Lichen sclerosus is a common disease that can significantly affect an individual’s quality of life. Despite this, it is a condition that is often overlooked by healthcare professionals. By identifying the underlying genetic pathways, we pave the way for disease risk prediction, better treatments and potentially prevention.
Dr Christos Tziotzios, Reader in Clinical and Molecular Dermatology at King’s College London and Consultant Dermatologist at Guy’s and St Thomas’ NHS Foundation Trust, senior author
19 March 2026
New study identifies genetic differences linked to common inflammatory skin condition
Researchers at King’s College London have conducted the largest genetic study of the chronic inflammatory skin condition lichen sclerosus, providing novel insights into the genetic variation seen in those with the condition.
The findings, published in the British Journal of Dermatology, could help to explain why some people are more susceptible to developing the condition than others and pave the way for earlier identification of people at risk, and better treatments.
Lichen sclerosus (LS) is a chronic and highly debilitating inflammatory condition that affects mostly the genital skin in both women and men. With an estimated 2% of the population affected by the condition at some point in life, LS can cause significant psychological suffering and impact on quality of life due to pain, stinging and effects on intimate relationships.
The condition has long been thought to be caused by irritation from urine, but it’s not clear why some people are more susceptible to developing LS than others.
To better understand the genetic basis of the condition, researchers studied the genomes of 6,681 women and 970 men with LS and compared them to the genomes of people without the condition. The team used national biobanks from the UK, Norway and Finland.
They found that the risk of developing LS was associated with differences in the DNA sequence at 14 different parts of the genome, highlighting a number of likely LS genes. The strongest genetic link identified by the team involved an immune system gene known as HLA-DRB1, which plays an important role in how the body recognises and responds to infections.
The findings also suggest that LS is driven by changes in immune system activity, particularly in pathways involved in T-cell responses (a type of immune cell), the way cells present antigens (molecules that trigger immune reactions), and processes linked to tissue scarring (fibrosis). The authors say these findings help to explain why LS is sometimes seen alongside other inflammatory and scarring skin conditions.
Interestingly, the researchers also discovered a link between LS and variation in the ALDH2 gene, which is involved in how the body processes alcohol and manages damage caused by toxic molecules in the body. This unexpected finding opens up new directions for research into how other chemical processes in the body might contribute to the disease.
It's great that, with the support of our Norwegian and Finnish colleagues, we have identified so many genetic factors that contribute to the development of lichen sclerosus. We know from our experience with other skin conditions that genome-wide association studies can instigate a wide range of research focused on preventing disease and improving outcomes for patients.
Dr Nick Dand, geneticist and lead analyst for the study at King’s College London
This study was supported by a research grant from the British Skin Foundation. Dr Tziotzios is supported by the Medical Research Council (Grant MR/X030466/1).
We are always encouraged to see the positive impact of research supported by the British Skin Foundation. These important discoveries play a vital role in improving patient outcomes over time, which remains central to our mission.
Phil Brady, Chief Operating Officer at the British Skin Foundation
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Adjunct Reader in Clinical and Molecular Dermatology
UKRI Innovation Fellow at HDR UK