Efficacy of Biologic Agents in Psoriatic Arthritis

MARCH 16, 2017
MD Magazine Staff

Allan Gibofsky, MD: When it comes to the choice of therapies in psoriatic arthritis, we start with the nonsteroidals to provide acute relief of pain and inflammation. We may use conventional synthetics, but we would like to use the biologic agents and, in particular, the TNF (tumor necrosis factor) inhibitors, as soon as we can because of evidence now from multiple sources. But these agents really improve signs and symptoms, improve patient reported outcomes, and inhibit the structural progression of disease. Also, by effectively treating the inflammatory burden of the disease, they will significantly reduce the long-term consequences of untreated or undertreated inflammation, such as malignancy and cardiovascular disease. I think that we should be using the TNF agents as early as we can in patients to get the disease under optimal control and to reduce the burden of inflammation that is causing the psoriatic arthritis, as well as the risk of long-term consequences.
 
TNF inhibitors do, of course, increase the risk of infections and, in some instances, the risk of malignancy. Whether the risk of increasing malignancy is due to the drug or whether it’s due to the enhanced inflammatory burden that we’re treating the patients with that drug for is an open question that remains to be teased out. That said, the significant risks of the TNF inhibitors we are most concerned about are infections.
 
We are most concerned about the increased risk of infections in patients who are taking TNF inhibitors for the treatment of their psoriatic arthritis. Before starting a TNF inhibitor, the patient should be screened for hepatitis and tuberculosis because we have seen viral reactivation, new cases of tuberculosis, and also the reactivation of tuberculosis that may already be latent in the patient’s body. If patients have a history of infection, an active infection, or an active malignancy, we would not use a TNF inhibitor until these conditions are taken care of and put into the background. In some instances, for example, we may treat or begin treatment for tuberculosis or latent tuberculosis and then just wait a very brief period of time and start the patient on a TNF inhibitor. While there are relatively few contraindications, they do need to be observed. But having said that, patients should be considered candidates for biologic therapy, in particular with TNF inhibitors, as early as possible.
 
In addition to the biologic agents that are referred to as the TNF inhibitors, there are other agents that can be used to inhibit other cytokines—inflammatory mediators that can also be abnormal in patients with psoriatic arthritis. For example, the most recent biologic is an agent called secukinumab, which is an inhibitor of interleukin (IL)-17. This agent also has shown efficacy in psoriatic arthritis. There is another agent called ustekinumab, which inhibits 2 other inflammatory mediators called IL-12 and IL-23. Clinical experience would suggest that while this agent is indicated for both skin disease and joint disease, it appears to work more in reducing the skin burden of disease than the joint burden of disease. Finally, we also have a small molecule called apremilast, which is a phosphodiesterase 4 (PDE4) inhibitor. That, too, has shown great efficacy in the treatment of patients with psoriasis and psoriatic arthritis.

Transcript edited for clarity.

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