HEPATITIS-C VIRUS-INFECTION IN ITALIAN PATIENTS WITH ORAL LICHEN-PLANUS - A PROSPECTIVE CASE-CONTROL STUDY

Citation
M. Carrozzo et al., HEPATITIS-C VIRUS-INFECTION IN ITALIAN PATIENTS WITH ORAL LICHEN-PLANUS - A PROSPECTIVE CASE-CONTROL STUDY, Journal of oral pathology & medicine, 25(10), 1996, pp. 527-533
Citations number
44
Categorie Soggetti
Dentistry,Oral Surgery & Medicine",Pathology
ISSN journal
09042512
Volume
25
Issue
10
Year of publication
1996
Pages
527 - 533
Database
ISI
SICI code
0904-2512(1996)25:10<527:HVIIPW>2.0.ZU;2-C
Abstract
To assess the aetiology of liver disease associated with lichen planus , we prospectively studied 70 consecutive newly diagnosed patients wit h oral lichen planus (OLP) living in northwest Italy (Piemonte) and 70 controls matched for age and sex with other oral keratoses coming fro m the same district. Twenty-two patients with OLP (31.4%) and 9 contro ls (12.9%) were found to be affected by chronic liver disease (CLD) (P =0.014). In sixteen of the 22 OLP patients with CLD the liver disease was hepatitis C virus (HCV)-related, whereas 2 of the 9 controls had a HCV-related CLD (P=0.016). In another OLP case, liver damage was rela ted to a combination of HCV and alcohol abuse. The prevalence of HCV a ntibodies in the whole OLP group (27.1%) was significantly higher than in controls (4.3%) (P=0.014), whereas no difference was found between the OLP and control groups regarding hepatitis B virus markers and ot her common causes of CLD. HCV infection was more frequently found in p atients with erosive OLP (58.8%) than in patients with non-erosive OLP (13.2%) (P=0.004). Serum HCV-RNA was detected by polymerase chain rea ction (RT-PCR) in the majority (93.7%) of OLP patients who had HCV ant ibodies. Excluding OLP and control patients with HCV markers, there wa s no difference between the two groups regarding frequency of CLD. Our data show that HCV is probably the main pathogenic factor in liver di sease of Italian patients with OLP, and suggests that HCV could be inv olved in the pathogenesis of OLP.