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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)

A 51-year-old patient with aplastic anaemia in whom a successful allogeneic bone-marrow transplantation had been performed developed acute graft-versus-host disease in spite of prophylactic administration of methotrexate. There was severe liver injury but no involvement of the skin or intestines. When prednisone therapy was introduced the fever and the eosinophilia disappeared and liver damage was rapidly reversed. There was no haematological impairment. It would seem warranted to consider a wider use of prednisone in the treatment of acute GVHD in human recipients of allogeneic bone-marrow.
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PMID:Successful treatment with prednisone and graft-versus-host disease in an allogeneic bone-marrow transplant recipient. 3

We report four cases of Omenn's syndrome (OS), an autosomal recessive disease characterized by early erythrodermia, protracted diarrhea, severe infections, lymphadenopathy, hepatosplenomegaly, failure to thrive, and leukocytosis with marked eosinophilia. The immunological investigations revealed B lymphopenia with increased levels of serum IgE and marked depression of T-cell activation, not restored by the addition of exogenous interleukin 2 (IL-2). IL-2 and interferon-gamma (IFN-gamma) production in vitro were very low or absent. One patient was treated with HLA-identical bone marrow transplant with a complete remission of the clinical picture and the immunological defect. The infant died of graft versus host disease 4 months after the graft. For the remaining three infants the outcome was also fatal within the first year of life. In conclusion, OS should be considered a severe combined immunodeficiency disease with peculiar clinical, immunological, and histological findings.
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PMID:Clinical and immunological findings in four infants with Omenn's syndrome: a form of severe combined immunodeficiency with phenotypically normal T cells, elevated IgE, and eosinophilia. 311 64

A disease similar to the chronic graft-versus-host disease (cGVHD) seen following transplantation of human bone marrow was observed after syngeneic and allogeneic bone marrow transplantation in rats. Bone marrow grafts were exchanged between donors and recipients that were syngeneic or genetically different for the RT2 erythrocyte antigen locus by the use of AUG/AUG.2B and PVG/PVG.2A congenic pair donor/recipient strain combinations. After an initial period of well-being (120-180 days posttransplantation), several AUG and AUG.2B recipients of syngeneic or RT2-mismatched bone marrow developed clinical signs compatible with cGVHD. The clinical signs of the disease included: erythema, diffuse alopecia, thickened skin folds, and conjunctivitis. Laboratory findings included peripheral blood eosinophilia and impaired in-vitro proliferative responses to third-party spleen cells in the mixed lymphocyte reaction. Histological examination of the tissues of a limited number of rats with cGVHD showed subepidermal mononuclear inflammation with atrophy of the epidermis and adnexa of the skin, as well as plasmacytic hyperplasia of the lymphoid tissues. None of the PVG or PVG.2A recipients of syngeneic or RT2-mismatched marrow developed cGVHD. The development of cGVHD in AUG.2B recipients of syngeneic marrow and the absence of the disease in reciprocal marrow grafts between the PVG/PVG.2A rat strains suggests that the development of the disease in the AUG and AUG.2B recipients of RT2-mismatched bone marrow is not due to the RT2 disparity, but may be due to an autologous immune reaction. Furthermore, the finding that the cGVHD is only observed when the AUG and AUG.2B strains are used as recipients--not when the PVG or PVG.2A strains are used as recipients--suggests that the development of the disease is associated with the genetic background of the host and is independent of the background of the donor. It is possible that the use of high-dose cyclophosphamide treatment is involved in the pathogenesis of cGVHD, because the disease is observed only when the recipients are conditioned for transplantation with this immunosuppressive agent.
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PMID:Chronic graft-versus-host disease in rats after syngeneic bone marrow transplantation. 315 5

Degenerative epithelial changes with cytoplasmic eosinophilia and nuclear pleomorphism were found in the intrahepatic periductal glands in two patients who died following allogeneic bone marrow transplantation. These changes, which have not been described in the literature to our knowledge, were closely associated with clinicopathologic signs of graft-versus-host disease (GVHD), and histologically they resembled small bile ductal lesions, a characteristic finding of hepatic GVHD. In addition, periductal glandular and small bile ductal lesions frequently coexisted. Neither livers from patients given autologous marrow transplantation nor other control livers including those from patients given abdominal irradiation revealed such glandular lesions. These results suggest that the observed changes in the intrahepatic periductal glands were a manifestation of GVHD.
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PMID:Intrahepatic periductal glands in graft-versus-host disease. 329 53

This report describes a patient in whom the clinical, laboratory, and histologic features of diffuse fasciitis with eosinophilia developed several months after allogeneic bone marrow transplantation for acute lymphoblastic leukemia. Numerous reports detail the association between diffuse fasciitis and hematologic diseases; a patient in whom diffuse fasciitis developed in the setting of chronic graft-versus-host disease following bone marrow transplantation for acute leukemia is discussed. Treatment of the chronic graft-versus-host disease improved the symptoms of the diffuse fasciitis.
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PMID:Diffuse fasciitis after bone marrow transplantation. 330 Mar 20

Damage of skeletal muscle in association with graft-versus-host disease (GvHD) has been referenced exceptionally. Eighteen months after bone marrow transplantation, a 22-year-old man developed polymyositis associated with manifestations of chronic GvHD, such as peripheral eosinophilia and localized morphea. Diagnosis of polymyositis was established by clinical, electromyographic, and histopathologic findings. His clinical condition improved with immunosuppressive therapy. At electronmicroscopy, some close and broad contacts between lymphocytes with activated appearance and degenerated muscle fibers were observed, suggesting a lymphocytotoxic mechanism. The findings support the idea that polymyositis can be considered a manifestation of chronic GvHD.
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PMID:Inflammatory myopathy associated with chronic graft-versus-host disease. 352 79

Inflammatory fasciitis without infection include different entity like eosinophilic fasciitis, the syndrome of eosinophilia-myalgia after tryptophan ingestion, toxic oil syndrome, exposure to trichlorethylene, phenylketonuria skin changes, the syndrome of palmar fasciitis, fasciitis in chronic graft-versus-host disease and fasciitis secondary to an adjacence process. The diagnosis of all these scleroderma-like skin changes is sometimes not easy because the clinical and sometimes the histopathological changes are bordeline manifestations with scleroderma. The most characteristic markers for non infectious fasciitis is eosinophilia and the infiltration of the fascia with eosinophilis, but it may be unremarkable or absent, only frequently present at the onset of the disease. Anamnesis is most important to guide the diagnosis. The eosinophils, but not only, may play a major role in the pathogenesis of this entity.
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PMID:[Non-infectious inflammatory fasciitis: a borderline syndrome]. 759 18

Eosinophilia may complicate allogeneic bone marrow transplantation (BMT) after treatment with preparative regimens that include total body irradiation (TBI). This complication is of uncertain significance and has not been reported after treatment protocols which do not contain TBI. We reviewed our experience using busulfan and cyclophosphamide (CY), instead of TBI, as the preparative regimen for allogeneic BMT to study the incidence and relationship to graft-versus-host disease (GVHD) of post-treatment eosinophilia. Fifty-five consecutive patients receiving busulfan 16 mg/kg and CY 120 mg/kg for the treatment of leukemia were reviewed. All patients received non-T cell-depleted, HLA-matched sibling or unrelated donor marrow 2 days after chemotherapy was complete. Cyclosporine (CYA) and methylprednisolone were given to prevent GVHD. Thirty-nine patients surviving 100 days post-transplant were evaluated; 11 (28%) patients developed eosinophilia (defined as an absolute eosinophil count of > 500 x 10(6)) after transplant. Only 2 patients were still taking methylprednisolone at the onset of eosinophilia. At the onset of eosinophilia 5 of these 11 patients (45%) and GVHD that worsened within 2 months. In the other 6 patients (55%), GVHD was not present initially but developed in all 6 patients at a median of 4 months after the onset of eosinophilia. We conclude that eosinophilia can complicate allogeneic BMT not preceded by TBI and that it often heralds the onset of worsening of, or de novo, GVHD.
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PMID:Eosinophilia after allogeneic bone marrow transplantation using the busulfan and cyclophosphamide preparative regimen. 883 34

A hypereosinophilic syndrome associated with dermatitis has been observed rarely in association with HIV infection. We describe the case of a young man with AIDS who came to us with a diffuse cutaneous eruption, fever, angioedema, eosinophilia, and a mildly elevated serum IgE level. No allergic or infectious cause of this illness could be determined, and the patient was treated with corticosteroids and PUVA therapy, resulting in complete resolution of the dermatitis and associated findings. In this case, there were clinical and histopathologic similarities to the idiopathic hypereosinophilic syndrome and to acute graft-versus-host disease. The serum level of the cytokine interleukin-5 (IL-5), which is associated with eosinophil production, was found to be mildly elevated during the peak of the eruption, while samples drawn previously and subsequently were not. Although it appears that the syndrome we describe is associated with the measurably elevated level of IL-5, further investigation is required to determine whether there is a cause and effect relationship between IL-5 and this entity. A brief review of the literature concerning eosinophils and HIV infection is also presented in the context of this case.
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PMID:Hypereosinophilic syndrome associated with HIV infection. Military Medical Consortium for Applied Retroviral Research. 815 85

A 39 year old patient diagnosed of severe aplastic anemia and treated with allogenic bone marrow transplantation and who presented chronic eosinophilic pneumonia eight months after the transplant is presented. The patient had no previous history of asthma or atopy. Conditioning was performed with cyclophosphamide and total body irradiation. Prophylaxis of the graft versus host disease was carried out with cyclosporin and short course of methotrexate. At day 30 mild graft versus host disease appeared which spontaneously resolved. A progressive increase in the number of eosinophils was observed from day +40 reaching 1.05 x 10(9)/l at day +180 coinciding with suspension of the cyclosporine. The patient remained asymptomatic with no evidence of chronic graft versus host disease. At 8 months following allogenic transplantation the patient developed three episodes of fever, cough, moderate dyspnea and pulmonary infiltrates. Respiratory tests showed a restrictive pattern. Bronchoalveolar lavage contained 20% of eosinophils. Upon lung biopsy alveolar infiltration by eosinophils, lymphocytes and mononuclear cells was observed. Diagnosis of chronic eosinophilic pneumonia was made with initiation of steroid treatment. A drastic response was observed. The patient remained asymptomatic without recurrence and without evidence of chronic graft versus host disease. This picture may have been caused by the donor eosinophils given that retrospective evaluation demonstrated a persistent moderate eosinophilia in the donor.
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PMID:[Chronic eosinophilic pneumonia in a patient treated with allogenic bone marrow transplantation]. 820 96


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