ABSTRACT
La artritis psoriásica (AP) es una enfermedad autoinmunitaria, inflamatoria, crónica que se caracteriza por artritis y psoriasis cutánea y se clasifica en el grupo de las espondiloartropatías (EA). Su gran heterogeneidad clínica ha dificultado el estudio de su patogenia y la realización de ensayos clínicos aleatorizados extensos con DMARD (disease-modifying anti-rheumatic drugs [fármacos antirreumáticos modificadores de la enfermedad]). La eficacia de las terapias biológicas en la AP ha suscitado un gran interés en esta enfermedad, en su clasificación clínica y en los mecanismos patogénicos subyacentes. A continuación, se revisan varios artículos recientes sobre la patogenia de la AP, centrados en la angiogénesis sinovial y su potencial como diana terapéutica; en la expresión sinovial de macrófagos y proteína p53 y su relación con la destrucción articular en la artritis reumatoide (AR) y AP. Finalmente, se analiza si la forma poliarticular de la AP comparte características inmunohistoquímicas con la AR o con las EA. Aunque la efectividad de las terapias anti-factor de necrosis tumoral [TNF]-á en la AR y la AP apoya que la patogenia de ambas enfermedades es similar, estos y otros estudios indican que existen diferencias en la expresión y el significado patogénico de ciertas células y moléculas. De confirmarse, existiría la posibilidad de desarrollar nuevas terapias específicas para la AP(AU)
Psoriatic arthritis (PsA) is a chronic inflammatory autoimmune disease characterized by arthritis and psoriasis of the skin. It is classified within the spondyloarthropathies (SpA) group. The wide clinical heterogeneity of PsA has hampered research into its pathogenesis and the performance of large randomised clinical trials with disease-modifying anti-rheumatic drugs. The success of biologic agents in PsA has stimulated wide interest in this disease as well as in its clinical classification and underlying pathogenic mechanisms. Several recent articles on the pathogenesis of PsA are reviewed, focussing on the potential of synovial angiogenesis as a therapeutic target and on synovial expression of macrophages and p53 protein related to joint damage in rheumatoid arthritis (RA) and PsA. Finally, the question of whether the polyarticular variant of PsA shares immunohistochemical features with RA or SpA is also discussed. Although the success of tumor necrosis factor-alpha antagonists in both RA and PsA supports a similar pathogenesis in both disorders, these and other studies suggest that there are differences in the synovial expression and pathogenic significance of certain cells and molecules. If confirmed, this phenomenon could open new avenues in specific therapy for PsA(AU)
Subject(s)
Humans , Psoriasis/complications , Synovitis/complications , Arthritis, Psoriatic/diagnosis , Neovascularization, Pathologic/physiopathology , Tumor Necrosis Factor-alpha/antagonists & inhibitors , Tumor Suppressor Protein p53/isolation & purification , Spondylarthropathies/complications , Rheumatic Diseases/complicationsABSTRACT
No disponible
Subject(s)
Humans , Arthroscopy/methods , Joint Diseases/diagnosis , Rheumatic Diseases/diagnosisABSTRACT
Psoriatic arthritis (PsA) is a chronic inflammatory autoimmune disease characterized by arthritis and psoriasis of the skin. It is classified within the spondyloarthropathies (SpA) group. The wide clinical heterogeneity of PsA has hampered research into its pathogenesis and the performance of large randomized clinical trials with disease-modifying anti-rheumatic drugs. The success of biologic agents in PsA has stimulated wide interest in this disease as well as in its clinical classification and underlying pathogenic mechanisms. Several recent articles on the pathogenesis of PsA are reviewed, focussing on the potential of synovial angiogenesis as a therapeutic target and on synovial expression of macrophages and p53 protein related to joint damage in rheumatoid arthritis (RA) and PsA. Finally, the question of whether the polyarticular variant of PsA shares immunohistochemical features with RA or SpA is also discussed. Although the success of tumor necrosis factor-alpha antagonists in both RA and PsA supports a similar pathogenesis in both disorders, these and other studies suggest that there are differences in the synovial expression and pathogenic significance of certain cells and molecules. If confirmed, this phenomenon could open new avenues in specific therapy for PsA.
ABSTRACT
No disponible
