Papel de los polimorfismos -238 y -308 del promotor del factor de necrosis tumoral alfa en la patogenia y respuesta al tratamiento anti- factor de necrosis tumoral alfa en artritis reumatoide
Rheumatoid arthritis (RA) is a systemic autoimmune disease that affects 0.8% of the world population, it affects the synovial membrane of joints and the clinical presentation encompasses a wide spectrum, ranging from a mild to a severe and erosive disease that causes joint and cartilage destruction...
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Sociedad Médica de Santiago
2005
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oai:scielo:S0034-988720050009000142005-11-09Papel de los polimorfismos -238 y -308 del promotor del factor de necrosis tumoral alfa en la patogenia y respuesta al tratamiento anti- factor de necrosis tumoral alfa en artritis reumatoideLlanos M,CarolinaSoto S,LilianSabugo S,FranciscaBastías Ch,M JoséSalazar A,LorenaAguillón G,Juan CCuchacovich T,Miguel Arthritis, rheumatoid Genotype Tumor necrosis factor-alpha Rheumatoid arthritis (RA) is a systemic autoimmune disease that affects 0.8% of the world population, it affects the synovial membrane of joints and the clinical presentation encompasses a wide spectrum, ranging from a mild to a severe and erosive disease that causes joint and cartilage destruction which finally provokes irreversible structural damage and patient disability. In the last years, there have been important advances in the pathogenesis of this disease, the efforts have been concentrated on pro-inflammatory cytokines such as tumor necrosis factor alpha (TNFalpha). This protein guides numerous events in the synovial and systemic inflammatory process and is encoded in the Major Histocompability Complex (MHC), one of the most polymorphic of the genome. Polymorphisms affecting the TNFalpha gene and its regulatory regions are associated with RA prevalence and course. There is a possible association between these polymorphisms and the clinical response to the use of monoclonal antibodies anti-TNFalpha. The possibility that the determination of genotypes -238 and -308 may have prognostic and therapeutic consequences is debated nowadays (Rev Méd Chile 2005; 133: 1089-95).info:eu-repo/semantics/openAccessSociedad Médica de SantiagoRevista médica de Chile v.133 n.9 20052005-09-01text/htmlhttp://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0034-98872005000900014es10.4067/S0034-98872005000900014 |
institution |
Scielo Chile |
collection |
Scielo Chile |
language |
Spanish / Castilian |
topic |
Arthritis, rheumatoid Genotype Tumor necrosis factor-alpha |
spellingShingle |
Arthritis, rheumatoid Genotype Tumor necrosis factor-alpha Llanos M,Carolina Soto S,Lilian Sabugo S,Francisca Bastías Ch,M José Salazar A,Lorena Aguillón G,Juan C Cuchacovich T,Miguel Papel de los polimorfismos -238 y -308 del promotor del factor de necrosis tumoral alfa en la patogenia y respuesta al tratamiento anti- factor de necrosis tumoral alfa en artritis reumatoide |
description |
Rheumatoid arthritis (RA) is a systemic autoimmune disease that affects 0.8% of the world population, it affects the synovial membrane of joints and the clinical presentation encompasses a wide spectrum, ranging from a mild to a severe and erosive disease that causes joint and cartilage destruction which finally provokes irreversible structural damage and patient disability. In the last years, there have been important advances in the pathogenesis of this disease, the efforts have been concentrated on pro-inflammatory cytokines such as tumor necrosis factor alpha (TNFalpha). This protein guides numerous events in the synovial and systemic inflammatory process and is encoded in the Major Histocompability Complex (MHC), one of the most polymorphic of the genome. Polymorphisms affecting the TNFalpha gene and its regulatory regions are associated with RA prevalence and course. There is a possible association between these polymorphisms and the clinical response to the use of monoclonal antibodies anti-TNFalpha. The possibility that the determination of genotypes -238 and -308 may have prognostic and therapeutic consequences is debated nowadays (Rev Méd Chile 2005; 133: 1089-95). |
author |
Llanos M,Carolina Soto S,Lilian Sabugo S,Francisca Bastías Ch,M José Salazar A,Lorena Aguillón G,Juan C Cuchacovich T,Miguel |
author_facet |
Llanos M,Carolina Soto S,Lilian Sabugo S,Francisca Bastías Ch,M José Salazar A,Lorena Aguillón G,Juan C Cuchacovich T,Miguel |
author_sort |
Llanos M,Carolina |
title |
Papel de los polimorfismos -238 y -308 del promotor del factor de necrosis tumoral alfa en la patogenia y respuesta al tratamiento anti- factor de necrosis tumoral alfa en artritis reumatoide |
title_short |
Papel de los polimorfismos -238 y -308 del promotor del factor de necrosis tumoral alfa en la patogenia y respuesta al tratamiento anti- factor de necrosis tumoral alfa en artritis reumatoide |
title_full |
Papel de los polimorfismos -238 y -308 del promotor del factor de necrosis tumoral alfa en la patogenia y respuesta al tratamiento anti- factor de necrosis tumoral alfa en artritis reumatoide |
title_fullStr |
Papel de los polimorfismos -238 y -308 del promotor del factor de necrosis tumoral alfa en la patogenia y respuesta al tratamiento anti- factor de necrosis tumoral alfa en artritis reumatoide |
title_full_unstemmed |
Papel de los polimorfismos -238 y -308 del promotor del factor de necrosis tumoral alfa en la patogenia y respuesta al tratamiento anti- factor de necrosis tumoral alfa en artritis reumatoide |
title_sort |
papel de los polimorfismos -238 y -308 del promotor del factor de necrosis tumoral alfa en la patogenia y respuesta al tratamiento anti- factor de necrosis tumoral alfa en artritis reumatoide |
publisher |
Sociedad Médica de Santiago |
publishDate |
2005 |
url |
http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0034-98872005000900014 |
work_keys_str_mv |
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