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Abnormal Urinary Coproporphyrin Levels in Patients Infected by Hepatitis C Virus With or Without Human Immunodeficiency VirusA Study of 177 Patients
Bernard Cribier, MD, PhD;
David Rey, MD;
Georges Uhl, MD;
Christophe Le Coz, MD;
Christine Hirth, MD;
Eric Libbrecht, MD;
Denis Vetter, MD;
J.-Marie Lang, MD;
Françoise Stoll-Keller, MD;
Edouard Grosshans, MD
Arch Dermatol. 1996;132(12):1448-1452.
Abstract
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Objective Many cases of porphyria cutanea tarda have been described in association with human immunodeficiency virus (HIV) infection in young individuals. The link between hepatitis C virus (HCV) and porphyria cutanea tarda is even stronger as more than 50% of patients who have this diagnosis in Italy, France, or Spain are also infected by HCV. To study the role of viral infections on the metabolism of porphyrins, we measured the urinary porphyrin levels in patients with HIV and HCV infections.
Design Survey; prospective study.
Setting University Hospital of Strasbourg, France.
Patients Sixty-one HIV-positive patients, 56 HCV-positive patients, 60 HIV- and HCV-positive patients, and 51 HIV- and HCV-negative control subjects were randomly selected. None had clinical signs of porphyria or a familial history of porphyria.
Main Outcome Measures The porphyrin-excretion profile was determined by high-performance liquid chromatography on fresh urine samples. The HIV and HCV viremias were quantified in the serum by the branched DNA assay. Measures were planned before data collection began.
Results The porphyrin-excretion profile typical of porphyria cutanea tarda was found in only 1 of 177 patients. In the remaining 176 patients, the mean coproporphyrin level was significantly raised in HCV-positive patients and even higher in patients who were HIV- and HCV-positive. The coproporphyrin level was not correlated to the alanine aminotransferase level, the CD4+ cell count, or the HCV and HIV viremias.
Conclusions In cases of infection with HIV, HCV, or both, the development of a porphyria cutanea tarda urinary profile is a rare event (0.56% in this study), but coproporphyrin excretion is increased. This could be related to hepatic changes induced by the viruses. Our results do not support the hypothesis of a direct viral effect on the porphyrin metabolism. Infection with HIV, HCV, or both may be a major triggering factor, but is not sufficient to induce porphyria.
Arch Dermatol. 1996;132:1448-1452
Author Affiliations
From the Dermatology Clinic (Drs Cribier, Le Coz, and Grosshans), Centre d'Information et de Soins de l'Immunodéficience Humaine (Drs Rey, Libbrecht, and Lang), the Hepatogastroenterology Department (Drs Uhl and Vetter), the Laboratory of Biochemistry (Dr Hirth), and the Institute of Virology (Dr Stoll-Keller), Strasbourg University Hospital, Strasbourg, France.
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Arch Dermatol 1996;132:1503-1504.
ABSTRACT
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