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Specific inhibition of the cytokine tumour necrosis factor α (TNFα) has yielded dramatic improvements in the symptoms, signs, and quality of life of patients with chronic inflammatory diseases of Th1 phenotype such as rheumatoid arthritis (RA),1–9 psoriatic arthritis (PsA),10–14 ankylosing spondylitis,15–17 psoriasis,18–21 and Crohn’s disease.22,23 The ability of anti-TNFα therapy to inhibit disease progression in RA5,6,24 and PsA14,25 as evidenced by retardation of joint destruction by x ray analysis, has also been documented. Although these clinical results have been clearly demonstrated, our understanding of disease pathophysiology and demonstration of the specific cellular and immunohistochemical effects of new treatments continue to evolve. This review focuses on what has been recently learnt about the mechanism of treatment in PsA and psoriasis.
Psoriasis, occurring in approximately 1–3% of the population,26,27 is a disease characterised by unsightly erythematous and indurated lesions, often with extensive silvery scale, which may cause significant impairment of quality of life and emotional wellbeing.28,29 Although the exact prevalence of PsA is not as precisely known, studies suggest that at least 7%30 and probably closer to 31%,31,32 or higher,26,33,34 of all patients with psoriasis may demonstrate this unique inflammatory arthropathy. It is probably underdiagnosed given that its various subtypes (oligoarticular, polyarticular, distal interphalangeal or axial predominant, and arthritis mutilans), originally described by Moll and Wright,35 may be confused with other conditions such as osteoarthritis, RA, other spondyloarthropathies, gout, and chronic tendonitis. A new classification scheme in development, through a patient database project known as CASPAR, led by Philip Helliwell, is expected to yield more sensitive and specific criteria for PsA and its subsets using clinical, laboratory, and radiological parameters. …
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