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July 1995

Porphyria Cutanea Tarda and Hepatitis C Viral InfectionA Clinical and Virologic Study

Author Affiliations

From the Dermatology Clinic, University Hospital (Drs Cribier, Petiau, Heid, and Grosshans), the Virology Institute (Dr Keller and Ms Schmitt), and the Hepatogastroenterology Service, University Hospital (Dr Vetter), Strasbourg, France.

Arch Dermatol. 1995;131(7):801-804. doi:10.1001/archderm.1995.01690190055010

Background and Design:  The role of hepatitis C virus (HCV) infection in porphyria cutanea tarda (PCT) is probable since the global HCV antibody prevalence among patients with PCT is about 70%. The purpose of this study was to evaluate the virologic characteristics in 12 patients with sporadic PCT and in one patient with familial PCT. Anti-HCV antibodies were detected by enzyme-linked immunosorbent assay and confirmed by recombinant immunoblot assay. Hepatitis B virus and antihuman immunodeficiency virus markers were also determined. The polymerase chain reaction was performed to detect the following: (1) both positive and negative HCV RNA strands, (2) HCV RNA titer, and (3) HCV RNA genotype.

Results:  Seven of the 12 patients with sporadic PCT were HCV positive, and the patient with familial PCT was HCV negative. The age at onset of PCT was significantly lower in HCV-positive patients than in HCV-negative pa- tients. The HCV RNA was detected in all patients who had HCV antibodies, and the replicative intermediate of HCV was detected in three of them. The positive RNA titer ranged from 1:10 to 1:106. Four patients were infected by HCV genotype I, two by genotype II, and one patient was coinfected by type I and type II. Three of the seven HCV-positive patients also had HBV antibodies, but HBV DNA was never detected. All patients were negative for the human immunodeficiency virus.

Conclusions:  The HCV infection rate was high (58%) in this series, and all HCV-infected patients had HCV RNA, reflecting an active replication of the virus. The young age at onset of PCT suggests that HCV is a major triggering factor of PCT. Nevertheless, the clinical changes of PCT were not related to the virologic findings, suggesting an indirect role of HCV.(Arch Dermatol. 1995;131:801-804)