Introduction

Lichen planus (LP) is a papulosquamous disorder characterized by pruritic, purple, polygonal, plain topped, papules occurring in the flexor aspects of the extremities with occasional nail (classically pterygium) and oral mucosal involvement. ₁ The exact etiology of lichen planus remains elusive. Several pathogenic mechanisms like immunogenic, genetic, infective, metabolic and many others, with emphasis on interaction between endogenous-genetic-autoimmune and exogenous-environmental components such as drugs or infections have been proposed to play a role in the etiology of the disease. ₂ The role of Hepatitis C virus (HCV) infection in the causation of lichen planus (LP) is controversial as many studies from around the world, ₃ including several studies from various parts of India, have shown contradictory results. We conducted a study to look for an association between Hepatitis C Virus infection and lichen planus in our institution in Pondicherry.

Materials and methods

Third generation ELISA (Innova HCV ELISA) for anti-HCV antibodies in the plasma/serum was performed in 40 consecutive cases of LP (confirmed by clinical examinations and histopathology) and an equal number of age- and gender-matched healthy volunteers from October 2001 to May 2003.

Results

The mean age of cases and control groups were 32.1±10.7 years (range of 19-56 years) and 32±9.3 years (range of 20-54 years), respectively. Number of cases and controls in the different age groups showed no significant difference. There were 19 males and 21 females in both the groups. There were 32 cases of LP involving the skin only, 4 cases involving the skin and the oral mucosa, 3 cases involving the oral mucosa only, and one case of nail LP. ELISA test for anti-HCV antibodies was negative in all the LP patients as well as in all the healthy volunteers.

Discussion

Mokni et al ₄ published the first report of LP associated with HCV infection. Subsequently, a number of studies claimed such a causal association between HCV infection and LP. ₃₅₆ A number of studies, on the other hand, failed to show any association between HCV and LP. _37891011 Nagao et al ₃ demonstrated the existence and replication (by RT-PCR) of HCV within oral LP lesions. Erkek et al ₃ found that the detection rate of HCV-RNA was higher in the lesional skin compared to non-lesional skin in HCV-infected LP patients. Oral LP after treatment of HCV infection with IFN-, ₁₂₁₃ and subsidence of such lesions after stopping IFN therapy ₁₃ have also been reported. The prevalence of HCV in LP patients shows wide geographic variations – 0% in England, ₁₄ 3.8-28.6% in France, ₃ 0-55% in USA, 37.8-62% in Japan, ₃ and 4-65% in Italy ₃ . The reason for such variability is not clear, but may be because of geographic variations or a genetic susceptibility.

From an epidemiological standpoint, the main studies describing a strong association with HCV have been conducted mostly in Japan, Italy and Spain, all areas with a high HCV endemicity. ₁₅ Campisi et al ₁₅ found that a weak association between oral LP and HCV infection may exist only in areas where HCV is endemic. In India, studies conducted in Calicut, ₁₆ Kolkata, ₁₀ New Delhi ₁₀ have failed to demonstrate a statistically significant association between HCV and LP, whereas studies conducted in Hyderabad and Bangalore ₁₀ have shown a significant association. We have not found any association between lichen planus and HCV infection in our tertiary care center in Pondicherry. Whether the absence or the presence of an association between HCV infection and LP in different parts of India is due to the varied prevalence of HCV infections in different parts of the country is difficult to emphasize, as no consistent association between high prevalence of HCV infection in the population and the occurrence of LP has been found in the Indian studies (Table 1).

Figure 1

Table 1: Association between HCV infection and LP compared with the prevalence of HCV infection in different parts of India

Very recently, Carrozzo and Gandolfo maintained that the substantial geographical heterogeneity could be partially explained by immunogenetic factors related to the population. ₁₇ Thus, the role of HCV in LP could be postulated to be one of a triggering factor in suitable environmental, immunogenetic and geographic conditions. ₁₇