The Pathogenesis of Plaque Psoriasis


Jayme Heim, MSN, FNP-BC, and Matthew T. Reynolds, PA-C, provide an overview of the pathogenesis of plaque psoriasis and how our understanding of the condition has evolved.

Jayme Heim, MSN, FNP-BC: Good evening. Welcome to this HCP Peers & Perspectives® presentation titled: “Expert Physician Assistant and Nurse Practitioner Insights on the Management of Plaque Psoriasis from Real-World Data.” I’m Jayme Heim. I’m a nurse practitioner in Grandville, Michigan, and I work at West Michigan Dermatology. Today I am joined by Matt Reynolds. Matt?

Matthew T. Reynolds, PA-C: Thanks, Jayme. My name is Matthew Reynolds. I’m a dermatology physician assistant located in Little Rock, Arkansas. I have been in practice for about 8 years in Arkansas, serving the rural and suburban communities. Our discussion today is going to focus on the role of long-term and real-world data regarding the safety and efficacy of IL-23 [interleukin 23] inhibitors in the management of patients with plaque psoriasis. Jayme?

Jayme Heim, MSN, FNP-BC: Let’s briefly review the pathogenesis of plaque psoriasis. How has our understanding of this condition evolved over the years?

Matthew T. Reynolds, PA-C: Psoriasis is a chronic inflammatory skin disease that classically presents with well-demarcated red plaques with silvery scale, commonly involving the scalp, elbows, knees, the presacral region. Some other areas of interest are the palms, soles, and even the nails and genitalia. Psoriasis is an inflammatory, immune-mediated condition involving cutaneous T cells, dendritic cells, and keratinocytes, with subsequent release of a variety of cytokines and other soluble mediators. Now, largely we believe that psoriasis is a TH1 [helper T cell type 1]-mediated disease, and there are several chemical signals that are responsible for the effects that we see in keratinocyte hyperproliferation that manifest as these scaly plaques that we see in our patients. They also contribute to the augmented inflammation underlying several systemic disease associations, such as metabolic syndrome, cardiovascular disease, and even psoriatic arthritis. Specifically, our understanding of the psoriasis pathway has evolved substantially over the past decade. We’ve identified more selective targets that involve immune suppression and overall, more effective treatment success. From the time of drugs like adalimumab and ustekinumab, we now know we have isolated select targets specifically on the IL-23 pathway that provide clear skin and minimal side effects in monitoring. Specifically, we have identified the specific subunit of IL-23 that is chiefly involved in the psoriasis pathway, in the P19 unit of IL-23, whereas previously it was thought that the P19 and the P40 subunits were important in the psoriasis pathogenesis. We’ve come a long way in our understanding of psoriasis as a whole. In addition, we now know that psoriasis and a plethora of other comorbid disease associations exist, such as IBD [inflammatory bowel disease], MS [multiple sclerosis], and metabolic syndrome, just to name a few.

Transcript edited for clarity

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