Abstract
Psoriatic arthritis (PsA) is a heterogeneous chronic inflammatory disorder of the peripheral joints, peripheral entheses, synovial sheaths of tendons, and spine associated with psoriasis. PsA is characterized by different clinical phenotypes and its course is variable1. Patients can also have gut2 and eye involvement3. In addition, patients with PsA or psoriasis have increased frequency of insulin resistance, obesity, type 2 diabetes, metabolic syndrome, hypertension, hyperlipidemia, and cardiovascular disease compared with the general population4. Recently, a new designation has been proposed with the aim to cover all these clinical situations: psoriatic disease5. In the past, PsA was considered a rare and mild disease. The prevalence of psoriasis in the general population is currently estimated to be around 2%–3%, with one-third of patients developing associated musculoskeletal manifestations. In the last 20 years, evidence has been gathered demonstrating that PsA is destructive and deforming in 40%–60% of patients, with joint damage emerging in the first years of the disease course6. It is believed that around 20% of patients with PsA develop a serious destructive disease. Patients with PsA suffer from functional impairment, decreased quality of life (QOL), and psychosocial disability, and have a significant increase in mortality versus the general population7,8. Therapies for PsA have been inadequate until recently. Nonsteroidal antiinflammatory drugs are useful in improving symptoms but have no effect on the progression of radiographic joint damage. Local corticosteroid injections may be of great aid in patients with persistent mono- or oligoarthritis but use of systemic glucocorticoid treatment is not supported by evidence. Traditional disease-modifying antirheumatic drugs (DMARD), which are the second-line treatment, are employed in PsA to control symptoms, but there is no evidence that they slow the progression of structural joint damage. The introduction of …
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