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)

Thirty-six patients received allogeneic (34) or syngeneic (two) bone marrow transplants as treatment for severe aplastic anaemia or acute leukaemia. Nineteen of the allogeneic recipients received methotrexate (MTX) and 15 received cyclosporin A (CyA) as the predominant immunosuppressive agent to minimize graft-versus-host disease (GVHD) post transplant. In the first 100 d post transplant renal dysfunction was much less frequent in the MTX recipients than in the CyA recipients who exhibited three distinct syndromes of nephrotoxicity: most commonly. CyA recipients developed asymptomatic azotaemia, proteinuria, urinary casts, impaired urinary concentrating ability and hypertension. Secondly, two CyA recipients developed acute reversible renal failure precipitated by systemic bacterial infection which required dialysis and in which the kidney was the sole target organ; thirdly, two recipients of HLA-genotypically non-identical grafts developed a rapidly progressive fatal syndrome with multiple organ involvement including lung, brain and kidney which clinically and histologically resembled thrombotic thrombocytopenic purpura.
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PMID:Cyclosporin A associated nephrotoxicity in the first 100 days after allogeneic bone marrow transplantation: three distinct syndromes. 634 55

Since 1976, 16 adult patients with acute leukemia have been treated by chemotherapy, total body irradiation (TBI) and allogeneic bone marrow transplantation (BMT) in the medical school hospital and the satellite hospitals of Nagoya University. The first group of 10 patients were given marrow grafts at the time of leukemic relapse and the second group of six patients were given the grafts in the period of remission of their disease. For the first group (ALL/ANLL 2:8, age (median) 33, M/F 8:2), HLA-identical donor cells (25 x 10(7)/kg [median]) were infused after the patients were conditioned with NSC D 245382 (ACNU) or daunorubicin, cyclophosphamide (CY) and a single shot of 1000 rad of TBI. For the second group (ALL/ANLL 4:2, age (median) 20, M/F 5:1), HLA-identical donor cells (22 x 10(7)/kg [median]) were infused after the patients were conditioned with CY and fractionated (250 rad x 4) TBI. All the patients were isolated in a laminar air flow room (LAF) after gut and skin decontamination. Engraftment of donor cells was confirmed in 15 out of the 16 patients. Febrile periods in LAF and the days required for platelet transfusion were prolonged in the first group. All the patients in the first group died within 12-214 days after BMT because of interstitial pneumonitis (7 patients) or bacterial infection (3 patients). On the other hand, five out of six patients in the second group are alive 84-540 days after BMT. For the surviving patients, the complications of chronic graft versus host disease, viral infections, tuberculosis, hepatitis, hemorrhagic cystitis and recurrence of leukemia are now the problems. It can be stated that the patient's clinical condition at the time of BMT is one of the most essential factors for the success of BMT although the effects of other variables, such a change in the conditioning regimens of the supportive care, must also be carefully analyzed.
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PMID:Sixteen adult patients with acute leukemia treated by chemotherapy, total body irradiation and allogeneic marrow transplantation. 639 11

We report here a case of 33 year-old-man with refractory bilateral pneumothoraces during the treatment for interstitial pneumonitis 6 months after bone marrow transplantation (BMT). He was diagnosed as having acute myelogenous leukemia (AML) M1. He was treated with chemotherapy, and cerebral irradiation. BMT was performed in August 1989 from a sibling donor whose human leukocyte antigen was matched, ABO blood type mismatched. Preconditioning regimen was cyclophosphamide and total body irradiation (TBI). BMT was successful without major graft versus host disease. Thereafter he complained of respiratory symptom and was admitted on June 14 1990. Computed tomogram (CT) scan showed interstitial and alveolar shadows. We started the treatment against bacterial infection, Pneumocystis carinii, cytomegalovirus (CMV) and against interstitial pneumonitis with bolus dose of steroid. The transbronchial lung biopsy specimen revealed interstitial pneumonitis without typical CMV nor pneumocystis carinii pneumonia. Although a CT scan showed improvement of pneumonitis, bilateral pneumothoraces occurred. The adhesion therapy became successful after the reduction of steroid dosage. A pneumothorax rarely occurs after BMT. In this case it is speculated that TBI might be responsible for interstitial pneumonitis, and the steroid might have inhibited the adhesion therapy of pneumothorax.
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PMID:[Refractory bilateral pneumothoraces complicated with interstitial pneumonitis after bone marrow transplantation]. 836 73

Bacterial complications develop mainly after transplantation during the period before engraftment takes place. Wound infections, urinary tract infection and pneumonia are the commonest complications of solid organ transplantation and generally involve Gram-negative bacilli and Staphylococcus aureus. However, Gram-positive cocci will predominate when selective oral antimicrobial prophylaxis is given as is frequently the case in bone marrow transplant recipients. Oromucositis, induced by total body irradiation or anthracyclines, result in more bacteraemia due to oral viridans streptococci. The use of central intravenous catheters leads to an increase in bacteraemia and infection due to coagulase-negative staphylococci. Patients requiring intensive care are also at risk of nosocomial infections including legionellosis. Once engraftment has occurred, there is much less risk of bacterial infection but patients remain vulnerable to the intracellular pathogens Listeria monocytogenes, non-typhoid salmonellae, Norcardia spp. and mycobacteria for as long as they require immunosuppression. Any rejection crisis must be treated aggressively with high-dose steroids or other agents which further undermine an already fragile immunity. In bone marrow transplant recipients, graft versus host disease and its treatment exerts a more profound effect on immunity and often coincides with cytomegalovirus infection which compromises the patient even further. Such patients are again at risk of infection with the same range of pathogens encountered during neutropenia since the oral mucosa, gut and catheter, if one is present, provide the same portals of entry. Immunosuppressive therapy, in some centres, is discontinued once the risk of graft versus host disease is reduced, although the reconstitution of the immune system is a lengthy process and there is a continued deficiency of IgG which renders patients unable to opsonise the encapsulated bacteria Streptococcus pneumonia and Haemophilus influenzae. In contrast to bone marrow transplant recipients, those with a solid organ transplant require life-long immunosuppression and so remain susceptible to infections with intracellular pathogens and, even with minimal immunosuppression, there will always be the risk that common bacteria will cause infection in unusual places and that uncommon organisms will be involved in apparently straightforward infections.
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PMID:Bacterial complications of transplantation: diagnosis and treatment. 860 44

Intravenous immune globulin (IVIG) has been used with success to prevent and treat infection in patients with immunodeficiencies of humoral immune function. More recently, IVIG has been shown to modulate immune responses and to treat successfully several autoimmune disease. Initial trials in bone marrow transplant recipients were aimed at the prevention of cytomegalovirus (CMV) disease. Although most studies showed such a benefit, CMV prophylaxis is now commonly provided by use of CMV-negative blood products or ganciclovir prophylaxis in, respectively, CMV-seronegative and CMV-seropositive patients. Acute and chronic graft-versus-host disease (GVHD) and associated infections remain critical barriers to the wider application of allogeneic blood or marrow transplantation, especially among patients given HLA-disparate grafts. To date, four controlled clinical trials have shown a significant reduction in acute GVHD in patients given IVIG (500-1000 mg/kg) weekly until 90-120 days post-transplant. In addition, bacterial infection in the early transplant period appears reduced. Meta-analysis of controlled trials reporting acute GVHD endpoints in 379 patients found a relative risk of acute GVHD of 0.68 (95% CI, 0.45-1.02) in IVIG recipients compared to untreated controls. Overall mortality reported in 809 patients in these trials showed an odds ratio of mortality of 0.74 (0.55-0.99) in IVIG recipients compared to controls (values < 1.0 suggest that IVIG was effective in preventing the event). More recently it has been shown that in the absence of hypogammaglobulinaemia, IVIG (500 mg/kg) given monthly from day 90 to 360 did not reduce the incidence of chronic GVHD or late complications. Future research is aimed at characterizing the mechanism of action of suppression of acute GVHD with weekly IVIG prophylaxis and the role of IVIG prophylaxis in patients receiving unrelated marrow grafts.
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PMID:Immunomodulation in allogeneic marrow transplantation: use of intravenous immune globulin to suppress acute graft-versus-host disease. 862 43

During the last 15 years, the techniques to prepare leukocyte-poor cellular blood components greatly improved, as well as our knowledge about the role of leukocytes in many adverse effects of transfusion. These two facts favor the extension of indication of leukocyte-poor blood components. Leukocytes in blood components may be detrimental to their storage, due to their metabolic needs and to their progressive lysis, leading to the release of cytokines. Leukocytes are the exclusive vector in blood of CMV and HTLV viruses. Leukocytes are a key element of the immune modifications induced by transfusion. HLA alloimmunization is favored by the transfusion of large quantities of leukocytes HLA different from the recipient whose immune functions are intact. Conversely, the risk of transfusion associated graft versus host disease is dependent of the transfusion of mature T lymphocytes sharing a partial identity with the recipient, and/or an immune deficient status of the recipient. Between these two extremes, many other effects related to the presence of leukocytes in cellular blood components, as are the transfusion effect observed in transplant recipients, the increased risk for bacterial infection after transfusion, the increased risk for tumor recurrence or the reactivation of virus infections, remain to be fully understood. Despite recent significant improvements, further studies, experimental as well as clinical, will be needed to expand the indications of leukocyte-poor blood components.
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PMID:[Why remove leukocytes from labile blood products in 1995?]. 864 Mar 15

We have previously demonstrated that administration of the nitric oxide (NO) synthesis inhibitor aminoguanidine (AG) to mice undergoing nonlethal graft-versus-host disease (GVHD) results in less destruction of host tissue and enhanced proliferative responses of splenic lymphocytes. Subsequently, we have determined whether the amelioration of GVHD pathology associated with inhibition of NO synthesis affects survival in a lethal GVHD model. Utilizing a C57BL/6 to C57BL/6xDBA2JF1 model, administration of parental lymph node lymphocytes instead of splenocytes results in 80-90% lethality by week 4 after GVHD induction. Administration of AG resulted in significantly decreased lethality coincident with decreased serum NO2- + NO3- levels. AG therapy had no effect on donor anti-host cytolytic T cell activity, which indicates that destruction of host tissue via this pathway was unaffected by the therapy. Histological evaluation of spleen, small intestine, bone, and mesenteric lymph node did not reveal any difference in the histological correlates of disease in the treated mice. AG increased various hematopoietic indices, including red blood cell count, white blood cell count, and hemoglobin, which indicates that the disruption of hematopoiesis during acute GVHD is mediated in part by NO. In addition, the number of GVHD mice with endogenous bacterial infections in the spleen and liver was significantly decreased in mice receiving AG therapy. These data indicate that NO plays a detrimental role during GVHD that appears to result in decreased hematopoietic indices and concomitant susceptibility to bacterial infection.
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PMID:Attenuation of lethal graft-versus-host disease by inhibition of nitric oxide synthase. 900 Jun 68

In order to investigate the mechanism of susceptibility to bacterial infection after bone marrow transplantation (BMT), we evaluated the neutrophil functions at 1, 3, 6, and 12 months after hematological reconstitution in a 29-year-old AML patient who received allogeneic bone marrow transplantation. Acute graft-versus-host disease (GVHD) was grade I, and chronic GVHD was not present. The patient exhibited complications of upper and lower respiratory infections several times after BMT, all of which subsided within a month. Chemotactic responses toward all three chemotactic factors, random mobility, phagocytosis, superoxide (O2-) release and bactericidal activity were severely impaired early after reconstitution. These neutrophil functions gradually improved with time after BMT, and all normalized at 12 months after reconstitution of transplanted bone marrow. Both O2- release and bactericidal activity of neutrophils were significantly enhanced at 6 and 12 months after marrow reconstitution following pretreatment of 50 ng/ml of granulocyte colony-stimulating factor (G-CSF) in vitro. These findings suggest that the combined disorders in neutrophil functions in early phase after BMT may play an important role in susceptibility to bacterial infections until one year after BMT. Administration of G-CSF, which potentiates the bactericidal activity of neutrophils, is recommended for preventing infectious complications and for treating prolonged and unmanageable infections after BMT.
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PMID:[Combined deficiency in neutrophil functions after bone marrow transplantation and the in vitro effect of granulocyte colony-stimulating factor]. 926 58

Two years have passed since the product liability(PL) law took effect in our country on July 1, 1995. At the start, we were uneasy about such things as an increase in lawsuits, the rise of medical care costs and the concealment of medical information. However, no-one has brought an action concerning blood products so far under the PL law. In terms of quality control of blood products, regular inspection of various instruments, reagents and manuals is the fundamental rule. Moreover, in order to ensure blood products of good quality, it is very important to select blood donors on the basis of physical examination and questionnaires on their medical condition, not to mention a range of screening tests to detect viral and bacterial infection. Since the first HIV infection through blood derived from an HIV-seronegative donor was reported in our country, it is especially desirable to improve measures for detecting HIV in window period blood for HIV antibody. There is also a problem concerning the irradiation of blood products to prevent PT-GVHD. We expect the PL law to provide a higher degree of safety of blood transfusion; however, it is also necessary to make proper use of blood products and to take the right measures in the event of adverse transfusion reaction, so as to raise the safety of blood transfusion.
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PMID:[Important points concerning quality control of blood products under the product liability law]. 930 Dec 79

Transfusion-associated graft-versus-host disease (TA-GVHD) is a fatal side effect of blood transfusion. The present study describes a case of TA-GVHD in a neonate treated with anti-CD3 monoclonal antibody (OKT3). The patient died of systemic bacterial infection. However, it is suggested that OKT3 suppressed the graft-versus-host reaction due to the improvement in the clinical signs and a change in the human leucocyte antigen (HLA) type on the surface of circulating lymphocytes. A relatively large dose of OKT3 together with steroid pulse therapy and cyclosporin A may be required for the control of TA-GVHD in neonates.
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PMID:OKT3 therapy for transfusion-associated graft-versus-host disease in a neonate. 931 93


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