Lead researcher Emma Guttman-Yassky, M.D., of the department of dermatology and Laboratory of Inflammatory Skin Diseases, Icahn School of Medicine at Mount Sinai, New York, told Dermatology Times the findings of the report have “the potential of changing the way we treat keloids, a painful and debilitating condition that, up to now, was primarily treated with surgery and radiation (as gold standard).”
The research team is now planning to conduct a study into the effectiveness of dupilumab and other immune-based treatments in patients with keloids.
While many keloid patients have some form of atopy, Dr. Guttman-Yassky says, “We now have a few more patients without atopic dermatitis that responded to dupilumab as well, so I believe it is going to work on all keloid patients regardless of atopic dermatitis.”
The New York researchers also used realtime PCR to evaluate Th2 gene expression (IL-4R, IL-13, CCL18) in lesional and non-lesional keloid skin taken from three female African American patients with severe chronic keloids but no atopic dermatitis and compared the results with those from skin samples taken from five African American patients with healthy skin.
They found that IL-4R, directly targeted by dupilumab, was highly up-regulated in keloid lesions versus controls, IL-13 was significantly increased in lesional and non-lesional keloids versus controls and CCL18 was highly increased in keloids, particularly in non-lesional skin.
Genes involved in cartilage/bone development and highly expressed in keloids, such as cadherin 11 and fibrillin 2, were all significantly increased in keloid lesions compared with non-lesional skin and controls.