Overview of Psoriatic Arthritis (PsA)


Leonard H. Calabrese, DO, provides insight on the pathophysiology of psoriatic arthritis [PsA].

Anthony M. Turkiewicz, MD: Hello, and welcome to this HCPLive® Peer Exchange titled “Evaluation and Management of Real-world Cases of Psoriatic Arthritis.” I’m Dr Anthony Turkiewicz, the director of the clinical research unit at Rheumatology Associates in Birmingham, Alabama. Joining me in this discussion are my colleagues Dr Leonard Calabrese, a professor of medicine at Cleveland Clinic in Cleveland, Ohio; Dr Sheetal Desai, an associate clinical professor of medicine at the School of Medicine at the University of California, Irvine; and Dr Ana-Maria Orbai, an assistant professor at John Hopkins University School of Medicine in Baltimore, Maryland.

Our discussion is going to focus on available biologic therapies for the treatment of psoriatic arthritis. We’ll also discuss diagnostic strategies and clinical clues in the evaluation of patients with PsA [psoriatic arthritis]. In addition, we’ll also look at some real-world cases and discuss some best-course actions for those patients. Let’s start with a brief overview diagnosis of a progression of psoriatic arthritis, and we’ll direct it to Dr Len Calabrese. It’s a loaded question, but if you don’t mind, briefly discuss the high-level overview of PsA pathophysiology for us.

Leonard H. Calabrese, DO: That’s a big question, so I’ll give you the 30,000-foot view of it. I look at psoriatic arthritis as a prototypical immune-mediated inflammatory disease state. Like all diseases, there’s a combination of genetic factors. This disease has been studied extensively genetically, through GWAS [genome-wide association studies] and candidate gene approaches, and we know that there’s the IL-23 gene. We know that there are some class 1 genes of C6 locus; there’s a genetic component.

Like all other IMiDs [immunomodulatory imide drugs], it’s not just the genes. While there’s strong hereditability, there are “extrachromosomal” factors, I like to say. It’s a neologism in biology of all these external environmental factors. Psoriatic arthritis is still a work in progress. There’s an association with obesity, cardiometabolic syndrome, and cardiovascular disease. There’s some suggestion of proinflammatory dietary changes. Something drives that.

Finally, for the pathogenesis, I like to think of psoriatic arthritis as a diverse disease and we’re going to get into this later when we start talking about domains. There are cytokine hubs that drive skin and musculoskeletal inflammatory disease. Engaged in that is IL-23, an upstream inflammatory cytokine that’s released by professional antigen-presenting cells. There are innate lymphoid cells that are involved like gamma delta T cells, ILC3 cells, and MAIT [mucosal-associated invariant T] cells, and they can amplify and become activated in the presence of the cytokine. Then adaptive immunity kicks in, and there’s strong evidence of Th17 [T-helper 17] and Th22 cells.

Once this inflammatory milieu is created, there’s further recruitment of innate cells—polymorphonuclear leukocytes, mast cells. These can enter the circulation—home to skin, home to joints—and result in inflammatory and potentially destructive disease. Over and above that, I’m sure we’re going to get into different clinical expressions: IL-17, IL-23, and I have to add TNF [tumor necrosis factor] because it’s critical to skin and joints in this milieu.

Anthony M. Turkiewicz, MD: Perfect. That was succinctly done in a very difficult question.

Transcript Edited for Clarity

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