Lichen Planus and Hepatitis Viruses

• Lichen planus has associations with liver diseases, including autoimmune chronic active hepatitis, primary biliary cirrhosis (PBC), and postviral chronic active hepatitis.
• PBC association occurs irrespective of penicillamine use.
• Hepatitis C virus (HCV) and lichen planus link is seen in specific endemic regions like East and Southeast Asia, South America, the Middle East, and Southern Europe.
• HCV prevalence is 16% to 29% in southern European lichen planus patients.
• Oral lichen planus patients with liver disease show significantly higher HCV rates in certain populations (78% versus 3%).
• No clear association exists between HCV and pure cutaneous lichen planus.
• Unidentified genetic factors may contribute to the co-occurrence of HCV and lichen planus.
• Human leukocyte antigen-DR6 (HLA-DR6) haplotype may relate to the heterogeneity of HCV and oral lichen planus in endemic regions for both.
• No strong link exists between hepatitis B virus (HBV) and lichen planus.
• Lichen planus patients reportedly have higher dyslipidemia rates and more cardiac risk factors.
• Metabolic syndrome may be more common in individuals who have oral lichen planus.
• Thyroid dysfunction, mainly hypothyroidism, is present in up to 34% of lichen planopilaris patients.
• Lichen sclerosus et atrophicus is observed in up to 16% of oral lichen planus patients, without increased oral lichen planus risk in individuals with lichen sclerosus et atrophicus.
• Recent studies show lichen planus correlates with autoimmune diseases like systemic lupus erythematosus, Sjögren disease, dermatomyositis, vitiligo, and alopecia areata, in the Taiwanese population.
• Lichen planus cases alongside internal malignancy may indicate paraneoplastic autoimmune multiorgan syndrome.

Malignant transformation

• Whether oral lichen planus has inherent malignant potential has been debated.
• Malignant transformation risk is currently believed to be low.
• Risk factors increasing oral cancer likelihood include long-standing disease, erosive or atrophic types, tobacco use, and possible esophageal involvement.
• Oncogenic HPV subtypes, including type 16, are more common in oral lichen planus and could partially explain the malignancy risk.
• Reported rates of SCC development vary: 0.8% of oral lichen planus in the United States, 1.9% in the United Kingdom, 0.6% in China, and 1% in Sweden.
• Most cases involve in situ carcinoma or a microinvasive pattern.
• The tongue is the most common cancer site, followed by the buccal mucosa, gingiva, and rarely, the lip.
• Lesions clinically manifest as indurated, nonhealing ulcers or exophytic lesions with a keratotic surface.
• Red atrophic plaques can also be seen and often correlate with in situ disease.
• Advanced cases can result in nodal metastases and death.
• No overall increased malignancy risk has been observed in cutaneous lichen planus.
• Rare case reports exist of cutaneous SCC arising in long-standing lichen planus lesions.
• Risk factors include hypertrophic or verrucous lichen planus, lower extremity location, history of arsenic or x-ray exposure, and long-standing disease (average, 12 years).