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Biologics represent useful treatment for PsA; other therapies, approaches require more study

Monday, June 18 2007 | Comments
Evidence Grade 0 What's This?
Good clinical data support the use of biologic drugs in psoriatic arthritis, but more research is necessary to find additional treatments and appropriate therapeutic methods to treat this condition, presenters said.

Douglas Veale, a professor at the University College Dublin, spoke about rheumatologists' approaches for treating patients with PsA.

Many patients may present with the classic disease in both the skin and joints. But Veale queried clinicians about how they make treatment decisions in more difficult cases, such as in patients with joint involvement but few or no skin manifestations, with disease in the skin but little joint involvement, or with eye disease, enthesitis, dactylitis, or spondylitis alone or in combination with vascular peripheral arthritis manifestations.

"[W]e should really always be striving for excellence and particularly when our patients are concerned. We should be striving for the best possible treatments, and not aim halfway and settle for second-best," he said. "The best treatments are most likely to benefit both the skin and joint symptoms."

Veale said that nonsteroidal antiinflammatory drugs, corticosteroids, disease-modifying antirheumatic drugs, and biologics are the evidence-based medicines currently used to treat PsA.

However, there are no robust data and a low grade of evidence for the use of NSAIDs in PsA, with no randomized controlled trials of coxibs and an uncertainty about whether NSAIDs actually exacerbate the psoriasis, he claimed.

Use of corticosteroids in PsA has grade D evidence, with no randomized controlled trials of oral and intraarticular corticosteroids. These drugs are commonly used, but their prescription is based on expert opinion, such that intraarticular steroids are often effective and can be used in mono- or oligo-disease.
For DMARDs, Veale said there have been clinical trials with sulfasalazine, methotrexate, cyclosporine, azathioprine, and leflunomide, but study subject numbers were low and results showed only minor or moderate efficacy. Rheumatologists often use methotrexate as first-line therapy for PsA, even though many studies with this drug have been poorly powered and inadequate. Evidence for its use is based mostly on rheumatoid arthritis and psoriasis literature, according to Veale.

Biologics that target tumor necrosis factor have demonstrated substantial improvements in PsA signs and symptoms, improved quality of life, and attenuation of radiographic joint damage in several randomized controlled trials. He pointed to some examples of these results with etanercept, adalimumab, and infliximab.

Veale noted, however, that there is still no evidence-based treatment for PsA that has spinal involvement.

"So, in summary, therefore, I hope that I've shared with you my thoughts suggesting ... that initial treatment decisions are currently based largely on expert opinion and data borrowed from the RA literature. We have good clinical data for biologic drug efficacy. However, the best treatment strategy for enthesitis, dactylitis, and spondylitis remains largely ill-defined," Veale said.

He added that rheumatologists should make treatment decisions after consulting colleagues, especially those in the field of dermatology, and that the decisions should be based on the disease as a whole. Also, more controlled studies are needed to research therapeutic approaches for enthesitis, dactylitis, and spondylitis in PsA, according to Veale.

Dr. Paul Peter Tak, who works at the University of Amsterdam, reviewed the pathogenesis of PsA and RA and suggested avenues for potential PsA treatments.

He explained that both RA and PsA are immune-mediated inflammatory disorders with different clinical, immunological, and genetic features as well as potentially different joint destruction and structural remodeling.

However, he said that such disorders share a common pathogenetic mechanism, so therapies that target these common pathways could work for both. Some therapeutic possibilities could be alefacept, abatacept, drugs that block TNF, interleukin (IL)-1, IL-6R, IL-18, IL-20, or others.

This information concerns uses that have not been approved by the Food and Drug Administration.

By Shayna Muckerheide

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