PORPHYRIA-CUTANEA-TARDA AND HEPATITIS-C VIRAL-INFECTION - A CLINICAL AND VIROLOGICAL STUDY

Citation
B. Cribier et al., PORPHYRIA-CUTANEA-TARDA AND HEPATITIS-C VIRAL-INFECTION - A CLINICAL AND VIROLOGICAL STUDY, Archives of dermatology, 131(7), 1995, pp. 801-804
Citations number
19
Categorie Soggetti
Dermatology & Venereal Diseases
Journal title
ISSN journal
0003987X
Volume
131
Issue
7
Year of publication
1995
Pages
801 - 804
Database
ISI
SICI code
0003-987X(1995)131:7<801:PAHV-A>2.0.ZU;2-U
Abstract
Background and Design: The role of hepatitis C virus (HCV) infection i n porphyria cutanea tarda (PCT) is probable since the global HCV antib ody prevalence among patients with PCT is about 70%. The purpose of th is study was to evaluate the virologic characteristics in 12 patients with sporadic PCT and in one patient with familial PCT. Anti-HCV antib odies were detected by enzyme-linked immunosorbent assay and confirmed by recombinant immunoblot assay. Hepatitis B virus and antihuman immu nodeficiency 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-n egative patients. The HCV RNA was detected in all patients who had HCV antibodies, and the replicative intermediate of HCV was detected in t hree of them. The positive RNA. titer ranged from 1:10 to 1:10(6). Fou r patients were infected by HCV genotype I, two by genotype II, and on e 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 dete cted. All patients were negative for the human immunodeficiency virus. Conclusions: The HCV infection rate was high (58%) in this series, an d all HCV-infected patients had HCV RNA, reflecting an active replicat ion 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 indirec t role of HCV.