The connection between prurigo nodularis and atopic dermatitis, particularly concerning chronic itch, was a key topic at the 44th Annual Fall Clinical Dermatology Conference. Shawn Kwatra, MD, Associate Professor of Dermatology at Johns Hopkins University School of Medicine, highlighted the shared pathophysiology between these conditions and its implications for therapeutic development.
Kwatra noted that while prurigo nodularis presents with fibrotic nodules and atopic dermatitis with eczematous lesions, the morphology is often genetically encoded, but there are shared elements of pathophysiology. Key cytokines such as IL-4, IL-13, and IL-31 are conserved between these diseases, driving similar mechanisms of itch and inflammation.
"In atopic dermatitis, you have many eczematous lesions and in prurigo nodularis, you have these fibrotic nodules," Kwatra explained. "What we know is the morphology of these lesions is oftentimes genetically encoded...but there's elements of shared pathophysiology. So IL-4, IL-13, and IL-31, many of these similar cytokines are conserved between these different diseases."
This shared pathophysiology has already led to therapeutic success, with dupilumab approved for both conditions. Furthermore, nemolizumab, already approved for prurigo nodularis, is anticipated to receive approval for atopic dermatitis as well, reinforcing the importance of targeting common pathways.
Novel Therapies on the Horizon
Kwatra emphasized the emergence of novel targeted therapeutics for atopic dermatitis, including nonsteroidal topical therapies. These include topical PDE4-inhibitors, topical JAK inhibitors, and aryl hydrocarbon modulators, which offer alternatives to the long-standing reliance on topical steroids.
"The latest advancements in atopic dermatitis are a whole host of novel targeted therapeutics," Kwatra said. "We have nonsteroidal topical therapies, topical PDE4-inhibitors, topical JAK inhibitors, and aryl hydrocarbon modulators..."
In addition to topical advancements, Kwatra highlighted the development of new biologics targeting interleukin (IL)-4 receptor alpha, as well as IL-13 and IL-31, which hold significant promise for managing chronic itch in both prurigo nodularis and atopic dermatitis. These advancements reflect a deeper understanding of the shared immunological mechanisms driving these conditions, paving the way for more effective and targeted treatments.
