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The Korean Journal of Gastroenterology ; : 235-244, 2011.
Artículo en Coreano | WPRIM | ID: wpr-212483

RESUMEN

Understanding of the pathophysiology of inflammatory bowel disease (IBD) is constantly evolving and, recently, a number of biologic agents have been developed. They selectively target specific molecule or pathways and correct the imbalance of the gut immune system. Among them, antibody to tumor necrosis factor (anti-TNF-alpha) is the first developed drugs, and it dramatically improved the IBD management. However, more than one-third of the patients do not respond to the drugs due to antibody formation. To increase treatment efficacy, enormous effort to develop novel anti-cytokines which can be an alternative to anti-TNF-alpha has been made. They are anti CD4+ T cell cytokine including interleukin (IL)-12/23 and IL-17 blockers, selective anti-adhesion molecule known as natalizumab, vedolizumab and alicaforsen, T-cell proliferation inhibitor, anti-inflammatory cytokine, immune stimulator, growth factor, and mitogen-activated protein kinase inhibitor. The efficacy and safety of each drugs are under investigation. Some drugs reported very promising data, however, others showed disappointing and different results. In addition, most of the trials were done in a very small number of patients, and there is no trial comparing to anti-TNF-alpha. The present paper reviews the action mechanism, short or long term efficacy and safety of variable drugs other than anti-TNF-alpha in IBD.


Asunto(s)
Humanos , Anticuerpos Monoclonales/uso terapéutico , Inhibición de Migración Celular , Factores Estimulantes de Colonias/uso terapéutico , Citocinas/antagonistas & inhibidores , Terapia Genética , Inmunosupresores/uso terapéutico , Enfermedades Inflamatorias del Intestino/tratamiento farmacológico , Péptidos y Proteínas de Señalización Intercelular/uso terapéutico , Proteínas Quinasas Activadas por Mitógenos/antagonistas & inhibidores , Trasplante de Células Madre , Factor de Necrosis Tumoral alfa/antagonistas & inhibidores
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