EPIDEMIOLOGY OF HEPATITIS-C AND HEPATITIS-G IN SPORADIC AND FAMILIAL PORPHYRIA-CUTANEA-TARDA

From 1995 to 1997, we prospectively evaluated the prevalence of hepati tis C virus (HCV) RNA in 124 patients with porphyria cutanea tarda (PC T) from Northern France (83 sporadic and 41 familial PCT). Serum sampl es were analyzed for ferritin, transaminases, HCV antibodies, and HCV RNA. In addition, genotyping of HCV and searches for HCV infection ris k factors (blood transfusion, iv drug abuse, and surgical intervention ) were performed. Twenty-six of 124 patients (21%; 95% CI: 13.9-28) we re positive for serum HCV antibodies. All of them were also positive f or HCV RNA. The prevalence of HCV infection was higher in the sporadic PCT group (26.5%, 22 out of 83) than in the familial PCT group (9.7%, 4 out of 41). Risk factors for hepatitis C infection were found to be significantly increased in the HCV-positive group when compared with the HCV-negative PCT group. In all HCV-positive patients with a risk f actor, the suspected date of exposure to the virus always preceded the clinical onset of PCT The HCV genotype pattern in PCT patients was si milar to that observed in nonporphyric HCV patients in western Europea n countries. Serum ferritin level was increased in both HCV-positive a nd HCV-negative porphyric patients. Transaminase levels were significa ntly higher in HCV-infected PCT patients. Sixty-seven out of 124 patie nts were retrospectively studied for hepatitis G virus (HGV) infection . Six of these 67 patients (8.9%; 95% CI: 2.1-15.8) were positive for HGV RNA. None of the six HGV;infected patients were positive for HCV R NA. The HGV-infected patients did not differ statistically from those without HGV infection with regard to age, ferritin, transaminase level s, and PCT treatment. These results support the view that sporadic cas es of HGV infection may occur frequently. This study of a large cohort of HCV and PCT patients further documents an increasing gradient in H CV prevalence from northern to southern Europe, and shows that HCV inf ection acts as a triggering factor of PCT. Finally, the HGV prevalence found in the PCT patients was comparable with that found in French bl ood donors, suggesting that HGV is not a PCT triggering factor.