Psoriatic arthritis: Current concepts on pathogenesis‐oriented therapeutic options

TLDR: A subset of patients with PsA fail to respond to conventional therapies and to anti–tumor necrosis factor (anti-TNF) agents that are currently approved for the treatment of PsA, underscoring the diverse mechanisms likely to be at play in these heterogeneous phenotypic subtypes ofPsA.

Abstract: Psoriatic arthritis (PsA) is a chronic inflammatory arthropathy of the peripheral joints, spine, and entheses, associated with psoriasis and characterized by diverse phenotypic subtypes and a variable clinical course. Much progress has been made in identifying the distinctive characteristics of this disease since Alibert first described the association between psoriasis and arthritis in 1818 in “Lepre squammeuse,” his discourse on skin diseases (1). Recent insights into the immunopathogenic mechanisms of PsA have revealed disease characteristics in the synovium, vascular structures, entheses, and bone of PsA patients that are similar to, and distinct from, those of rheumatoid arthritis (RA) as well as other forms of spondylarthritis (SpA), including ankylosing spondylitis (AS), reactive arthritis, and enteropathic arthritis. Such investigations, along with advances in biotechnology and the development of a number of targeted biologic response modifiers (BRMs) with demonstrated effectiveness for both skin and joint manifestations, have led to substantial progress in the treatment of PsA and a renewed interest in the mechanistic processes behind this complex disease. As with RA and SpA, a subset of patients with PsA fail to respond to conventional therapies and to anti–tumor necrosis factor (anti-TNF) agents that are currently approved for the treatment of PsA. A number of novel agents beyond TNF blockade are under investigation for PsA, underscoring the diverse mechanisms likely to be at play in these heterogeneous phenotypic subtypes of PsA.