The pathophysiologic mechanisms of TNFi-induced psoriasis are not completely understood. I suspect that TNFi agents may downregulate some of the inhibitory cells of the immune system that hold psoriasis in check before actually improving psoriasis. TNFi agents can induce psoriatic eruptions or worsen preexisting psoriatic skin disease in patients with rheumatoid arthritis (RA) and inflammatory bowel disease (IBD). One theory is that some individuals with RA and IBD may have a genetic predisposition to TNFi-induced psoriasis; another is that TNFi therapy increases risk for infection-induced psoriasis. While these mechanistic suggestions are possible, they are, at this time, speculative. I am not aware of any data that prove any of them. From my perspective, the mechanisms are mostly irrelevant as long as you are making the right diagnosis and treatment recommendations, including the consideration of agents outside of the class, when warranted.

TNFi-induced psoriasis is a rare phenomenon, although it is likely underrecognized by rheumatologists and gastroenterologists. For example, as a dermatologist treating psoriasis, I may not perform a complete musculoskeletal examination looking at range of motion and gait as often as a rheumatologist treating RA would. Likewise, a rheumatologist who is treating the patient’s RA may not be as likely to perform a complete skin examination. So, there is the potential for selection bias in recognizing TNFi-induced psoriasis. Another relevant example of selection bias is that when TNFi agents were first approved by the US Food and Drug Administration for RA, there was some inkling that they might be effective for psoriasis, but this had not been my experience. None of the patients with psoriatic arthritis who were prescribed TNFi therapy by their rheumatologist and referred to me for psoriasis had clearing of their psoriasis. I would see patients with psoriatic arthritis, who had been treated previously by rheumatologists, for their psoriasis because it had not cleared up; every time a patient’s skin cleared with the TNFi, they would not have to schedule an appointment with me because there were no skin problems to report. 

If you are a medical dermatologist and you care for patients with inflammatory dermatologic conditions, there is a good chance that you will never see a case of TNFi-induced psoriasis. If you are a psoriasis specialist, you will probably see a few cases over the course of your career. I suspect that most RA or IBD specialists who are regularly treating patients with TNFi therapy will likely never see a case of TNFi-induced psoriasis. Finally, it is worth noting that some genes that are linked to psoriasis, RA, and IBD are shared by all 3 of these disorders. This means that some patients with RA or IBD who develop TNFi-induced psoriasis may have been on the road to developing psoriasis at some point anyway.