John Tesser, MD; Nehad Soloman, MD; and Jennifer Simpson, DNP, review the pathophysiology of psoriatic arthritis.
John Tesser, MD: Hello, I’m Dr John Tesser, and I am a clinical rheumatologist in Phoenix, Arizona. I am with the group known as Arizona Arthritis and Rheumatology Associates.
I am joined here today in this panel discussion on psoriatic arthritis by one of my partners and colleagues, Nehad Soloman, and one of the nurse practitioners [Jennifer Simpson, DNP], who makes up 1 of 15 advanced practice clinicians that we have in our group. We have 15 rheumatologists, 13 others besides Dr Soloman and myself. We have a very interesting team structure in our group, which I think is important to bring up. It has the compliance of a number of teams of rheumatologists and advanced practice clinicians, which when it’s full is 1 and 2, respectively.
We work as teams of 3 and see a panel of patients that belong to our team, and with 15 different teams within the practice, you can see that we’re a pretty large practice. But I think it’s helpful to see how we all work in 1 practice, in that you will get the perspectives of 2 rheumatologists and 1 nurse practitioner, and we’re all representing different teams. So although we’re in the same group, we don’t necessarily practice exactly the same. As the spirit of this discussion is to review psoriatic arthritis and its management, I think it will be very interesting to get perspective from each of us in how we approach it. I’m very excited to hear Jen’s approach and Nehad’s approach to how we do things.
Let me kick this discussion off by launching into a very brief overview of the disease psoriatic arthritis. We know that it is a disease that affects somewhere between 0% and 6% of the population. We know that, for the most part, patients develop psoriasis well before they develop arthritis, usually on average 10 or 11 years before. We know that around 30% of patients with psoriasis may develop psoriatic arthritis. There’s a fair amount of heritability involved with it, and when we see patients we always ask if there are family members, particularly first-degree family members, who may have the disease. That has some implications in helping us diagnose patients who may not actually have psoriasis when we’re seeing them for their arthritis, a situation that occurs very infrequently, but up to 15% of the time.
There are certain genetic types that key into and increase the risk of patients developing psoriatic arthritis. Certainly, we’re all familiar with HLA-B27, as opposed to the HLA-C family of genes that seem to confer risk for psoriasis. That’s an interesting divergence there that I think is not well understood or well known. The pathophysiology of the disease is very fascinating. We understand that interleukin-23 is extremely important and is one of the upstream cytokines that is important in causing activation of downstream cytokines, including the interleukin-17 family, the TNF [tumor necrosis factor] family. And certainly, the interplay of interleukin-12/23 is also very important. Understanding those cytokine families is the beginning of understanding the different categories of medications that we use as they inhibit different members of these cytokine classes. We’ll get into the treatment of the disease in depth a bit later, but it’s important to point that out.
The other thing about the pathophysiology of the disease that is really important to understand is that we appreciate the focus of the immunologic and inflammatory attack is on the enthesis. That is the insertion of both ligaments and tendons into bone, and it’s one of the ways in which we understand how the disease manifests, where to examine around the joints where the ligaments and tendons are found, as well as in the joints.
The focus is actually on the inflammation in those tissues. Synovitis is almost a secondary phenomenon, although a very important one, and certainly there could be bone erosion as well as deformity, which it will lead to. And all of this is in conjunction with the immediate effects of inflammation of pain, swelling, and stiffness will combine to contribute to functional difficulties. Taking into account functionality is of ultimate importance, and in fact, is very important to the agencies that approve medications. Because if you can’t demonstrate that your medication improves function, you will have a hard time getting approval through the various agencies, and specifically the FDA in the United States.
We appreciate that the disease affects both peripheral joints and the spine, and the sacroiliac joints. The spine in particular is very interesting because the entire spine, vertebrae, and discs, are encased in a very thick network of fibers of ligamentous origin. This helps to understand and explain why back pain in those individuals who are affected can be so diffuse and debilitating. Then of course, involvement of the sacroiliac joints leads to very important pain located in the very lower back and the pelvic region. That’s a very short overview of the disease.
This transcript has been edited for clarity.