Could a Faulty Hormone in the Skin be the Key to Psoriasis? Study Sheds Light - Video

New research strongly suggests the hormone hepcidin may trigger the onset of the condition. This marks the first time hepcidin has been considered a potential causal factor. In mammals, hepcidin is responsible for regulating iron levels in the body. The findings were published in Nature Communication.

The international research team behind this discovery, which includes Dr Charareh Pourzand from the Department of Life Sciences, the Centre for Therapeutic Innovation and the Centre for Bioengineering and Biomedical Technologies at the University of Bath in the UK -- hopes their finding will lead to the development of new drugs able to block the action of the hormone.

Those most likely to benefit from such a treatment are patients with pustular psoriasis (PP) -- a particularly severe and treatment-resistant form of the disease that can affect a patient's nails and joints as well as skin.

Dr Pourzand said, "A new treatment targeting iron hormone imbalance in the skin offers hope. This innovative approach could significantly enhance the quality of life for millions, restoring their confidence and wellbeing."

Currently there is no cure for psoriasis, though treatments that include topical creams, light therapy and oral drugs can help keep symptoms under control for patients with some forms of the condition. Recent treatments have focused on targeting the immune pathways that contribute to psoriasis developing.

Dr Pourzand believes a drug targeting hepcidin has the potential to dramatically improve treatment options for all psoriasis patients.

She said: "Our data strongly suggests hepcidin would be a good target for skin psoriasis treatment. A drug that can control this hormone could be used to treat flare-ups and keep patients in remission to prevent recurrence.

Reference: Abboud, E., Chrayteh, D., Boussetta, N. et al. Skin hepcidin initiates psoriasiform skin inflammation via Fe-driven hyperproliferation and neutrophil recruitment. Nat Commun 15, 6718 (2024). https://doi.org/10.1038/s41467-024-50993-8