ArticleInternational journal of women's dermatology2025
Prior anogenital herpes and human papillomavirus infections are associated with increased risk of lichen sclerosus in a large retrospective cohort study.
Article in International journal of women's dermatology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.
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Who cites it
5 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Molecular Mechanisms in the Etiopathology of Lichen Sclerosus: A Systematic Review.International journal of molecular sciences · 2026Pooled it
- Genital Lichen Sclerosus: From Hidden Mechanisms to Healing Horizons.International journal of molecular sciences · 2026Review
- Comparative Outcomes of GLP-1 Therapy vs. Bariatric Surgery in Patients with Cirrhosis.Obesity surgery · 2026Article
- Stigmatization and bias in interpreting lichen sclerosus risk factors.International journal of women's dermatology · 2025Article
- Increased risk ofAnnals of gastroenterologyArticle
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Lichen sclerosus (LS) is an inflammatory mucocutaneous disorder typically affecting the anogenital region with unknown etiology. It is postulated that infectious etiologies could play a role in pathogenesis. Objective: Herein, we analyze for potential associations between LS and infectious agents. Methods: The TriNetX research network was utilized to compare prevalence of prior infections in patients with versus without LS and risk of LS in patients with versus without prior infections. Results: Patients with versus without LS had a higher prevalence of prior herpes simplex virus (HSV), human papillomavirus (HPV), gonorrhea, chlamydia, Lyme disease, hepatitis B virus, and hepatitis C virus diagnosis. Preceding infections with HSV and HPV were associated with increased risk of developing LS. Preceding vaccination for HPV was associated with decreased risk of LS. Limitations: We were limited to ICD-10 codes and their accuracy. We could not confirm LS histopathologically, separate genital and extragenital LS, or assess specific HPV types. Conclusion: Our study suggests that HSV and HPV infections may be potential LS risk factors.
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