Low prevalence of hepatitis C virus infection in porphyria cutanea tarda in germany

Stölzel, Ulrich; Köstler, E; Koszka, Christiane; Stöffler‐Meilicke, Marina; Schuppan, Detlef; Somasundaram, Rajan; Doss, M.; Habermehl, Karl O.; Riecken, E. O.

doi:10.1002/hep.1840210604

Cited by 91 publications

(45 citation statements)

References 24 publications

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“…However, recent studies in Spain, France, and Italy [4][5][6] indicated that a substantial majority (71%-91%; average, 77%) of subjects with PCT had evidence of infection with the hepatitis C virus (HCV). In contrast, the prevalence of HCV infection was low (0%-18%) in PCT patients from Northern or Central Europe, 3,[7][8][9][10] Australia, 11 or New Zealand. 12 Until now, the relationship of HCV to PCT has been studied in few North American patients.…”

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confidence: 99%

Porphyria cutanea tarda, hepatitis C, and HFE gene mutations in north america

et al. 1998

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In some, but not all countries, porphyria cutanea tarda (PCT) has been associated with chronic infection with the hepatitis C virus (HCV). Recently, PCT has also been associated with mutations in the HFE gene that are associated with HLA-linked hereditary hemochromatosis. Until now, few studies of these associations have been reported from North America. The aims of this study were: 1) to assess the prevalence of HCV infection and HFE mutations in North American patients with PCT; 2) to compare demographic and laboratory features between those who are HCV-positive and HCV-negative; and 3) to study urinary porphyrin excretions in American HCV-positive patients without clinically manifest PCT. Clinical and laboratory data, including tests for HCV and urinary porphyrins, were collected from 70 unselected patients with typical PCT. Urinary porphyrins were also measured in 110 non-PCT patients with chronic hepatitis C. Mutational analyses of the HFE gene were performed in 26 PCT patients. Thirtynine of 70 (56%) of the PCT patients had evidence of HCV infection. Thirty-two of 39 PCT patients with HCV were men, all of whom used alcohol. In contrast, 22 of 31 PCT patients without HCV infection were women, 12 of whom had taken estrogens. The HCV-positive group was more likely to have used illicit intravenous drugs (45% vs. 0%; P ‫؍‬ 0.01), to have had several (G4) sex partners (48% vs. 13%; P ‫؍‬ 0.005), and less likely to have no known risk factors for HCV infection (33% vs. 78%; P ‫؍‬ 0.004). Total urinary porphyrin excretion was the same in the two groups, but those with HCV infection had a significantly lower percentage of uroporphyrin and higher percentages of hepta-and hexa-carboxy porphyrins in urine. Sixteen of 110 (15%) HCV-positive subjects without PCT had increased urinary porphyrins, but, unlike PCT, these were mainly coproporphyrin. Forty-two percent of PCT patients carried the C282Y mutation of HFE (15% homozygous), and another 31% carried the H63D mutation (8% homozygous). Thus, 73% of PCT patients had one of these mutations. The prevalence of HCV infection (56%) and mutations in the HFE gene (73%) are high among North American patients with PCT. Alcohol and estrogen use are important additional risk factors. All PCT patients should be tested for HCV infection and for HFE gene mutations. Although HCV infection is a trigger for PCT, preclinical PCT is rare in chronic HCV hepatitis C in the United States. (HEPATOLOGY 1998;27:1661-1669.)

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Porphyria cutanea tarda, hepatitis C, and HFE gene mutations in north america

et al. 1998

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“…The identification of chronic viral hepatitis C as a frequent coexisting disease in porphyria cutanea tarda (PCT) with an increasing gradient from northern to southern Europe (1)(2)(3)(4) suggests association between viral hepatitis and porphyrinopathies. Increased urinary porphyrin excretion has been recognised for many years in various hepatobiliary diseases (5,6).…”

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Urinary Porphyrin Excretion in Hepatitis C Infection

Vogeser¹,

Jacob²,

Zachoval³

1999

CCLM

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A high prevalence of hepatitis C virus infection in porphyria cutanea tarda in some populations suggests a close link between viral hepatitis and alteration of porphyrin metabolism. Moreover, there is evidence of a role of porphyrinopathies in hepatocarcinogenesis. The aim of our study was to obtain data on the prevalence and patterns of heme metabolism alterations in patients with chronic hepatitis C virus infection. Urinary porphyrin excretion was prospectively studied in 100 consecutive outpatients with chronic hepatitis C infection without signs of photosensitivity, using an ion-pair high-performance liquid chromatography method. Increased total porphyrin excretion was found in 41 patients, with predominant excretion of coproporphyrins (whole study group: mean 146 µg/g creatinine, interquartile range 76-186; normal < 150), in 10 patients excretion exceeded 300 µg/g creatinine. In the majority of all patients studied (75/100) an increased ratio of the relatively hydrophobic coproporphyrin isomer I to isomer III was found. In just one case, urinary porphyrin pattern characteristic for chronic hepatic porphyria was present (uroporphyrin > coproporphyrin, heptacarboxyporphyrin III increased) but the total porphyrin excretion was only slightly elevated in this case. In the whole group, total urinary porphyrin excretion correlated well with serum bilirubin and was inversely correlated with albumin and thrombin time. In conclusion, secondary coproporphyrinuria occurs frequently in heptatitis C infection, whereas in Germany, preclinical porphyria cutanea tarda seems to be rare in these patients.

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“…In Italy and in other Mediterranean countries hepatitis C virus (HCV) infection is the single most frequent cause of liver disease in PCT patients, 6,21,22 while it is rare in Northern European countries. 23,24 The aim of this work is to investigate whether HFE mutations have a role as genetic susceptibility factors for PCT in a population with a high prevalence of an acquired triggering factor, such as HCV chronic infection.…”

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High prevalence of the His63Asp HFE mutation in italian patients with porphyria cutanea tarda

et al. 1998

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Sporadic porphyria cutanea tarda (PCT) is caused by a reduced activity of uroporphyrinogen decarboxylase (URO-D) in the liver. Mild to moderate iron overload is common in PCT, as iron is one of the factors which trigger the clinical manifestations of the disease through the inactivation of URO-D. A role for genetic hemochromatosis in the development of iron overload in sporadic PCT has been hypothesized in the past. The aim of this work was to investigate whether mutations of HFE, which is a candidate gene for hemochromatosis, play the role of genetic susceptibility factors for PCT in Italian patients, who have a high prevalence of acquired triggering factors, such as hepatitis C virus (HCV) chronic infection and alcohol. We determined HFE genotypes of 68 male patients with PCT. Our data do not confirm an association of PCT with the Cys282Tyr HFE mutation, strongly associated with hemochromatosis in Northern European countries. A second mutation of HFE, His63Asp, however, had a significantly increased frequency as it was present in half of the patients. Surprisingly, the presence of the His63Asp mutation was not related to the iron status of patients, suggesting that a subtle abnormality of iron metabolism induced by this mutation could escape detection by the standard parameters of iron status. In PCT patients with liver disease, the presence of the mutation could contribute to the inactivation of URO-D, either directly or through a synergistic action with other factors that cause liver damage. (HEPATOLOGY 1998;27;181-184.)

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Low prevalence of hepatitis C virus infection in porphyria cutanea tarda in germany

Cited by 91 publications

References 24 publications

Porphyria cutanea tarda, hepatitis C, and HFE gene mutations in north america

Porphyria cutanea tarda, hepatitis C, and HFE gene mutations in north america

Urinary Porphyrin Excretion in Hepatitis C Infection

High prevalence of the His63Asp HFE mutation in italian patients with porphyria cutanea tarda

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