Hepatitis C virus antibodies and liver disease in patients with porphyria cutanea tarda

Decastro, Mar; Sánchez, Javier; Herrera, Juan José Durán; Chaves, A.; Durán, Rafael; Buey, L. García; García‐Monzón, Carmelo; Sequí, Julia; Moreno–Otero, Ricardo

doi:10.1002/hep.1840170405

Cited by 143 publications

(42 citation statements)

References 32 publications

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“…60 Viral infections -The role of hepatotropic viruses in triggering PCT has been reported since 1992. 61 the prevalence of anti-HCV antibodies ranges from 8% to 90%, and it is related to its endemicity in the population, 9,11,62 being higher in some regions of Europe (France, 63 Spain, 64 Italy 31,61 e Poland 65 ) and in the United States. 53 There is no predominance of HCV genotype in porphyrias.…”

Section: Triggerrring Factorsmentioning

confidence: 99%

“…68 As PCT may be the first indication of an HCV infection, it is important to be searched in all patients. 69 The hypotheses explaining the role of HCV in PCT encompass: (1) lower Urod activity secondary to hepatocyte injury; 64,70 (2) changes in the cytochrome P450 oxidase-dependent system; 70 and (3) increased auto-immune response in the liver.31 Auto-antibodies would occur due to a mechanism of molecular mimicking 71 and they act as inhibitors of the Urod catalytic activity. 72 There is also slight increase in the prevalence of hepatitis B.…”

Section: Triggerrring Factorsmentioning

confidence: 99%

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Porfiria cutânea tardia

Vieira

Martins

2006

An. Bras. Dermatol.

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Section: Triggerrring Factorsmentioning

confidence: 99%

Section: Triggerrring Factorsmentioning

confidence: 99%

Porfiria cutânea tardia

Vieira

Martins

2006

An. Bras. Dermatol.

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“…[3][4][5][6][7][8][9][10][11][12][13][14][15] A frequent association has also been reported between PCT and the hepatitis B virus 34 and also between PCT and the HIV. [35][36][37] This close association and the finding that the age at onset of PCT was significantly lower in HCV patients 38 suggests that HCV infection is a precipitating factor of PCT.…”

Section: Discussionmentioning

confidence: 99%

“…In addition, patients present with chronic liver disease, moderate iron overload; in some countries, patients present with a high association with hepatotropic virus infections. High prevalence of hepatitis C virus (HCV) markers were recently reported in Southern European patients (76%-95%), [3][4][5][6][7][8][9] and patients from the United States (50%-75%). [10][11] In contrast, lower prevalence has been reported in Northern Europe (8%-18%) [12][13][14] and New Zealand (0%).…”

Section: Porphyria Cutanea Tarda (Pct) Is Caused By a Decreased Activmentioning

confidence: 99%

Hepatic uroporphyrinogen decarboxylase activity in porphyria cutanea tarda patients: The influence of virus C infection

et al. 1998

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Porphyria cutanea tarda (PCT) is caused by a decreased activity of the hepatic enzyme uroporphyrinogen decarboxylase (URO-D). This deficiency causes overproduction, hepatic deposition, and increased excretion of uroporphyrin. Iron overload and hepatic viral infections are considered aggravating factors of the disease. Two forms of PCT have been described, as follows: a familial one with an inherited decrease of URO-D activity in all tissues and a sporadic one with a decreased activity of URO-D restricted to the liver. To assess whether the hepatic URO-D returns to normal during a remission of the disease, this activity was measured in liver biopsy samples in 24 sporadic PCT patients. The hepatic and urinary porphyrin concentrations were also measured. Viral status and histopathological findings were analyzed to assess their involvement in PCT. Six patients treated by phlebotomy to reduce hepatic iron and who were considered to be in clinical remission, characterized by a disappearance of cutaneous lesions, showed higher hepatic URO-D activities and lower hepatic porphyrin concentrations than did patients with overt PCT. The medians of these variables, however, did not achieve normal values. The hepatic URO-D activity showed a significant inverse relationship with both hepatic porphyrins and urinary uroporphyrin excretion. Hepatic URO-D activity was not reduced by hepatitis C virus (HCV) infection and liver damage. We conclude that the achievement of remission in PCT largely depends on the transient normalization of hepatic URO-D activity. A small increase in hepatic coproporphyrin in nonporphyric patients could reflect hepatic injury/iron/alcohol-induced oxidative stress oxidizing the accumulated heme precursors rather than a direct effect on hepatic URO-D enzyme. (HEPATOLOGY 1998; 27:584-589.)

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“…It has been recommended that all patients presenting with PCT be screened for hepatitis C infection (7)(8)(9)(10). In addition, there has been evidence presented (1 [1][2][3][4][5][6][7][8][9][10][11][12][13][14] which shows that hepatitis C viral infection can induce high-titer antinuclear antibodies, other autoantibodies including anti-DNA in low titer, and clinical immunologic disorders which in combination may cause a patient to meet the American College of Rheumatology (ACR) 1982 criteria for SLE (15).…”

Section: To the Editormentioning

confidence: 99%

Hepatitis C as another possible cause of porphyria cutanea tarda and systemic lupus erythematosus: Comment on the article by Kutz and Bridges

Nepveu

Libman

1996

Arthritis & Rheumatism

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LETTERSmight be a precipitating factor for AAU among Japanese patients with AS, but not in persons who are otherwise healthy.We agree that in those of our patients who had AAU, the onset of AS was earlier than in those who had not developed AAU; however, this difference was not statistically significant (Student's t-test). We also compared the age at onset of AS between DR8-positive and DR8-negative patients. No significant difference in the age at onset was observed between these 2 groups. In our study, the only significant difference observed was in the association of HLA-DR8 in patients with versus those without AAU. There was only 1 patient who was positive for DR8 but did not have AAU. Since the number of DR8-positive AS patients with the early-onset type of the disease in our study population was not large enough to enable statistical analysis, it was difficult to conclude whether DR8 had any relation to the age of onset of AS. More studies with more patients are needed in order to support the hypothesis that HLA-DR8 is specifically associated with the early-onset type of AS.With regard to the LMP2 genes, it is difficult to comment about which class I1 specificity occurs with the LMP;! gene for linkage disequilibrium, since this has not been studied in a Japanese population. This might be a useful area for further investigation.In conclusion, this first study with a small number of Japanese AS patients indicated a significant association of HLA-DR8 among patients who later developed AAU. A firm conclusion can be reached only when further studies reconfirm the same observation.

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Hepatitis C virus antibodies and liver disease in patients with porphyria cutanea tarda

Cited by 143 publications

References 32 publications

Porfiria cutânea tardia

Porfiria cutânea tardia

Hepatic uroporphyrinogen decarboxylase activity in porphyria cutanea tarda patients: The influence of virus C infection

Hepatitis C as another possible cause of porphyria cutanea tarda and systemic lupus erythematosus: Comment on the article by Kutz and Bridges

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