Impact of smoking on histological liver lesions in chronic hepatitis C.

AIMS AND METHODS: To examine the association between smoking and histological liver lesions in chronic hepatitis C, we studied 244 consecutive patients (152 men, 92 women; mean age 45.9 (12.6) years) with histologically proven chronic hepatitis C. Daily tobacco consumption during the six months preceding liver biopsy was recorded as the number of cigarettes smoked daily. Total lifetime tobacco consumption was recorded as the number of cigarette packs smoked per year (packs-years). Liver biopsy specimens were graded for histological activity and fibrosis according to the METAVIR scoring system. RESULTS: The proportion of patients with moderate (A2) or marked (A3) activity increased gradually from 62.0% in non-smokers to 81.7% in patients who smoked more than 15 cigarettes per day (p<0.009). A similar relationship was observed with total lifetime tobacco consumption: 59.0% of patients who had never smoked had grade A2 or A3 disease activity compared with 84.6% of patients who smoked more than 20 packs per year (p<0.002). Multivariate analysis showed that age over 50 years (odds ratio (OR) 5.4), alcohol intake exceeding 20 g/day (OR 2.75), and tobacco consumption of more than 15 cigarettes/day (OR 3.6) were independently related to the histological activity score. No relationship was found between the severity of fibrosis and either daily tobacco consumption or total lifetime tobacco consumption. Multivariate analysis showed that only age over 50 years (OR 8.8), daily alcohol intake exceeding 30 g/day (OR 3.4), and histological activity score (OR 7.9) were independently related to the fibrosis score. CONCLUSION: This study suggests that smoking, independent of alcohol, could aggravate the histological activity of chronic hepatitis C and that patients with chronic hepatitis C virus infection should be advised to reduce or stop smoking.

Lichen planus and hepatitis C virus--related chronic active hepatitis.

BACKGROUND AND DESIGN: An increased prevalence of chronic liver disease has been reported in patients with lichen planus (LP). We report six cases of LP associated with chronic active hepatitis and actively replicating hepatitis C virus (HCV). RESULTS: We studied six patients (three men and three women; mean age, 61 years; age range, 47 to 70 years) with various forms (cutaneous and/or mucosal) of LP and abnormal liver test results. Four patients had severe mucosal lesions. Cutaneous and mucosal lesions had a long-term evolution. Liver disease was discovered 2 to 6 years before LP in three cases and was diagnosed at the same time as LP in the three other cases. Liver biopsy performed in five patients showed chronic active hepatitis without cirrhosis in all five cases. Anti-HCV antibodies were detected in all cases by second-generation enzyme-linked immunosorbent assay and confirmed by second-generation recombinant immunoblot assay. Hepatitis C virus RNA was evidenced by means of polymerase chain reaction in the serum samples from the six patients, proving active viral replication. CONCLUSIONS: Lichen planus may be associated with HCV-related chronic active hepatitis. As interferon treatment may induce viral inactivation in some patients with HCV-related chronic liver disease, a search for HCV infection should be systematically performed in patients with chronic LP.

Hepatitis C virus infection can mimic type 1 (antinuclear antibody positive) autoimmune chronic active hepatitis.

Hepatitis C virus (HCV) has been shown to induce anti-liver-kidney microsomal-1 (LKM1) antibody positive chronic active hepatitis, simulating type 2 autoimmune chronic active hepatitis. The cases of five patients presenting with features of type 1 (antinuclear antibody positive) autoimmune chronic active hepatitis and extrahepatic autoimmune manifestations, in whom immunosuppressive treatment had no effect on liver disease are presented. In these patients, HCV infection could be shown by the presence in serum of anti-HCV antibodies and HCV-RNA detected by polymerase chain reaction. These cases suggest the following: (a) chronic HCV infection can mimic type 1, as well as type 2, autoimmune chronic active hepatitis; (b) HCV infection might be systematically sought in patients presenting with features of type 1 autoimmune chronic active hepatitis, with special care in patients who are unresponsive to immunosuppressive treatment.