Erin Boh, MD, PhD, FAAD, shares insight into clinical manifestations of plaque psoriasis, and panelists emphasize how disease characteristics may be mistaken for signs and symptoms of commonly comorbid diseases.
Brad Glick, DO, MPH: What about the clinical manifestations of plaque psoriasis?
Erin Boh, MD, PhD, FAAD: George hit on it a little. We see the classic psoriasis: scaling, erythematous plaques that are often bilateral or symmetrical, involving elbows and knees. The scalp is a very common area that is involved and difficult to treat, I might add, but we also have other forms of psoriasis. You want to remember that you can have inverse psoriasis. It is not the classic, scaling plaque that you might see with regular psoriasis. It might present as beefy, red, macerated skin in the groin, not unlike HS [hidradenitis suppurativa] or other comorbidities that share the same cytokine. I think you want to look at all the parts of the body: nails, scalp, the skin, and certainly, do not forget the genitals. I find that is one that, as dermatologists, we often forget to look at because we do not want to go there. We did a study in our clinic that showed that patients do not bring it up, but would like people to look there, because they often cannot. They might have itchy skin and they do not put that together and realize it is psoriasis. You do not see pictures of that often. I think the thing to think about is what George said, because of the pathophysiology, these inflammatory cytokines share characteristics with a lot of other disease states. We must think of immune-mediated inflammatory disease as a whole group and psoriasis is just 1 of them. We must be aware, when we examine our patients, to look for HS, to ask them questions about IBD [inflammatory bowel disease] because they all share those same cytokines. The end result is scaling in the skin, the scalp, mucosa, and other places.
Brad Glick, DO, MPH: Talking about the cytokines makes me think about background comorbidities. Tell us about some of the comorbidities associated with psoriatic disease and what the impact is on those comorbidities.
Erin Boh, MD, PhD, FAAD: Obviously, the one that is the elephant in the room is psoriatic arthritis, correct? We all know that psoriasis and psoriatic arthritis go together, but there are a number of them, like obesity or metabolic syndrome. We know that the same inflammatory cytokines are involved in making atherosclerotic plaque. We have coronary artery disease, obesity, psoriatic arthritis, and even inflammatory bowel disease, because they share some of the common cytokines such as TNF [tumor necrosis factor]. Those sorts of things occur in much greater incidences in patients with psoriasis. We need to ask our patients about those comorbidities, because that too can help when you come down to what your treatment algorithm is going to be. We want to treat as many of the disease processes with 1 drug as we can. It is logical to ask those questions of patients and then look for other disease processes that have much higher incidences in patients with psoriasis.
Brad Glick, DO, MPH: Neal, do you have any other comments relating to comorbidities, your perspective, how you approach patients, and the impact on comorbidities as it relates to psoriatic disease?
Neal Bhatia, MD: I think Erin hit a big one about being cognizant about what is under the hood with a lot of these patients. If we are not looking into their weight, their lifestyle, their cardiovascular risk, and history, then all of that discussion of systemic therapy could be for naught. I think, as a specialty, we need to ramp up our inquiries of these patients and how much is going on in their medical history. I want to go back to one of the things George said about the characterization of the immune mechanisms, hypersensitivity, and autoimmune diseases. These are words that get thrown around a lot by patients who sit there on Dr Google and go to the chat rooms.
I always must make sure that I am reminding patients about what is truly autoimmune. In some cases, they tend to cross more the Th2 [T helper cell type 1] side of the fence if anything, but we do not want patients to equate psoriasis with lupus in terms of approaches because they may be the exact opposite part of the immune shelf. I think the one thing that both George and Erin brought up nicely is process. If we are not stopping the process in its tracks and are just constantly mopping up the mess, we are not going to get patients out of their own way in terms of their futures. We want patients to think about what their outcome is going to be in 6 months, not just 6 days or 6 weeks. We want them to think about what we can do to change the quality of their lives with these interventions. I think a lot of that goes hand in hand with the way we define it ourselves.
Brad Glick, DO, MPH: Well said.
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Transcript edited for clarity.