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)

The pathogenetic mechanisms underlying common, and less common but severe, adverse cutaneous drug reactions are reviewed. Pharmacogenetic variability may account for a susceptibility to serious drug reactions to sulphonamides and anticonvulsants, as well as to lupus erythematosus (LE)-like syndrome. Exanthematous drug reactions may have an immunological basis. Cell mediated cutaneous drug reactions, including lichenoid reactions, LE-like syndrome, fixed drug eruption, erythema multiforme, Stevens-Johnson syndrome and toxic epidermal necrolysis, will inevitably involve elements of the skin immune system. Graft-versus-host disease provides a useful model for aspects of these drug-induced disorders. Urticaria, angioedema, anaphylaxis and anaphylactoid reactions may involve Type I immunoglobulin (Ig)-mediated or Type III hypersensitivity, or may be caused by pharmacological, non-allergic means. Drug-induced vasculitis, serum sickness and the Arthus phenomenon are manifestations of the immune complex disease. Drug-induced pemphigus may involve immune dysregulation, but several thiol-containing drugs are able to cause antibody-independent acantholysis directly.
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PMID:Mechanisms of drug eruptions: Part I. 748 37

Graft-versus-host disease (GVHD), induced by the reaction of donor T cells to recipient histoincompatible antigens, is a serious complication of allogeneic bone marrow transplantation (BMT), resulting in considerable morbidity and mortality. In MHC-disparate BMT, donor T cells directly react with major histocompatibility complex (MHC) antigens, while in MHC-matched BMT, T cells react with minor histocompatibility antigens (miHA) presented by shared MHC molecules. Clinically, acute and chronic GVHD can be distinguished on the basis of the time of onset, clinical manifestations and distinct pathobiological mechanisms. Acute GVHD usually occurs within 2 to 6 weeks following allogeneic BMT and primarily affects the skin, liver and the gastrointestinal tract with T cell infiltration of the epithelia of the skin, mucous membranes, bile ducts and gut. In addition, hair follicle cells, airways, bone marrow, and a variety of other tissue systems can be involved. Acute GVHD occurs in up to 50% of allogeneic HLA-matched and 70% of HLA-disparate BMT recipients despite prophylactic immunosuppressive drugs. Chronic GVHD involves a wider range of organs and clinical manifestations include scleroderma, liver failure, immune complex disease, glomerulonephritis, and autoantibody formation.
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PMID:T cell immunity and graft-versus-host disease (GVHD). 1633 5