The biologic agents currently approved for treatment of PsA, i.e., those targeting the pro-inflammatory cyto-kine, tumor necrosis factor-alpha (TNF- ), have produced dramatic improvements in arthritis, enthesitis, dactylitis and psoriatic skin lesions, as well as function, quality of life, and inhibition of structural damage as measured radiographically (Antoni et al. 2005a, b; Mease 2003, 2004; Mease and Antoni 2005; Mease et al. 2000, 2004, 2005; Mease and van der Heijde et al. 2006). Current anti-TNF-a agents include etanercept, infliximab, and adalimumab. Some of the observed histological and immunohistochemical effects of TNF-inhibition include reduction of: synovial lining layer thickness, vascularity, endothelial expression of avb3 and vascular cell adhesion molecule (VCAM)-1, sublayer expression of intercellular adhesion molecule (ICAM-1) and E-selectin, T-cell and macrophage infiltration, vascular endothelial growth factor (VEGF) expression, synovial flk-1 expression and reduction in osteoclast differentiation and in the numbers of osteo-clast precursors (Mease 2004b).
Studies of patients with RA show that many of those who have inadequate efficacy with one anti-TNF-a medication may switch to another and attain a good response (Hansen et al. 2004; Haraoui et al. 2004). Preliminary evidence suggests this is true in PsA as well (van den Bosch et al. 2006).
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