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)

There is evidence that epidermal stem cells or their early progeny may be the targets in graft-versus-host disease (GVHD). The early progeny should be a proliferating group of daughter cells more concentrated in areas just above or adjacent to stem cell regions. We have, therefore, compared proliferative rates of keratinocytes within relevant subregions of the epidermis using the AgNOR stain on biopsies from patients with GVHD, non-specific inflammatory infiltrates (NSI) and normal skin. We concurrently evaluated T cell infiltration using immunohistology on paraffin-embedded tissue with UCHL-1 antibody. Fifty-one bone marrow transplant patients were evaluated in each of three temporal groups (days 7-20 post-transplant, days 20-40 post-transplant, and days 80-100 post-transplant). In each of these groups, 5-9 patients with a histological diagnosis of GVHD were compared to similar numbers of patients with a histological diagnosis of non-specific dermatitis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Proliferation rates in epidermis of patients with graft-versus-host disease, non-specific inflammation and normal skin. 151 75

Lethally irradiated rats, reconstituted with syngeneic bone marrow and given Cyclosporin A (CyA) for 6 weeks, developed disease resembling allogeneic graft-versus-host disease 2 weeks after withdrawal of CyA. Other studies have demonstrated the pivotal role of the thymus in the etiology of this CyA-induced autoimmune disease (CyA-AI). In this study the question was addressed whether inducer/effector cells of CyA-AI are generated in the thymus during or after CyA administration; whether these cells stay in the thymus, or, if they don't, whether they home to the secondary lymphoid organs. Adoptive transfer of thymocytes from donors treated for induction of CyA-AI obtained one and 14 days after cessation of CyA administration did not elicit CyA-AI in irradiated secondary recipients. Furthermore, adult thymectomy of rats immediately after the course of CyA did not influence the kinetics of development of skin pathology, although weight loss commenced later in thymectomized than in sham-thymectomized rats. Lymph node and spleen cells obtained from donors treated for induction of CyA-AI one and 14 days after withdrawal of CyA-AI caused CyA-AI upon adoptive transfer to secondary recipients, but the symptoms of acute disease (dermatitis, alopecia and weight loss) were strikingly less severe upon transfer of lymphoid cells obtained one day after stopping CyA than 14 days thereafter. Therefore, this study demonstrates that CyA-AI inducer/effector cells are generated in the thymus during the administration of CyA. These cells exit from the thymus during CyA administration; either they home predominantly peripherally (i.e. in the skin) rather than in the secondary lymphoid organs, or they leave the thymus as inducer cells which home in the lymphoid organs where they subsequently may trigger potentially autoreactive lymphocytes as probably also present in normal individuals, or both pathways may be operative.
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PMID:On the localization of effector cells in cyclosporin-induced autoimmunity. 177 63

AR can be regarded as the most severe variant of the spectrum of chronic actinic dermatitis. The exact etiology is still unknown, but is probably multifactorial, involving contact allergic, photoallergenic, phototoxic, immunologic, and metabolic factors. A diagnosis of AR should only be made when the following criteria are present: (1) persistent infiltrated papules and plaques on light-exposed skin, often with extension to covered areas or generalized infiltrated erythroderma; (2) photosensitivity to a broad spectrum of wavelengths, including UV-B, UV-A, and part of the visible spectrum; and (3) on histologic examination, a dermal infiltrate with presence of atypical lymphoid cells. When one or two criteria are lacking, the more general term chronic actinic dermatitis should be preferred. The presence of a lymphoid infiltrate dominated by CD8+ cells seems to be useful as an additional marker for a diagnosis of AR. A CD8+ predominance in dermal infiltrates is exceptional and has been reported in clinically distinguished conditions such as graft-versus-host disease, lichen planus, erythema multiforme, and pityriasis lichenoides acuta, as well as chronica, and, finally, in mycosis fungoides. In erythrodermic patients, the presence of a CD8+ -dominated dermal infiltrate and, especially, a reversed CD4+ to CD8+ ratio in the peripheral blood are highly characteristic for a definite diagnosis of AR. It is not known why preferentially CD8+ lymphocytes occur in AR. Exposure to UV radiation can induce the presence of suppressor cells. In late lesions of polymorphic light eruption, there is also an increase of CD8+ cells as compared with early lesions, perhaps contributing to local suppression of the inflammatory response.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Actinic reticuloid. 187 48

Small bowel and its mesentery contain considerable amounts of lymphoid tissue that can mediate graft-versus-host disease in small bowel transplant (SBT) recipients. Present studies determined the existence of GVHD in a fully allogeneic SBT model and examined the effect of donor pretreatment with ALS in eliminating GVHD. Adult male Lewis (Lew) rats received orthotopic small bowel transplants from untreated (LewxBN)F1 (LBNF1) donors (group 1) or Brown Norway (BN) donors that were untreated (group 2) or pretreated with ALS (days -2 and -1) (group 3). All recipients were treated with cyclosporine 15 mg/kg/day i.m. on days 0-6 postoperatively. Animals were weighed and examined daily for signs of rejection and GVHD. No animals in groups 1 or 3 showed any physical signs of GVHD, but all of those in group 2 had characteristic weight loss, diarrhea, and dermatitis between 4 and 6 weeks postoperatively, from which they all recovered. Histologic examination of skin and spleen at this time confirmed the presence of GVHD. The relative spleen weight [( spleen weight/body weight] x 100) of group 2 animals was also significantly greater than that of unoperated control Lew animals. Spleen cells obtained from group 2 animals at the time of subclinical GVHD, but not cells from group 1 or 3 animals, caused enlargement of popliteal lymph nodes when they were injected into the footpads of Lew rats. This study shows that GVHD can manifest itself in recipients of a fully allogeneic small bowel transplant even when rejection is prevented by effective immunosuppression with CsA. However, combined use of recipient treatment with CsA and pretreatment of donor animals with ALS eliminates all manifestations of GVHD.
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PMID:Graft-versus-host disease in fully allogeneic small bowel transplantation in the rat. 291 75

The histopathologic changes of radiation dermatitis have been classified either as early effects (necrotic keratinocytes, fibrin thrombi, and hemorrhage) or as late effects (vacuolar changes at the dermal-epidermal junction, atypical radiation fibroblasts, and fibrosis). Two patients, one exposed to radiation therapeutically and one accidentally, are described. Skin biopsy specimens showed an interface dermatitis characterized by numerous dyskeratotic epidermal cells with lymphocytes in close apposition (satellite cell necrosis); that is, the epidermal changes were similar to those in acute graft-versus-host disease. Because recipients of bone marrow transplants frequently receive total body irradiation as part of their preparatory regimen, the ability of radiation to cause persistent epidermal changes similar to those in acute graft-versus-host disease could complicate the interpretation of posttransplant skin biopsy specimens.
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PMID:Subacute radiation dermatitis: a histologic imitator of acute cutaneous graft-versus-host disease. 291 58

Acute graft-versus-host disease (GVHD) was induced in newborn Brown-Norway (BN) and DA rats by i.v. injection of 3 X 10(7) Lewis (L) lymph node cells. Control BN and DA rats received syngeneic cells. Rats were injected i.v. with [methyl-3H]thymidine for 1 h before being killed at 1, 2, 4, 5, 6, 8, 10, 11, 12, 13, and 14 days after the cellular inoculum. A piece of ventral abdominal skin was removed. Autoradiography was used to determine cell proliferative activity (labeling index, LI) in mast cells and fibroblasts of the dermis and basal cells of the epidermis. In addition, the number of mast cells per high-power field was determined for all 4 groups of rats: control DA, GVHD-DA, control BN, and GVHD-BN. Only GVHD-BN rats demonstrated extensive dermatitis. The LI of mast cells, fibroblasts, and basal cells decreased in control rats with increasing age. Although there were differences between DA and BN rats, there was a general pattern of increased proliferation of mast cells at early time points of GVHD followed by a decrease to or below control levels. The number of mast cells per high-power field also increased at early time intervals in both the DA and BN GVHD rats, but decreased significantly at later time points. These data confirm previous studies on chronic GVHD which demonstrated a decrease in the number of mast cells in the skin. Fibroblast LI was decreased at day 1 in both DA and BN GVHD rats. In GVHD-DA, fibroblast LI remained depressed while GVHD-BN demonstrated a second peak in LI at day 10 before declining below control levels. The most prominent basal cell response occurred in GVHD-BN between days 6-14 and is probably indicative of an attempted reparative response associated with GVHD dermatitis in this species. These data demonstrate that the activation of mast cells (proliferation and subsequent degranulation) correlates temporally with cell kinetic alterations occurring in the dermis and epidermis during acute GVHD.
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PMID:Kinetics of mast cell, fibroblast, and epidermal cell proliferation during acute graft-versus-host disease in the neonatal rat. 355 63

The histopathological changes and the course of graft-versus-host (GVH) disease were studied in the rat model of small-bowel transplantation using the Lewis----LBN-F1 strain combination. Allograft-induced GVH disease led to the recipients' death from enteritis, dermatitis and emaciation after 14.4 +/- 2.9 days (heterotopic grafts) and 14.0 +/- 0.7 days (orthotopic grafts). Histologic evidence of dermatitis (epidermal hyperkeratosis and cutaneous infiltration by mononuclear and polymorphonuclear cells) and enteritis (villous blunting and sloughing, inflammatory infiltrate of the recipient's own intestine) appeared on the 9th to 13th postoperative days, and these changes became fulminant within 2-3 days. The lymphatic tissues of the Lewis grafts and the LBN-F1 host underwent a course of progressive lymphoid depletion and loss of follicular architecture beginning on the 5th postoperative day. Throughout the postoperative course, the small-bowel graft remained intact. The relative spleen weight progressively increased until shortly before death, when a marked reduction was observed. The clinical triad of diarrhea, diffuse dermatitis, and hypertrophy of the lymphoid organs followed by their atrophy suggests a diagnosis of GVH disease rather than rejection of the small-bowel allograft. The diagnosis can be confirmed by biopsy of a recipient lymph node or the intestinal allograft (cave perforation) if it is accessible.
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PMID:Graft-versus-host disease induced by small bowel allografts. Clinical course and pathology. 395

A 50-year-old severely immunodeficient woman with malignant non-Hodgkin lymphoma died from graft-versus-host disease due to transfusion of a single unit of packed red cells. Three days after this transfusion a maculo-papular rash appeared, followed by generalized erythroderma refractory to therapy and eventually progressing into generalized ulcero-squamous dermatitis. This case, and a review of other similar cases published elsewhere, prompt the authors to recommend prophylactic irradiation of blood products prior to their administration to patients with cellular immunodeficiency, particularly in cases of acute leukaemia or malignant lymphoma where patients receive intensive radio- and/or chemotherapy regimens. To appreciate the degree of cellular immunodeficiency in such risk patients, simple criteria should be developed to assess the efficiency of the cellular immune system.
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PMID:[Acute graft-versus-host disease following a single transfusion of erythrocytes]. 396 40

A 23-year-old woman gravely ill with Pseudomonas septicemia secondary to presumed drug-induced bone marrow aplasia received marrow transplantation from two male HL-A identical sibling donors. She had a successful engraftment with excellent but temporary clinical improvement. Subsequently she succumbed to graft-versus-host disease manifested by Pseudomonas and Candida albicans septicemia, cytomegalovirus pneumonitis, three phases of dermatitis, nausea, vomiting, dysphagia, diarrhea, fever, edema and bone pain, with gradual but complete graft suppression by the 74th day after the transplantation. A second marrow transplant on the 70th day was unsuccessful.
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PMID:Bone marrow transplantation in a patient with drug-induced aplastic anemia. 440 93

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.
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PMID:New insight into the causes of immunodeficiency disorders. 638 1


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