[Skip to Content]
Access to paid content on this site is currently suspended due to excessive activity being detected from your IP address 54.166.74.94. Please contact the publisher to request reinstatement.
[Skip to Content Landing]
Article
December 1996

Hepatitis C Virus and Human Immunodeficiency Virus Infection Can Alter Porphyrin Metabolism and Lead to Porphyria Cutanea Tarda

Author Affiliations

Dermatology Branch National Cancer Institute Bldg 10/Room 12N238 10 Center Dr MSC 1908 Bethesda, MD 20892-1908 (e-mail: Andrew_Blauvelt@nih.gov)

Arch Dermatol. 1996;132(12):1503-1504. doi:10.1001/archderm.1996.03890360095016
Abstract

DAMAGE TO the liver with impairment of hepatic uroporphyrinogen decarboxylase can lead to the development of sporadic porphyria cutanea tarda (PCT).1 In older studies, agents most commonly implicated in the induction of PCT included alcohol, estrogens, iron, polychlorinated hydrocarbons, and hepatitis B virus. Recently, however, PCT has been frequently associated with infections by other viruses, namely, hepatitis C virus (HCV)2-5 and human immunodeficiency virus (HIV).6-9 Two studies in this issue of Archives examine these associations in more detail.10,11 The purposes of this editorial are to review recent information on this topic and to provide practical guidelines to dermatologists on the evaluation for underlying HCV and HIV infection in patients with photosensitivity or overt PCT.

Screening measures to detect hepatitis A and B viruses in the blood supply were developed in the early 1970s, and soon thereafter it became surprisingly clearthat most cases of transfusion-associated hepatitis were not due to these viruses, but to another agent,

First Page Preview View Large
First page PDF preview
First page PDF preview
×