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)

Transfusion-associated graft-versus-host disease (TA-GVHD) is a devastating immunologic complication of blood transfusion. Patients at highest risk include premature infants and other patients who are immunosuppressed as a result of either congenital or acquired disease or because of the administration of immunosuppressive therapy. An additional high-risk group is immunocompetent patients who are heterozygous at a particular HLA locus and who receive blood from a donor who is homozygous at the same locus. The clinical syndrome consists of fever, skin rash, diarrhea, hepatic dysfunction, and bone marrow aplasia. The outcome is nearly always fatal, despite attempted treatments that have included the use of immunosuppressive agents. Hemorrhage and infection are the most common causes of death. Both humoral and cytotoxic mechanisms have been implicated in the pathophysiology of TA-GVHD. The complication of TA-GVHD can be prevented by the use of irradiated blood components. The use of ultraviolet B light-irradiated blood products and leukoreduction filters are also being investigated as potential preventive treatment modalities.
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PMID:Transfusion-associated graft-versus-host disease. 935 3

An 8-month-old child with an immunodeficiency disorder characterized by abnormal lymphocyte function and by low IgG and IgA levels had combined liver and small bowel transplantation under tacrolimus and steroid immunosuppression for the treatment of short gut syndrome and hepatic cirrhosis. The patient developed an early postoperative episode of Pneumocystis carinii pneumonia, and a subsequent surgical complication, prompting discontinuance of tacrolimus. A skin rash eventually shown to be graft-versus-host disease (GVHD) developed in the flank on the 12th post-transplant day and gradually became generalized. Peritonitis, sepsis, multisystem organ failure including the liver allograft led to death on the 23rd post-operative day. The mechanisms leading to post-transplant GVHD under the specific circumstances in this case are discussed.
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PMID:Graft-versus-host disease after liver and small bowel transplantation in a child. 936 21

Although drug eruptions resembling graft-versus-host disease are rare, GvH-like reactions to the sulfhydryl group of drugs (penicillamine, captopril, gold sodium), phenobarbital and hepatitis vaccine have been described. Clinical reports concerning acute GvH-like drug rash are very uncommon and restricted to acetylsalicylic acid and spironolactone. We report on a patient who developed an acute GvH-like drug reaction caused by allopurinol. To our knowledge this variant of cytotoxic drug eruption has not yet been reported in literature.
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PMID:[Allopurinol as an inducer of acute graft-versus-host-like drug reaction. Case report with review of the literature]. 955 35

Four cases of a Grover's-like disease in patients with leukemia/lymphoma, who underwent high-dose chemotherapy and either allogeneic/autologous bone marrow transplantation or autologous stem cell infusion, are described. Three of four patients had fever prior to the onset of their rash. In addition to suprabasilar clefts, acantholysis, and dyskeratosis, typical of Grover's disease, there was a chemotherapeutic effect in the form of keratinocytes with atypical nuclei. So-called "starburst cells," which have been purported to be specific for high-dose etoposide (VP-16) therapy, were seen in two cases, but only one of these patients received etoposide. In one patient with clinical vesicles, direct immunofluorescence ruled out paraneoplastic pemphigus. In conjunction with 18 similar cases in the literature, the following conclusions were reached: (a) the pathogenesis probably involves the combined effects of fever (with sweating), occlusion, and chemo/radiation therapy; (b) no single chemotherapeutic agent can be consistently implicated; and (c) in addition to graft-versus-host disease, the eruption of lymphocyte recovery, and other cutaneous eruptions in the setting of bone marrow transplantation, the differential diagnosis includes paraneoplastic pemphigus, which direct immunofluorescence excludes.
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PMID:Grover's-like disease in the setting of bone marrow transplantation and autologous peripheral blood stem cell infusion. 1002 36

Cyclosporin A (CsA) can induce graft-versus-host disease (GVHD) following autologous bone marrow transplantation (ABMT) and autologous peripheral blood stem cell transplantation (APBSCT) in adults. We investigated whether GVHD can be induced following ABMT and APBSCT in childhood, and which cells are involved in the pathogenesis of this syndrome. We conducted a prospective study of 20 children and adolescents with hematological malignancies receiving CsA after ABMT and APBSCT. Skin biopsies were obtained on day 21 after transplantation or in the event of a rash. Immunophenotypic analysis of peripheral blood lymphocytes was performed on days 14, 21, 28 and 60 after transplantation. Clinical GVHD of the skin, confirmed by histological criteria, occurred in five patients. Five patients had no clinical GVHD but had acute GVHD alterations on routine skin biopsy. In all 10 patients with a positive skin biopsy for GVHD, CD4+ lymphocytes were the predominant cells in the epidermis. Immunophenotypic analysis of peripheral blood lymphocytes revealed a significantly increased CD4/CD8 ratio in patients with a positive skin biopsy (P < 0.01). Our findings indicate that it is possible to induce acute GVHD following ABMT and APBSCT in childhood. In addition, CD4+ lymphocytes play an important role in the pathogenesis of CsA-induced GVHD.
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PMID:Cyclosporin A-induced graft-versus-host disease following autologous bone marrow and stem cell transplantation in hematological malignancies of childhood. 961 82

Human herpesvirus 6 (HHV-6) infections following bone marrow transplantation (BMT) have been shown to be associated with fever, skin rash, graft versus host disease, encephalitis, delay in engraftment, marrow suppression, and pneumonia. Unfortunately several of these studies were case reports and although the results were suggestive they prompted us to study these pathological events systematically. These associations were primarily based on either HHV-6 isolation, HHV-6 DNA detection, antigen detection or increases in HHV-6 specific antibodies. HHV-6 activity was more frequent during the post- rather than the pre-transplantation period. All HHV-6 isolates from BMT patients have been shown to be variant B. A better understanding of HHV-6 associated pathogenesis gained by larger prospective trials is needed to facilitate proper treatment of cases of idiopathic illnesses or those associated with symptoms (fever, skin rash) similar to those caused by HHV-6.
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PMID:Human herpesvirus 6 infection and associated pathogenesis following bone marrow transplantation. 986 89

Patients undergoing bone marrow transplantation are at high risk of developing acute graft-versus-host disease (GVHD) which is a primary limiting factor for this procedure inasmuch as it is responsible for high morbidity rates and is associated with poor survival outcome. To provide improved treatment assessment and better interpretation of clinical outcomes, we need a precise and objective assessment of GVHD. Severity of GVHD is commonly assessed using an imprecise categorical grading system that incorporates skin, gut and liver grades, as well as subjective assessment of clinical performance. These organ grades are based on arbitrary cutpoints of skin rash, diarrhoea volume and bilirubin level. The International Bone Marrow Transplant Registry proposed an alternative grading system based on different combinations of organ involvement and provided estimates of relative risk of treatment failure. On the basis of that work, we developed an empirical mathematical model that quantifies GVHD severity, and that uses continuous, rather than categorical, daily measurements for each organ system. We use model-predicted values as an index of severity for any combination of values. The proposed index allows a more precise comparison of GVHD profiles across different treatment protocols and also permits more refined analyses to address relationships between GVHD and clinical outcomes.
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PMID:A multivariate approach for assessing severity of acute graft-versus-host disease in bone marrow transplantation. 1007 Jun 84

We previously demonstrated findings suggestive of autologous GVHD in patients receiving IL-2-activated peripheral blood stem cells (PBSC) with IL-2 after transplantation. A pilot study was designed to test tolerability, feasibility and frequency of autologous GVHD and engraftment using IL-2 and alpha-IFN post-transplantation. After cyclophosphamide (6 g/m2) and carboplatin (1800 mg/m2), patients with high-risk stage II or III breast cancer received chemotherapy and rhG-CSF mobilized autologous PBSC that had been cultured in IL-2 for 24 h. Subcutaneous administration of IL-2 began on day 0 at 6 x 10(5) IU/m2/day for 5 of 7 days each week and continued for 4 weeks. Once engraftment occurred, alpha-IFN was initiated at a dose of 1 x 10(6)/m2/day subcutaneously for 30 days. Thirty-four consecutive patients with stage II (n=20), IIIA (n=6) and IIIB (n=8) disease were treated. All patients were without evidence of disease at the time of transplantation. The average time required for the ANC to reach 500/mm3 was 10 days (range: 8-11 days) and for platelets to reach 20000/mm3 was 10.7 days (range: 6-21 days). Forty-seven percent of patients (n=16) completed the full course of immunotherapy; the remaining patients received attenuated doses due to patient's request (n=6), development of temperature >38 degrees C (n=3), development of neutropenia (n=3), serious infection (n=1) and miscellaneous reasons (n=5). Four patients experienced transient moderate toxicities (level 3) including elevated liver function tests, nausea, rash and capillary leak syndrome. Pathological findings suggestive of skin GVHD developed in 43% of patients (12/28 patients) when skin biopsies were evaluated in a blinded fashion. At 13 months post-transplant (median; range: 5-24 months), 28 patients (82%) remain disease-free. These results demonstrate the feasibility and toxicity of this regimen along with pathological findings compatible with autologous GVHD of the skin.
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PMID:Immunotherapy with interleukin-2 and alpha-interferon after IL-2-activated hematopoietic stem cell transplantation for breast cancer. 1021 42

During cardiac surgery for transposition of the great arteries at age 7 weeks, a female infant received blood, fresh frozen plasma and platelet transfusions. Eleven days postoperatively, she developed bloody diarrhoea, fever, an erythematous macular rash, hepatomegaly, seizures and pancytopaenia. A clinical diagnosis of transfusion related graft-versus-host disease (GVHD) was supported by skin histopathology. DNA polymorphism studies confirmed that circulating lymphocytes in peripheral blood and infiltrating cells in the skin were foreign in origin and were derived from transfused blood cells. No underlying immunodeficiency was identified. Treatment with steroids cyclosporin and antithymocyte globulin was unsuccessful and death occurred 2 months after surgery. The features of fever, rash, diarrhoea, liver dysfunction and pancytopaenia which characterize GVHD may mimic drug reactions or viral infection. In addition to histological features on skin biopsy. DNA polymorphism studies on skin and blood samples provide a unique and sensitive method to confirm GVHD. Irradiation of blood products should be considered for acutely compromised infants requiring urgent cardiac surgery.
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PMID:DNA polymorphism analysis in transfusion-associated graft-versus-host disease. 1023 46

Relapse remains the major cause of mortality in haematological malignancies treated with autologous stem cell transplantation (ASCT). Graft versus tumour reaction (GVT) associated to autologous graft versus host disease (GVDH) may contribute to eliminate minimal residual disease (MRD) after ASCT. Eighty patients with several diagnostics were submitted to ASCT. After stem cell infusion, patients randomised in 4 groups. Groups were treated as follows: Group A received either a IFN (alpha Interferon--1,000,000 U/d), Cyclosporine A (CSA--1 mg/-kg/d intravencus) for 28 days, and granulocyte-macrophage colony stimulating factor (GM-CSF-250/m2/d) until engraftment; B: CSA (same dose and way) and GM-CSF; C: CSA (1 mg/kg/d orally) and GM-CSF and D: only GM-CSF. Patients were inspected daily and if skin rash was detected, a skin biopsy was obtained at that moment, otherwise biopsies were obtained at day 21 after ASCT. GVHD was positive in 23 patients (13 from group A and 10 from group B). All cases were grades I and II. A majority of CD4+ T lymphocytes was seen in skin infiltrates. No significant differences were seen in WBC and platelets engraftment times, antibiotic administration or hospitalisation days required among the four groups. With a median follow up of 18 months, there were no differences in disease free survival (DFS) or overall survival (OS) between the patients who developed GVHD and the others. However, considering that myeloma cells do not express antigen MCH II, which is necessary for GVT effect, we excluded patients with multiple myeloma (MM) from survival analysis, thus obtaining a significant difference in OS results between patients who developed GVHD and those in whom this reaction was not observed (81% vs 58% p:0.05). We conclude that pharmacological induction of GVHD in ASCT is possible with CSA administration (1 mg/kg/d i.v.). Development of GVHD showed a better outcome for patients in our study except for those patients with MM. This results must be confirmed by a longer follow up of our patients and further studies.
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PMID:Graft versus host disease in autologous stem cell transplantation. 1046 7


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