Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0018133 (graft-versus-host disease)
 18,032 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Antibodies to Merkel cells (MC) are not known to occur in human sera. Using a newly described technic, we looked for the presence of antibodies directed against skin structures in sera from 2,300 patients with various dermatologic and hematologic disorders, as well as graft-versus-host disease (GVHD). Three of these sera (0.1%) were found to react with MC. One monoclonal IgM antibody was present in serum obtained from a patient with chronic cold agglutinin disease, the second from a patient with GVHD, and the third from a patient with pemphigus vulgaris. The present inadequate knowledge about normal MC function and the absence of described symptoms of MC dysfunction preclude analysis of the pathogenic significance of these MC antibodies in human sera.
J Am Acad Dermatol 1984 Oct
PMID:Antibodies to Merkel cells in human sera. Incidence and significance. 620 22

Cutaneous graft-versus-host disease in humans can be regarded as a potential model for the study of lymphocytotoxic reactions directed against the epidermis, and immunologically mediated cutaneous sclerosis. Toxic epidermal necrolysis and lichen planus are closely reproduced in graft-versus-host disease; sclerosis of chronic graft-versus-host disease cannot be regarded as strictly similar to any type of scleroderma. Sclerosis is the most consistently reproducible feature of cutaneous graft-versus-host disease in mouse chimeras; it offers the opportunity to study a dermal sclerosing reaction which may be considered as T cell dependent. Murine graft-versus-host disease presently appears debatable for use as a model of T cell dependent injury of the epidermis since stable established epidermal lesions are difficult to reproduce.
Br J Dermatol 1984 Jul
PMID:Human and murine cutaneous graft-versus-host diseases. Potential models for the study of immunologically mediated skin diseases. 623 23

Oral Cyclosporin A (CyA) was given for the prophylaxis of graft-versus-host disease (GVHD) to sixty-seven patients receiving a bone marrow transplant, and was found to be extremely effective in reducing the severity of acute GVHD. Side-effects of CyA included hypertrichosis, gum hypertrophy, and a rare but serious 'capillary leak' syndrome.
Br J Dermatol 1984 Apr
PMID:Dermatological aspects of the use of Cyclosporin A for prophylaxis of graft-versus-host disease. 637 Feb 94

We report the occurrence of benign angiomatous and mesenchymal tumors following chronic graft-versus-host disease. Our patient is a 23-year-old man who had undergone allogenic bone marrow transplantation for chronic myelogenous leukemia in 1978. Over the past 3 years he has developed poikiloderma and sclerodermatous tightening of the upper and lower extremities. From 1981 until the present time, violaceous to black friable tumors have erupted on the lower extremities. Histopathologic findings show an active mesenchymal and vascular tumorous response of variable-sized channels.
J Am Acad Dermatol 1984 May
PMID:Eruptive vascular tumors associated with chronic graft-versus-host disease. 637 61

The ability to define subpopulations of immunologically competent lymphocytes has permitted an enhanced understanding of the interaction between functionally distinct components of the immune system. T cells can provide help in antibody formation or they may suppress antibody production. Abnormal immunoregulatory mechanisms have been demonstrated in the hyperimmunoglobulin E-recurrent infection syndrome. This disorder is associated with a marked elevation of IgE and specific elevations of IgE antibodies directed toward staphylococcal antigens. Abnormal T cell regulation of immune responses has been demonstrated. Graft-versus-host disease (GVHD) occurs in an immunodeficient patient who has received an infusion of immunocompetent cells. The diagnosis of graft-versus-host (GVH) reaction may be complicated by the protean manifestations of the disorder. The acute form, consisting of a maculopapular rash, fever, and diarrhea, may be confused with acute infection or drug reaction. Chronic GVHD has been incorrectly diagnosed as histiocytosis X, acrodermatitis enteropathica, or scleroderma. Utilizing chromosome markers and/or identification of histocompatibility antigens, the presence of circulating lymphocytes from donor immunocompetent cells (blood transfusion, maternal source) can be documented. The development of sensitive technics for identifying cells can establish a precise diagnosis. Certain immunodeficiency disorders can be identified by biochemical means. Biotin-dependent multiple carboxylase enzyme deficiency is associated with a chronic dermatitis, alopecia, ataxia, and secondary infection of the skin with Candida. The disorder responds promptly to the administration of biotin with correction of dermatologic, neurologic, and immunologic abnormalities.
J Am Acad Dermatol 1984 Oct
PMID:New insight into the causes of immunodeficiency disorders. 638 1

Transfusion of blood products containing immunocompetent lymphocytes may cause graft-versus-host disease (GVHD) in immunosuppressed recipients. We describe fatal GVHD which occurred in a 30-year-old renal transplant patient 2 weeks after transfusion of 1.0 x 10(8) lymphocytes/kilogram. In addition to typical cutaneous and gastrointestinal manifestations, she developed irreversible bone marrow failure. Acute GVHD following blood product transfusion from normal donors has a mortality of 88%. Treatment is unsatisfactory, but irradiation of blood products prior to administration is preventive.
J Am Acad Dermatol 1983 Sep
PMID:Graft-versus-host disease from leukocyte transfusions. 663 Jun 3

Human graft-versus-host disease (GVHD) has several cutaneous manifestations, including a lichenoid and a sclerotic injury pattern. A versatile animal model of graft-versus-host skin disease (GVHSD) would facilitate study of the pathophysiology of these two cutaneous injury patterns. We have examined two murine chimeras histologically and have found two distinct patterns. Allogeneically transplanted B1/6 mice show a prolonged lichenoid-interface dermatitis that eventuates in clinical alopecia, whereas LP/J recipients of allogeneic cells do not show hair loss. Their histopathology consists of an early lichenoid phase that abates and is replaced by dermal sclerosis. Because of the versatility of the mouse as a laboratory animal, we feel that this model provides an excellent opportunity to define the immunopathologic mechanisms responsible for skin injury in GVHD. In addition, an understanding of the pathogenesis of the T cell-dependent, lichenoid, and sclerotic patterns of tissue injury in GVHSD might well provide insight into the pathogenesis of the GVHSD analogs, cutaneous lupus erythematosus and scleroderma.
J Invest Dermatol 1983 Nov
PMID:Murine graft-versus-host skin disease: a chronologic and quantitative analysis of two histologic patterns. 663 Oct 52

The exact pathogenic mechanism involved in lichen planus (LP) remains obscure. Two patients who have severe immunodeficiency diseases and who developed LP during the course of their illness are reported here. Both patients had hypogammaglobulinemia and disturbed immune function prior to the development of LP. Although such an association could be coincidental, the development of LP may be related to the underlying immune disturbances. Association of LP with several other disorders of the immune system has been previously observed. Other evidence for the possible involvement of an immunopathogenic mechanism in LP includes (1) deposition of immunoglobulin within the colloid bodies and at the dermoepidermal junction, (2) predominantly T cell dermal infiltrate in LP lesions, and (3) existence of clinical and histologic similarities between graft-versus-host disease and LP.
J Am Acad Dermatol 1982 May
PMID:Lichen planus in two immunodeficient hosts. 698 Feb 33

Human graft versus host disease is composed of 2 distinct clinical entities, acute graft versus host disease and chronic graft versus host disease, which have different pathogenesis. Acute graft versus host disease is produced by the attack of donor immunocompetent T or null lymphocytes against recipient histocompatibility antigens. The null lymphocytes may attack antigens shared by the donor and recipient and are autocytotoxic lymphocytes which can produce acute graft versus host disease in recipients of identical twin transplants. The cessation of acute graft versus host disease occurs when suppressor lymphocytes appear in the recipient's peripheral circulation. Chronic graft versus host disease is produced by immunocompetent lymphocytes that differentiate in the recipient. Its control is unknown. Some patients with chronic graft versus host disease have in vivo activated suppressor lymphocytes which produce a secondary immunoincompetence and an increased susceptibility to bacterial sepsis and death.
J Invest Dermatol 1980 May
PMID:Human graft versus host disease. 699 70

Graft versus host disease (GVHD) occurs in 50% to 70% of patients receiving bone marrow transplants. It can also develop in immunosuppressed patients with malignancies who receive nonirradiated blood transfusions. Most work indicates that the primary mechanism of GVHD is cell-mediated. It is likely that humoral factors are involved as well. Cutaneous manifestations are the earliest and most frequent sign of the disease. These may be morbilliform, scarlantiniform, lichenoid, or sclerodermoid lesions. In acute GVHD, the skin, gastrointestinal tract, and liver are commonly affected. In chronic GVHD, findings similar to collagen vascular disorders are present. A skin biopsy establishes the diagnosis.
J Am Acad Dermatol 1981 Nov
PMID:Graft versus host disease. 702 7


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>