function in 171 recipients of an HLA-matched bone marrow transplant (BMT). Only patients with detectable hemopoiesis as indicated by leukocyte counts greater than 1.0 x 10(9)/l and platelet counts greater than 25 x 10(9)/l who were alive on day 30 were entered in the study. Poor marrow function was detected in 24 (14%) patients as indicated by a decrease in the peripheral blood counts to less than 40% of the maximal preceding values post-transplant in association with reduced marrow cellularity. Leukopenia (n = 4), thrombocytopenia (n = 3) or a combination of the two (n = 17) occurred 62 +/- 23 (SEM) days post-transplant and was associated with acute graft-versus-host disease (AGVHD) grade II or more and infection (n = 19) in the absence of clear rejection or persistence/recurrence of malignant disease. A multivariate analysis showed that AGVHD was the major risk factor (p = 0.001) for developing poor graft function. In the 24 patients with poor graft function, hemopoietic recovery was strongly associated with resolution of AGVHD and of infections. Their survival (27%) was the same as survival for other patients matched for GVHD who had no pancytopenia. The causes of death were GVHD (n = 13), pneumonia (n = 3) and infections (n = 1). This study draws attention to a particular type of poor graft function following allogeneic BMT that is characterized by (1) normal timing and quality of engraftment, (2) AGVHD of grade II or greater, (3) progressive and severe pancytopenia, and (4) multiple infections with poor clinical condition.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Poor graft function associated with graft-versus-host disease after allogeneic marrow transplantation. 333 76

CMV infection is one of the major infection after bone marrow transplantation. CMV viremia was systematically studied in 66 patients with aplastic anemia or leukemia undergoing BMT. 57% patients had CMV viremia with a frequency peak between 7 and 9 weeks after transplant. Clinical symptoms found during viremia were pancytopenia, fever, cytolytic hepatitis. Interstitial pneumonitis was found only in 4 cases. In 3 cases, viremia was not associated with clinical symptoms. Survival was identical to the group of patients without viremia. Viremia was positively associated with the presence of high anti-CMV antibody titer in donor or recipient before transplant, or to a lymphocyte proliferative response against CMV antigens in donor or recipient before BMT. Granulocyte transfusions increased the frequency of CMV viremia. CMV infection was significantly associated with acute and chronic graft versus host disease. The relation showed between these parameters and viremia provides a basis for an accurate diagnosis of CMV infection and a better background for the study of prophylactic or curative treatment of CMV infection.
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PMID:[Clinical aspects of cytomegalovirus infection after allogenic bone marrow grafts]. 609 Dec 25

By induction of a graft-vs.-host reaction (GVHR) in nonirradiated H-2-different F1 mice, one can induce stimulatory pathological symptoms, such as lymphadenopathy and hypergammaglobulinemia, combined with the production of autoantibodies characteristic of systemic lupus erythematosus (SLE). Alternatively, the GVHR can lead to the suppressive pathological symptoms, such as pancytopenia and hypogammaglobulinemia, characteristic of acute GVH disease (GVHD). Whether stimulatory or suppressive symptoms are induced by a GVHR depends, in our view (2-4), on the functional subset of donor T cells activated in the F1 host. The purpose of the present study was to investigate whether class I and/or class II H-2 alloantigens can selectively trigger, out of a pool of unselected donor T cells, those subpopulations of T cells responsible for the stimulatory and suppressive GVH symptoms, respectively. For the induction of the GVHR, 10(8) lymphoid cells from C57BL/6 (B6) donors were injected into three kinds of F1 hybrid mice, which had been bred from H-2 mutant strains on a B6 background. Whereas the I-A-disparate (B6 X bm12)F1 recipients exclusively developed stimulatory GVH symptoms, including SLE-like autoantibodies and immune complex glomerulonephritis, the K locus-disparate (B6 X bm1)F1 recipients showed neither clearly stimulatory nor clearly suppressive GVH symptoms. In marked contrast, the (bm1 X bm12)F1 recipients, which differ from the B6 donor strain by mutations at both K and I-A locus, initially developed stimulatory GVH symptoms, but rapidly thereafter showed the suppressive pathological symptoms of acute GVHD and died. Moreover, spleen cells obtained from (B6 X bm12)F1 mice injected with B6 donor cells helped the primary anti-sheep erythrocyte (SRBC) response of normal (B6 X bm12)F1 spleen cells in vitro, whereas spleen cells (bm1 X bm12)F1 mice injected with B6 donor cells strongly suppressed the primary anti-SRBC response of normal (bm1 X bm12)F1 spleen cells. Spleen cells from the K locus-disparate (B6 X bm1)F1 recipients also suppressed the primary anti-SRBC of normal (B6 X bm1)F1 spleen cells; this suppression, however, was weak when compared with the suppression induced by spleen cells from GVH (bm1 X bm12)F1 mice. Taken together, these findings indicate that a small class II (I-A) antigenic difference suffices to trigger the alloreactive donor T helper cells causing SLE-like GVHD. In contrast, both class I (H-2K) and class II (I-A) differences are required to trigger the subsets of donor T cells responsible for acute GVHD. It appears that alloreactive donor T helper cells induce the alloreactive T suppressor cells, which then act as the suppressor effector cells causing the pancytopenia of acute GVHD. These findings may help to understand the variability of GVH-like diseases caused by a given etiologic agent, their cellular pathogenesis, and association with certain HLA loci.
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PMID:Allosuppressor and allohelper T cells in acute and chronic graft-vs.-host disease. II. F1 recipients carrying mutations at H-2K and/or I-A. 621 18

Groups of nonirradiated BDF1 mice were injected with unseparated spleen cells from B10, B10.D2, or DBA/2 donors. The diverse clinical and pathologic symptoms that developed during the course of the ensuing graft-vs-host reaction (GVHR) were related to the functional subsets of donor-T cells activated in the host. The activation of F1-specific donor T suppressor (TS) cells was confined to those GVH F1 mice that developed acute GVH disease (GVHD) (donor B10 or B10.D2). Moreover, activation in these GVH F1 mice of the Lyt-1-2+ donor TS cells sharply preceded the onset of and coincided with (week 2 to 6) the suppressive pathologic symptoms characteristic of acute GVHD, such as pancytopenia and suppression of splenic IgG production. The activation of these alloreactive TS effector cells was briefly preceded by the activation of F1-specific Lyt-1+-2- donor T helper (TH) cells and stimulation of the host's lymphoid tissue. Thus, in acute GVHD, a sequential alloactivation first of donor TH and then of TS cells was found. Those F1 mice that recovered from acute GVHD and developed stimulatory pathologic symptoms showed a concomitant loss of donor TS cell activity. An initial activation of F1-specific Lyt-1 +2- donor TH cells was also found in that parent----F1 combination (donor DBA/2), which failed to develop acute GVHD. Significantly in that combination, the alloactivation of donor TH cells was not followed by activation of significant numbers of donor TS cells. Instead, the DBA/2-injected BDF1 mice directly developed a persistent increase in splenic Ig formation and lupus-like GVHD.
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PMID:Allosuppressor- and allohelper-T cells in acute and chronic graft-vs-host disease. IV. Activation of donor allosuppressor cells is confined to acute GVHD. 623 Mar 90

2 fatal cases of graft-versus-host disease (GvHD) occurred following blood product transfusions given to patients receiving standard chemotherapy for Hodgkin's disease. GvHD was established by HLA typing, clinical course, and compatible skin biopsy. 23 cases of GvHD following transfusion of blood products from normal donors are also reviewed. It should be suspected when fever or rash appear 1-2 weeks after transfusion of unirradiated blood products into a compromised host or when pancytopenia following chemotherapy is prolonged or unexpectedly severe. Prevention of GvHD by irradiation of granulocytes, platelets and packed red blood cells given to immunosuppressed patients is recommended to prevent this often fatal disease.
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PMID:Acute graft-versus-host disease resulting from normal donor blood transfusions. 642 40

A young man with acute lymphoblastic lymphoma on chemotherapy developed acute graft-versus-host disease following nonirradiated blood transfusions during a period of pancytopenia. The importance of the cutaneous manifestations, in particular the histopathologic changes, in facilitating an early diagnosis of the disease are stressed. The question of irradiating blood transfusions for immunosuppressed patients with malignancies is discussed.
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PMID:Graft-versus-host disease in a patient with acute lymphoblastic lymphoma. 658 51

Graft versus host disease (GVHD) is a well recognized entity following bone marrow transplantation. Similar syndromes have been described after blood product transfusions, notably in patients with primary immunodeficiency syndromes and in patients with malignancies associated with immune deficiency or under immunosuppressive treatment. Review of the literature shows that posttransfusion GVHD is characterized by maculopapular skin rash, gastro-intestinal symptoms, liver disease, severe pancytopenia and, in some cases, hepatosplenomegaly and lymphadenopathy. The time to onset and the duration of the disease are short (10 days) and the mortality approaches 90%. The clinical features of this rare disorder are presented in the hope that, with increased awareness of this complication, clinicians will take preventive measures in patients at risk because no satisfactory therapy yet exists.
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PMID:[Clinical characteristics and evaluation of risk in the graft versus host reaction following transfusion]. 663 42

A 45-year-old female developed cytogenetic relapse of chronic myelogenous leukemia 4 years after allogeneic bone marrow transplantation. To induce a graft-versus-leukemia effect, peripheral blood buffy-coat cells were collected from the original marrow donor during 5 rounds of leukapheresis over 3 weeks, and 2.47 x 10(8) cells/kg were infused into the patient. Acute graft-versus-host disease (GVHD) did not develop even after an interval of 50 days from the last donor leukocyte transfusion (DLT). However, karyotypic analysis of bone marrow cells performed on the same day showed an apparent decrease in the proportion of Ph1 chromosome-positive cells (1/20) among all dividing cells, compared with the proportion (13/20) observed before DLT. At the same time, the proportion of red blood cells (RBCs) of donor origin among the peripheral RBCs of the patient, which was less than 10% before DLT, began to rise and reached 100% at 4 months after DLT. The karyotype of bone marrow cells obtained on day 90 after DLT was completely normal. Although chronic GVHD of the buccal mucosa and liver developed in association with pancytopenia on day 71 after DLT, this improved rapidly with oral administration of cyclosporine. The clinical course of this patient suggests that acute GVHD is not a prerequisite for elimination of Ph1-positive cells by DLT.
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PMID:[Successful treatment of recurrent chronic myelogenous leukemia in allogeneic marrow transplant recipient with the donor leukocyte transfusion, without induction of acute graft-versus-host disease]. 756 96

Posttransfusion graft-versus-host disease (PTGVHD) is known to develop in immunocompetent patients exhibiting clinical symptoms such as erythroderma, fever, liver dysfunction, diarrhea and pancytopenia. It is speculated that transfused blood donors' lymphocytes might recognize the recipients' HLAs as alloantigens. The thus stimulated lymphocytes might proliferate, expand and finally attack the host's immune system or tissues. However, details regarding these expanded donor cells such as: (1) whether they represent one clone or more, (2) the composition of lymphocyte subsets, and (3) the target HLA antigens of recipients, are not clear, since T-cell lines derived from PTGVHD patients have not yet been obtained. The aim of this study is to characterize T-cells responsible for PTGVHD and to identify their target molecules. For that purpose, we attempted to establish T-cell lines derived from a PTGVHD patient. We show that the established T-cell line, proven to be derived from donor lymphocytes, showed a CD4+ phenotype and had cytotoxic activities. Furthermore, we describe that the target of the cytotoxic T-cell line (CTL) is an HLA-DRB1*0405-related molecule of the patient.
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PMID:Establishment of a T-cell line from lymphocytes presumably implicated in posttransfusion graft-versus-host disease. 762 73


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