Scientists now believe that hepcidin, a hormone produced in the skin, might be the primary cause of psoriasis— a chronic and sometimes severe skin condition affecting 2-3% of people worldwide.
Recent findings suggest that psoriasis, which manifests as red, scaly patches that can severely impact a person’s quality of life, may be linked to hepcidin. The disease is not only persistent and debilitating but can also lead to life-threatening situations.
The latest research points to hepcidin as a significant trigger for psoriasis, marking the first time this hormone has been linked to the condition. In mammals, hepcidin plays a crucial role in regulating iron levels in the body.
The international team involved in this groundbreaking research, including Dr. Charareh Pourzand from the Department of Life Sciences and other centers at the University of Bath in the UK, aims to develop new medications that could inhibit the hormone’s action.
Such treatments would be particularly beneficial for patients dealing with pustular psoriasis (PP), a severe and often treatment-resistant type of the disease that affects skin, nails, and joints.
Dr. Pourzand emphasized that psoriasis significantly alters the lives of those affected. Many experience lifelong issues that can lead to disfigurement, physical pain, and emotional turmoil. The condition can also trigger other serious health problems.
“A novel treatment designed to correct iron hormone imbalance in the skin brings hope. This fresh approach could greatly improve the quality of life for millions, helping to restore their self-esteem and overall well-being,” she stated.
Iron is essential for skin health—but moderation is key
Iron is an important trace element essential for transporting oxygen throughout the body and supporting skin health; it plays vital roles in wound healing, collagen production, and immune response. However, excessive iron in the skin can lead to complications, worsening the negative effects of UV light and contributing to chronic conditions like psoriasis where skin cells multiply excessively.
For over 50 years, studies have indicated increased iron levels in the skin of individuals with psoriasis, but the reasons behind this excess and its implications have been unclear until now.
The current study, published in the prestigious journal Nature Communications, is the first to identify hepcidin as the likely contributor to this phenomenon.
Hepcidin regulates the absorption of iron from food and its release into the body. While it is typically produced by the liver in healthy individuals, this study revealed that in psoriasis patients, it is also synthesized in the skin.
High levels of hepcidin lead to iron overload
In the study, mice—which share many genetic and physiological traits with humans—developed a similar condition to psoriasis after high levels of hepcidin were produced in their skin.
This surplus of hepcidin led to a significant retention of iron in the skin cells, which then caused abnormal skin cell growth and an increased number of neutrophils (a type of immune cell) in the skin’s outer layer.
Both an excess of skin cells and neutrophils are hallmarks of psoriasis.
Psoriasis often runs in families, yet experts also believe that environmental factors, such as obesity, infections, and smoking, contribute to its development.
A chronic disease without a cure
Even though no cure exists for psoriasis, various treatments including topical medicines, light therapy, and oral medications can help manage symptoms for some patients. Recent therapies have focused on targeting the immune responses associated with the disease.
Dr. Pourzand is optimistic that targeting hepcidin could vastly improve treatment options for all those suffering from psoriasis.
She noted, “Our findings suggest that hepcidin could be a valuable target for treating skin psoriasis. A medication that controls this hormone might help manage flare-ups and maintain remission, reducing the chance of recurrence.”
“Moreover, regulating the excess iron in psoriatic skin through tailored iron chelators (compounds that bind to excess iron for removal) may help arrest the unrestrained growth of skin cells—a major focus of our lab’s research in collaboration with experts worldwide from the Skin@Bath Network, including those involved in this study.”
Dr. William Tillett, a senior lecturer at the University of Bath and a consultant rheumatologist with a focus on psoriatic arthritis, commented: “This research conducted by Dr. Pourzand and her team represents significant progress for individuals with psoriasis and the medical teams that treat them.”
“Although we do not fully understand the reasons behind psoriasis development, recognizing hepcidin as a crucial factor opens pathways for new treatment options and actions to prevent the disease in high-risk individuals. Current biologic drugs can be effective but are expensive and not universally available in the UK. Also, they do not work for everyone and may lose effectiveness over time, so exploring new treatment avenues is essential.”
He also cautioned: “However, the process of developing new medications is typically lengthy and expensive, so it is important for patients to have realistic expectations.”
Dr. Penelope Pratsou, a consultant dermatologist and representative for the British Skin Foundation, remarked: “The findings of this study provide fresh insights into the underlying mechanisms of psoriasis. The overproduction of hepcidin in psoriatic skin appears to be a significant factor. This discovery is encouraging for patients, though further studies are necessary to clarify hepcidin’s role and its potential as a treatment target for psoriasis.”
This research initiative is part of the Skin@Bath network, which has been advancing science since 2017 under Dr. Pourzand’s leadership, in partnership with RUH (Bath) and the Bath Institute for Rheumatic Diseases.
