Psoriatic arthritis (PsA) is among the most disabling forms of arthritis, even though it affects fewer people than other types of arthritis. PsA has a highly variable presentation, which generally involves pain and inflammation in joints and progressive joint involvement and damage. The condition is associated with the skin disease psoriasis, but not all people with psoriasis will develop PsA. Additionally, PsA may predate the development of skin disease, leading to some diagnostic uncertainty. Among people with psoriasis, the prevalence of arthritis varies from 6 percent to 42 percent. In the general population, the prevalence of PsA is estimated to be 0.3 percent to 1 percent. Based on estimates from the 2000 U.S. Census, 520,000 people ages 18 or older in the United States have PsA. Treatment of patients with PsA aims to control pain and inflammation and, ultimately, to slow the progression of joint destruction and disability. Available therapies for PsA include corticosteroids, oral disease-modifying antirheumatic drugs or DMARDs (hydroxychloroquine, leflunomide, methotrexate [MTX], and sulfasalazine), and biologic DMARDs. Five biologics (adalimumab, certolizumab pegol, etanercept, golimumab, and infliximab) are also classified as antitumor necrosis factor (anti-TNF) drugs. The U.S. Food and Drug Administration (FDA) has approved adalimumab, etanercept, golimumab, and infliximab for use in patients with PsA. This report also reviews evidence for abatacept, anakinra, certolizumab, rituximab, and tocilizumab, which are approved for rheumatoid arthritis (RA). Historically, few trials have been conducted with patients having PsA, with only minimal research before biologic agents were introduced; management options tended to be adapted from RA trial evidence. Similar to RA trials, many questions remain about the risks of these agents across a spectrum of adverse events from relatively minor side effects such as injection-site reactions to severe and possibly life-threatening problems such as severe infections or infusion reactions. Experts have not arrived at a consensus about the comparative effectiveness of corticosteroids, oral DMARDs, and biologic DMARDs for treating PsA. More importantly, it is unclear how the effectiveness and safety of different types of combination therapy compare. In addition, there is debate about how early in the disease process combination therapy should be initiated and whether patients will respond to a biologic agent if they have previously failed a different biologic agent. Finally, very little is known about the benefits or risks of these drugs in different patient subgroups, including ethnic minorities, the elderly, pregnant women, and patients with other comorbidities. This report summarizes the evidence on the comparative efficacy, effectiveness, and harms of corticosteroids, oral DMARDs, and biologic DMARDs in the treatment of patients with PsA. The Key Questions (KQs) are as follows: KQ 1: For patients with PsA, do drug therapies differ in their ability to reduce disease activity, to slow or limit the progression of radiographic joint damage, or to maintain remission? KQ 2: For patients with PsA, do drug therapies differ in their ability to improve patient reported symptoms, functional capacity, or quality of life? KQ 3: For patients with PsA, do drug therapies differ in harms, tolerability, patient adherence, or adverse effects? KQ 4: What are the comparative benefits and harms of drug therapies for PsA in subgroups of patients based on stage of disease, prior therapy, demographics, concomitant therapies, or comorbidities?
