Edward W. Cowen, MD, MHSc, senior clinician and acting branch chief, Dermatology Branch, National Institutes of Health, speaks on cytokines involved in the pathophysiology in pustular psoriasis and off-label therapy use.
There are several important cytokines involved in the pathophysiology of pustular psoriasis, with current treatment relying on a trial and error approach for the off-label use of psoriasis therapies, said Edward W. Cowen, MD, MHSc, senior clinician and acting branch chief, Dermatology Branch, National Institutes of Health.
Can you describe the pathophysiology of pustular psoriasis and how it compares with psoriasis?
So, targeting specific cytokines, including TNF [tumor necrosis factor], IL [interleukin]-12, IL-23, and IL-17, this has risen as a very effective way to manage classic plaque psoriasis. Pustular psoriasis may share overlapping pathways of inflammation, but we've also learned over the past several years that IL-36 is a particularly important cytokine in patients who have an inherited form of pustular psoriasis.
How has off-label use of approved psoriasis therapies fared in addressing treatment needs for those with pustular psoriasis?
Most of the data for use of the newer targeted therapies for pustular psoriasis is really based on anecdotal reports or small open-label trials. So, in part this is due to the relative rarity of the pustular forms of psoriasis, but this has also resulted in a bit of a trial-and-error approach to see which treatment might work best for a given patient with either localized or generalized disease.