Clinical Management of Psoriatic Arthritis

Allan Gibofsky, MD: The first thing to be aware of is that not all joint pain in patients with psoriasis is psoriatic arthritis. Even when patients are referred to the rheumatologist, they’re often referred back with the diagnosis of osteoarthritis or mechanical joint pain that is noninflammatory in nature. These patients can generally be managed fairly well, by the general physician, with nonsteroidals and mild analgesics (where appropriate). It is only when the patient has inflammatory arthritis (confirmed by the rheumatologist as psoriatic arthritis) that other considerations begin to apply.

The nonsteroidals are generally the first line of therapy, but those only affect the pain and inflammation. One needs agents that will actually affect the disease process itself to deal with the cause of the pain and inflammation. And so, in psoriatic arthritis, the conventional synthetic agents, such as methotrexate, leflunomide, and sulfasalazine, are often used (although the evidence for their effectiveness in each of the subgroups of psoriatic arthritis is really not as good as one would think). Nevertheless, these agents are often used, and sometimes in some patients, these agents are able to effectively control the symptoms and possibly even slow down the course of the disease.

In the majority of patients, however, we tend to move beyond conventional synthetic disease-modifying agents to the biologic agents. The biologic agents have really been a game changer, or a paradigm shift (depending upon your perspective), in the management of the seronegative spondyloarthropathies and, in particular, psoriatic arthritis. In the class of agents called the biologic agents, we have a subclass called the TNF inhibitors. TNF stands for tumor necrosis factor inhibitors. This is a class of agents that inhibits a naturally occurring substance in the blood and tissues that, when elevated, can cause significant inflammation in the joints as well as in other tissues. So, the TNF inhibitors—agents like adalimumab, etanercept, infliximab, certolizumab, and golimumab—are often used in the treatment of rheumatoid arthritis in varying doses (depending upon the severity of the disease), sometimes with an underlying conventional synthetic DMARD (disease-modifying antirheumatic drug), although more often without it because of their effectiveness and their ability to modify the disease even when given as monotherapy.

There are 5 agents in the class of TNF inhibitors—adalimumab, etanercept, golimumab, infliximab, and certolizumab. They differ in terms of their routes of administration as well as their frequency of administration (depending upon the patient). For example, infliximab is given exclusively, intravenously and it is weight-based, as so many milligrams per kilogram. Adalimumab and etanercept, as well as certolizumab, are given as subcutaneous injections. They are different in terms of how often they are given, and also there is the possibility of being given in the doctor’s office. Finally, you have golimumab, which is available in both an intravenous and subcutaneous formulation. Most patients, if not all, do prefer (if they can get it) a subcutaneous administration that they can self-administer as opposed to an intravenous administration that requires a trip to the physician’s office or an infusion center. Taken together, these are the [ways] that the 5 TNF inhibitors work—meaning by inhibiting the agent tumor necrosis factor.

The flip side of efficacy is, of course, safety. There’s no such thing as a free lunch, and by that I mean that there is an increased risk of infection with all of these agents. There is an increased risk of malignancy, there is an increased risk of the potential for autoimmune reactions, and so on. Because of the risk of infection, we mandate that patients be tested for tuberculosis and hepatitis—both before these agents are started as well as periodically during the course of treatment (depending upon whether the circumstances of the patient has changed). By that I mean that if a patient is stable on a TNF therapy, I would generally only check and recheck him/her once a year. But if the patient, though stable, travels to an endemic area of the world where there is tuberculosis, or is admitted to jail, or is a resident in a nursing home or some other congregate care facility, I might check them after they emerge from that facility because these are known to be areas where there is a higher risk of contracting the disease. And we know that TNF inhibitors lower their likelihood of being able to defend against tuberculosis because of the way that they work.

Transcript edited for clarity.