The possible role of human papillomavirus infection in the development of lichen sclerosus

Abstract

Lichen sclerosus (LS) is a chronic inflammatory skin disease of unknown origin predominantly affecting the anogenital area that causes pruritus and pain and is associated with an increased risk of malignancy. In some cases, LS vanishes after application of imiquimod, raising the question whether human papillomavirus (HPV) may have an etiopathogenic role in anogenital LS. The databases MEDLINE and Embase were systematically searched using the PRISMA guidelines. Twenty-seven papers were included that reported the prevalence of HPV in LS and in LS associated with neoplasia. HPV was identified in 0-80% (median 22%) of all LS cases. The prevalence of HPV was higher among male patients with LS (median 29%) than among female patients (median 8%). HPV16 was the most prevalent genotype, but the distribution of genotypes indicates that even low-risk HPV can cause LS. The diverging detection rates are probably due to small sample sizes in the reviewed papers and different detection methods. Factors possibly underestimating the prevalence of HPV are a selective search for high-risk HPV, DNA destruction in fixed tissue, focally residing HPV, and possibly a clearing of HPV before the time of biopsy. Seventy-five percent of sexually active people acquire HPV during their lifetime, thus HPV alone is not a cause of LS. Genetic and immunological host factors and viral factors other than type are likely to contribute. Future studies should include patients with a short duration of symptoms, and biopsies should be multiple and fresh.

Coexistence of genital lichen sclerosus and genital warts

“…HPV infection has been implicated as a causative agent of genital LS (1,6). The median prevalence of HPV in genital LS is 22% (6). One could expect a much higher prevalence of HPV in genital LS because the lifetime prevalence of HPV is high (4).…”

“…One could expect a much higher prevalence of HPV in genital LS because the lifetime prevalence of HPV is high (4). There are some facts that contradict the association of genital LS and HPV as a causative agent, such as the fact that genital LS is never seen in sexual partners; moreover, despite widespread immunization against HPV, there is no decline in the genital LS incidence, and so it can be concluded that there is a lack of clinical correlation of LS with HPV infection (6)(7)(8). Von Krogh et al found that 32% of men afflicted with LS revealed a positive history of penile warts (7).…”

“…HPV reactivation seemed to increase after local corticosteroid therapy. Reactivation of a latent HPV infection may be evoked following topical corticosteroid therapy because of an altered immune response (6,7).…”

Balanitis xerotica obliterans: a review of diagnosis and management

“…Furthermore, a recent systematic search of 27 papers reporting the prevalence of HPV in LS identified that HPV was present in 22% of LS cases. It also highlighted HPV 16 as the most common genotype …”

“…It also highlighted HPV 16 as the most common genotype. 21 There is also growing evidence for a possible autoimmune cause. In vulvar LS lesions, Farrell et al 22 demonstrated increased levels of interferon gamma, tumor necrosis factor, and interleukin-1.…”