Video
Allan Gibofsky, MD: Like rheumatoid arthritis, there are 3 domains of efficacy that we look for in the treatment of psoriatic arthritis. They are relief of signs and symptoms, improvement in patient-reported outcomes, and, more appropriately, inhibition of structural progression. The inhibition of structural progression is important because that actually shows whether or not you’re affecting the disease or just the symptoms. But let’s face it, no patient ever comes in complaining of structural progression. They come in complaining of pain, or limitation of motion, or inability to perform their routine activities of daily living. So those become the paramount domains that we look to affect. Patients need to be advised that agents, when used appropriately, can affect, significantly, all the domains of efficacy. And while we may only look at x-ray progression every year or so, the patients are told that we are going to be looking at their spine, if necessary, or their joints, primarily, to see whether we can inhibit the formation of erosions and, if possible, affect some reduction of the erosions that are already there when they are noticed. We are moving away from studies that involve X-rays to studies that involve MRI or ultrasound to give us the same information about the joint patterns of destruction even earlier and, in doing so, expose patients to less radiology procedures and fewer doses of X-rays.
When we do x-ray the hands of people with psoriatic arthritis, we often see not just erosions which may be nonspecific, but we also may see, in some patients, the characteristic erosion pattern called “pencil-in-cup deformity.” In that situation, the fingers are affected, primarily. You see the second phalanx eroded and the first phalanx eroded, but the characteristic picture is that the second phalanx has been eroded symmetrically to look like a pencil and the first phalangeal joint has been affected to flair out like a cup—hence the term, “pencil-in-cup deformity.”
There are a number of things that people will ascribe the occurrence of their disease to. The fact is that we don’t really have hard evidence that any one thing is a trigger, either for the disease or for any of the features of the disease. Our overriding belief is that inflammatory diseases occur in genetically susceptible individuals who encounter an environmental trigger or triggers. Having said that, while we are learning more about some of the genetic background that may predispose to psoriatic arthritis, we really don’t have a good idea of what the environmental trigger, or triggers, may be in that instance. We do know, for example, that similar features to the axial form or spine form of psoriatic arthritis also may occur in people who have inflammatory bowel disease and a different genetic composition. We also know that similar features to the spine involvement in psoriatic arthritis may occur in people with axial spondyloarthropathy or ankylosing spondylitis and there, too, may be different genetic susceptibility factors and different environmental triggers.
Transcript edited for clarity.