Graft-versus-host disease
Article Abstract:
A review is presented of the major features, clinical and pathologic aspects, and methods of prevention and treatment, of graft-versus-host disease (GVHD), the main complication of organ transplantation. The normal host-versus-graft reaction occurs when the immune cells of an organ recipient recognize transplanted cells as foreign because they carry on their surfaces foreign proteins encoded by the major histocompatibility complex (MHC), called human leukocyte-associated (HLA) antigens in humans. GVHD results when immune cells in the grafted tissue attack the host's ''foreign'' HLA antigens. It can develop in transplanted organs, blood products, or bone marrow. The cells responsible for GVHD are mature T cells (the major cell type of the cellular immune system). GVHD develops in patients whose immune systems are compromised; normally, the host's immune system rejects donated cells and GVHD cannot develop. Unfortunately, transplant patients and patients undergoing chemotherapy must be immunosuppressed to prevent transplant rejection. Descriptions of acute, chronic, and syngeneic (self-limited, occurring after transplants of the patient's own or HLA-compatible tissue) GVHD are presented. The disease has two phases: the first involves the activation of T cells in the graft by tissues in the recipient (afferent phase); the second involves secretion of factors by these activated cells and their attack on host tissue (efferent phase). The pathophysiology of GVHD is reviewed. Approaches to preventing and treating the disease usually focus on the afferent phase and try to prevent activation of donor T cells. Immunosuppressive drugs (cyclosporine, glucocorticoids) are administered for this purpose. In the case of bone marrow transplants, one approach is to remove all the T cells from the transplanted bone marrow, but this leads to a higher incidence of graft failure. Other methods are described. Future approaches to GVHD will use the methods of cell biology to deplete specified subgroups of immunologically active donor cells, and will focus on developing immunosuppressant drugs more suited to this purpose than those currently available. (Consumer Summary produced by Reliance Medical Information, Inc.)
Publication Name: The New England Journal of Medicine
Subject: Health
ISSN: 0028-4793
Year: 1991
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Vancomycin-induced immune thrombocytopenia
Article Abstract:
A study examines whether vancomycin-dependent antibodies in patients being treated with the antibiotic cause thrombocytopenia. Evidence indicates that severe bleeding can occur in patients with vancomycin-induced thrombocytopenia and that vancomycin-dependent antiplatelet antibodies are the cause of the thrombocytopenia.
Publication Name: The New England Journal of Medicine
Subject: Health
ISSN: 0028-4793
Year: 2007
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