Management of graft-versus-host disease
Identifieur interne : 002519 ( Main/Exploration ); précédent : 002518; suivant : 002520Management of graft-versus-host disease
Auteurs : S. Arai [États-Unis] ; G. B. Vogelsang [États-Unis]Source :
- Blood Reviews [ 0268-960X ] ; 2000.
English descriptors
- Teeft :
- Abstr, Acute disease, Acute gvhd, Allogeneic, Autoimmune, Bone marrow transplantation, Bronchiolitis, Bronchiolitis obliterans, Chronic, Chronic disease, Chronic graft, Chronic gvhd, Corticosteroid, Cyclosporine, Cytokine, Graft, Gvhd, Hepatic, Host disease, Immunosuppressive, Lichenoid, Lymphocyte, Marrow, Methotrexate, Mofetil, Mucosal, Mycophenolate, Mycophenolate mofetil, Myositis, Obliterans, Pentostatin, Prophylaxis, Przepiorka, Puva, Receptor, Refractory, Regimen, Risk factors, Sclerodermatous, Steroid, Storb, Tacrolimus, Thalidomide, Thymic, Transplant, Transplantation, Vogelsang.
Abstract
Abstract: The increasing number of allogeneic stem cell transplants, particularly those involving donors other than HLA-identical siblings, has made the management of acute and chronic graft-versus-host disease (GVHD) a continuing problem for transplant experts. There have been improvements in the prevention of acute GVHD with cyclosporine- and FK506-based combination therapies, as well as lymphocyte depletion. However, fewer than 50% of patients have durable improvement after initial treatment. FK506 and mycophenolate mofetil (MMF) are promising salvage therapies in steroid-resistant GVHD, as are the anti-cytokine antibodies and the purine nucleoside analog, pentostatin. The incidence of chronic GVHD has unfortunately not decreased, despite advances in treatment of acute GVHD. Treatment of chronic GVHD involves treatment of the underlying immunologic process and supportive therapies. Initial therapy has tended to be cyclosporine and prednisone. Refractory patients have hope with combination MMF and FK506, etretinate, plaquenil, and nonpharmacologic approaches, such as PUVA. Supportive care is an integral part of chronic GVHD management with emphasis on infection control and symptom control. Death in chronic GVHD is still largely attributable to infection. The progress in therapies for GVHD has been encouraging, but the future of GVHD management lies in a better understanding of its pathogenesis.
Url:
DOI: 10.1054/blre.2000.0137
Affiliations:
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Arai</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Johns Hopkins Oncology Center, Baltimore, MD</wicri:regionArea><placeName><region type="state">Maryland</region></placeName></affiliation></author><author><name sortKey="Vogelsang, G B" sort="Vogelsang, G B" uniqKey="Vogelsang G" first="G. B." last="Vogelsang">G. B. Vogelsang</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Johns Hopkins Oncology Center, Baltimore, MD</wicri:regionArea><placeName><region type="state">Maryland</region></placeName></affiliation></author></analytic><monogr></monogr><series><title level="j">Blood Reviews</title><title level="j" type="abbrev">YBLRE</title><idno type="ISSN">0268-960X</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="2000">2000</date><biblScope unit="volume">14</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="190">190</biblScope><biblScope unit="page" to="204">204</biblScope></imprint><idno type="ISSN">0268-960X</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0268-960X</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Abstr</term><term>Acute disease</term><term>Acute gvhd</term><term>Allogeneic</term><term>Autoimmune</term><term>Bone marrow transplantation</term><term>Bronchiolitis</term><term>Bronchiolitis obliterans</term><term>Chronic</term><term>Chronic disease</term><term>Chronic graft</term><term>Chronic gvhd</term><term>Corticosteroid</term><term>Cyclosporine</term><term>Cytokine</term><term>Graft</term><term>Gvhd</term><term>Hepatic</term><term>Host disease</term><term>Immunosuppressive</term><term>Lichenoid</term><term>Lymphocyte</term><term>Marrow</term><term>Methotrexate</term><term>Mofetil</term><term>Mucosal</term><term>Mycophenolate</term><term>Mycophenolate mofetil</term><term>Myositis</term><term>Obliterans</term><term>Pentostatin</term><term>Prophylaxis</term><term>Przepiorka</term><term>Puva</term><term>Receptor</term><term>Refractory</term><term>Regimen</term><term>Risk factors</term><term>Sclerodermatous</term><term>Steroid</term><term>Storb</term><term>Tacrolimus</term><term>Thalidomide</term><term>Thymic</term><term>Transplant</term><term>Transplantation</term><term>Vogelsang</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: The increasing number of allogeneic stem cell transplants, particularly those involving donors other than HLA-identical siblings, has made the management of acute and chronic graft-versus-host disease (GVHD) a continuing problem for transplant experts. There have been improvements in the prevention of acute GVHD with cyclosporine- and FK506-based combination therapies, as well as lymphocyte depletion. However, fewer than 50% of patients have durable improvement after initial treatment. FK506 and mycophenolate mofetil (MMF) are promising salvage therapies in steroid-resistant GVHD, as are the anti-cytokine antibodies and the purine nucleoside analog, pentostatin. The incidence of chronic GVHD has unfortunately not decreased, despite advances in treatment of acute GVHD. Treatment of chronic GVHD involves treatment of the underlying immunologic process and supportive therapies. Initial therapy has tended to be cyclosporine and prednisone. Refractory patients have hope with combination MMF and FK506, etretinate, plaquenil, and nonpharmacologic approaches, such as PUVA. Supportive care is an integral part of chronic GVHD management with emphasis on infection control and symptom control. Death in chronic GVHD is still largely attributable to infection. The progress in therapies for GVHD has been encouraging, but the future of GVHD management lies in a better understanding of its pathogenesis.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Maryland</li></region></list><tree><country name="États-Unis"><region name="Maryland"><name sortKey="Arai, S" sort="Arai, S" uniqKey="Arai S" first="S." last="Arai">S. Arai</name></region><name sortKey="Vogelsang, G B" sort="Vogelsang, G B" uniqKey="Vogelsang G" first="G. B." last="Vogelsang">G. B. Vogelsang</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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