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Abstract
Hepatitis C virus may cause hepatic and extrahepatic diseases. Extrahepatic manifestations range from disorders for which a significant association with viral infection is supported by epidemiologic and pathogenetic data, to anecdotal observations without clear proof of causality. This article describes the diagnosis and treatment of these diseases.
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Abstract
Iron is an essential element involved in various biological pathways. When present in excess within the cell, iron can be toxic due to its ability to catalyse the formation of damaging radicals, which promote cellular injury and cell death. Within the liver, iron related oxidative stress can lead to fibrosis and ultimately to cirrhosis. Here we review the role of excessive iron in the pathologies associated with various chronic diseases of the liver. We also describe the molecular mechanism by which iron contributes to the development of hepatic fibrosis.
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Affiliation(s)
- Marie-A Philippe
- Hepatic Fibrosis Group, The Queensland Institute of Medical Research, PO Royal Brisbane and Women's Hospital, Brisbane 4029, Australia
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3
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Zignego AL, Ferri C, Pileri SA, Caini P, Bianchi FB. Extrahepatic manifestations of Hepatitis C Virus infection: a general overview and guidelines for a clinical approach. Dig Liver Dis 2007; 39:2-17. [PMID: 16884964 DOI: 10.1016/j.dld.2006.06.008] [Citation(s) in RCA: 181] [Impact Index Per Article: 10.1] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 10/28/2005] [Revised: 06/03/2006] [Accepted: 06/06/2006] [Indexed: 02/08/2023]
Abstract
Hepatitis C Virus is associated with a wide series of extrahepatic manifestations. Based on available data the link between the virus and some of these extrahepatic diseases is only suggested and needs further confirmation. Hepatitis C Virus-related lymphoproliferative disorders, whose prototype is mixed cryoglobulinaemia, represent the most closely related extrahepatic manifestations of Hepatitis C Virus. Other Hepatitis C Virus-associated disorders include nephropathies, thyreopathies, sicca syndrome, idiopathic pulmonary fibrosis, porphyria cutanea tarda, lichen planus, diabetes, chronic polyarthritis, cardiopathy and atherosclerosis. A pathogenetic link between Hepatitis C Virus and some extrahepatic manifestations was confirmed by their responsiveness to antiviral therapy, which is now deemed the first therapeutic option to consider. By contrast, there are diseases where treatment with interferon was ineffective or dangerous. The aim of the present paper is to outline the most recent evidence concerning extrahepatic disorders that are possibly associated with Hepatitis C Virus infection. Special emphasis will be given to discussion of the most appropriate clinical approaches to be adopted in order to diagnose, treat (possibly prevent) and follow-up extrahepathic diseases in patients with Hepatitis C Virus infection.
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Affiliation(s)
- A L Zignego
- Department of Internal Medicine, Medical School, Center for Research, Transfer and High Education DENOthe, Center for the Study of Systemic Manifestations of Hepatitis Viruses MaSVE, University of Florence, Florence, Italy.
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4
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Gandolfo LD, Ameglio F, Biolcati G, Pimpinelli F, Trento E, Galante M, Nardi A, Topi G. Anti-HCV-core specific IgM in porphyria cutanea tarda. J Eur Acad Dermatol Venereol 2006. [DOI: 10.1111/j.1468-3083.1996.tb00175.x] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/28/2022]
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Durazzo M, Premoli A, Di Bisceglie C, Bertagna A, Faga E, Biroli G, Manieri C, Bo S, Pagano G. Alterations of seminal and hormonal parameters: An extrahepatic manifestation of HCV infection? World J Gastroenterol 2006; 12:3073-6. [PMID: 16718790 PMCID: PMC4124384 DOI: 10.3748/wjg.v12.i19.3073] [Citation(s) in RCA: 63] [Impact Index Per Article: 3.3] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/06/2023] Open
Abstract
AIM: To evaluate the possible influences of HCV infection and relative antiviral treatment on seminal parameters and reproductive hormonal serum levels.
METHODS: Ten male patients with HCV-related chronic hepatitis and 16 healthy male volunteers were studied. In all subjects seminal parameters (nemaspermic concentration, progressive motility, morphology) and hormonal levels were determined. Seminal parameters and inhibin B, follicle-stimulating hormone, luteinizing hormone, total and free testosterone, estradiol, prolactine in patients were measured after six and twelve months of antiviral combined (interferon + ribavirin) treatment.
RESULTS: Patients before treatment showed a significantly lower nemaspermic motility and morphology as well as lower inhibin B and free testosterone levels than controls. Inhibin B levels in cases were improved six and 12 mo after treatment in five responders (161.9 ± 52.8 pg/mL versus 101.7 ± 47.0 pg/mL and 143.4 ± 46.1 pg/mL versus 95.4 ± 55.6 pg/mL, respectively). Hormonal pattern of patients did not significantly change after treatment, with the exception of estradiol levels with an initial reduction and an overall subsequent increment (19.7 ± 6.4 pg/mL versus 13.6 ± 5.0 pg/mL versus 17.3 ± 5.7 pg/mL). However in 1-year responders a significant increment of free testosterone (14.2 ± 2.54 pg/mL versus 17.1 ± 2.58 pg/mL) occurred. An impairment of nemaspermic morphology occurred, while other seminal parameters did not change significantly during antiviral treatment.
CONCLUSION: Patients with HCV infection show worse spermatic parameters than controls, suggesting a possible negative influence of virus on spermatogenesis, with further mild impairment during antiviral treatment. However therapy could improve the spermatic function, as suggested by the increased inhibin B levels and improved hormonal pattern in responders. Further studies are needed to confirm these preliminary intriguing results.
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Affiliation(s)
- Marilena Durazzo
- Department of Internal Medicine, Corso A.M.Dogliotti 14, 10126, Turin, Italy.
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6
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Gisbert JP, García-Buey L, Pajares JM, Moreno-Otero R. Prevalence of hepatitis C virus infection in porphyria cutanea tarda: systematic review and meta-analysis. J Hepatol 2003; 39:620-7. [PMID: 12971974 DOI: 10.1016/s0168-8278(03)00346-5] [Citation(s) in RCA: 121] [Impact Index Per Article: 5.5] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/18/2022]
Abstract
BACKGROUND/AIMS To conduct a systematic review and meta-analysis on the prevalence of hepatitis C virus (HCV) infection in porphyria cutanea tarda (PCT). METHODS Studies evaluating prevalence of HCV infection in patients with PCT were considered. Bibliographical searches were conducted in several electronic databases. Studies comparing HCV prevalence in PCT (cases) and in a reference group (controls) were included in the meta-analysis, combining the Odds Ratios (OR) of the individual studies. RESULTS Fifty studies including 2,167 patients were identified. Mean HCV prevalence by serology was 47%, and 50% with polymerase chain reaction (PCR). HCV prevalence markedly varied depending on the country and the type of PCT (57% in the sporadic and 26% in the familial form). Eight case-control studies were identified. Seven studies compared HCV prevalence in PCT vs. healthy controls: 40% vs. 0.24%, respectively (OR=275; 95% confidence interval=104-725). Heterogeneity disappeared when only studies evaluating HCV infection by PCR were included. CONCLUSIONS HCV prevalence in patients with PCT is approximately 50%, much higher than that reported in general population, suggesting a possible etiopathogenic role of HCV in PCT. The striking geographical variation in this association suggests that genetic and/or environmental factors may also be involved in the pathogenesis of this disorder.
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Affiliation(s)
- Javier P Gisbert
- Servicio de Gastroenterología y Hepatología, Universidad Autónoma de Madrid, Hospital Universitario de la Princesa, Diego de León, 62. 28006, Madrid, Spain.
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Nishioka E, Funasaka Y, Bito T, Ito A, Tani M, Kawara A, Yoon S, Kondo M, Ichihashi M. Porphyria cutanea tarda with menopausal exacerbation: the possible role of menstruation as natural phlebotomy. J Am Acad Dermatol 2003; 49:547-50. [PMID: 12963930 DOI: 10.1067/s0190-9622(03)00483-3] [Citation(s) in RCA: 4] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/22/2022]
Abstract
We describe a 48-year-old woman with a 12-year history of porphyria cutanea tarda who showed a remarkable exacerbation of her eruptions accompanied by high serum levels of iron and ferritin at menopause. As iron storage is known to be a triggering factor of porphyria cutanea tarda, the possible role of menstruation as natural phlebotomy to prevent porphyria cutanea tarda exacerbation is discussed.
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Affiliation(s)
- Eri Nishioka
- Department of Dermatology, Kobe University School of Medicine, Japan
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8
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Yoshida K, Nakano H, Yoshitomi F, Oshika T. Prevalence of seropositivity for hepatitis C virus in cataract patients and the general population. J Cataract Refract Surg 2002; 28:1789-92. [PMID: 12388029 DOI: 10.1016/s0886-3350(02)01335-4] [Citation(s) in RCA: 8] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/01/2022]
Abstract
PURPOSE To investigate the epidemiologic relationship between hepatitis C virus (HCV) infection and cataract. SETTING Yoshida Eye Clinic, Fukuoka, Japan. METHODS This study included 492 patients with age-related cataract and 2624 controls who had a municipal mass health screening. All subjects were 60 years or older and inhabitants of Chikugo City (population 45000), Fukuoka, Japan. Each subject was serologically tested for HCV using the third-generation enzyme immunoassay. Seropositivity was compared in subgroups consisting of patients by decade; that is 60 to 69 years of age, 70 to 79 years of age, and 80 to 90 years of age. RESULTS The prevalence of HCV in the cataract group and health-screening (control) group was 18.3% and 7.1%, respectively, in the 60- to -69 year subgroup; 17.8% and 6.6%, respectively, in the 70- to 79-year subgroup; and 15.1% and 3.7%, respectively, in the 80- to 90-year subgroup. In each subgroup, the prevalence of HCV was significantly higher in the cataract group than in the control group (P <.01, chi-square test). In the cataract group, the HCV seropositive and seronegative groups did not differ significantly in the prevalence of hepatitis B virus (P =.548, Fisher exact probability test). CONCLUSIONS Patients with age-related cataract had significantly higher seropositivity for HCV than an age-matched general population. This suggests that HCV infection may play a role in the development and/or progression of cataract.
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Affiliation(s)
- Koichi Yoshida
- Yoshida Eye Clinic, Yoshitomi Eye Center, Fukuoka, Japan
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Brudieux E, de Lédinghen V, Moran MJ, Fontanellas A, Oui B, Trimoulet P, Belleannée G, Piton A, Raymond JM, Doutre MS, Amouretti M, de Verneuil H, Couzigou P. Hepatic porphyrin concentration and uroporphyrinogen decarboxylase activity in hepatitis C virus infection. J Viral Hepat 2001; 8:41-7. [PMID: 11155151 DOI: 10.1046/j.1365-2893.2001.00266.x] [Citation(s) in RCA: 5] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/09/2022]
Abstract
Previous studies have shown a high prevalence of hepatitis C virus (HCV) infection in patients with porphyria cutanea tarda (PCT). The aim of this study was to assess hepatic porphyrin concentrations (HPC) and hepatic uroporphyrinogen decarboxylase (UROD) activity in HCV-infected patients free of PCT. Thirty-two HCV-infected patients (20 M, 12 F, mean age 51 years) and seven control patients (4 M, 3 F, mean age 59 years) free of liver disease, were studied. Knodell's score was determined on liver biopsy by two independent anatomopathologists. Measurement of HPC and hepatic UROD activity levels were carried out on liver biopsy. Relative to controls, HCV-infected patients had high HPC levels (mean +/- SD: 47 +/- 20 vs. 17 +/- 6 pmol/mg protein, P < 0.001) and low hepatic UROD activity levels (514 +/- 95 vs. 619 +/- 125 pmol Copro/h/mg protein, P < 0.05). HPC was not correlated with hepatic UROD activity and the increase was due to coproporphyrin accumulation. No correlation was observed between HPC or hepatic UROD activity values and HCV-RNA concentrations, Knodell's score, hepatic fibrosis, periportal necrosis, periportal inflammation or hepatic iron content in HCV-infected patients. Hepatocellular necrosis was significantly correlated with HPC value (P < 0.005). Hence, in HCV-infected patients, HPC is significantly increased and hepatic UROD activity is very slightly decreased as compared to controls. HPC values and UROD activity are not correlated with HCV-RNA concentrations, hepatic iron content and hepatic fibrosis. The small increase in HPC values in hepatitis C infection is linked with hepatic injury and not with a direct effect on hepatic UROD enzyme.
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Affiliation(s)
- E Brudieux
- Département d'Hépato-Gastroentérologie, Hôpital Haut-Levêque, Pessac, France
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Theodore D, Fried MW. Natural history and disease manifestations of hepatitis C infection. Curr Top Microbiol Immunol 1999; 242:43-54. [PMID: 10592655 DOI: 10.1007/978-3-642-59605-6_3] [Citation(s) in RCA: 15] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/07/2023]
Affiliation(s)
- D Theodore
- Division of Digestive Diseases, University of North Carolina at Chapel Hill 27514, USA
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11
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Affiliation(s)
- A L Zignego
- Department of Internal Medicine, University of Florence, Italy.
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12
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Kazemi-Shirazi L, Datz C, Maier-Dobersberger T, Kaserer K, Hackl F, Polli C, Steindl PE, Penner E, Ferenci P. The relation of iron status and hemochromatosis gene mutations in patients with chronic hepatitis C. Gastroenterology 1999; 116:127-134. [PMID: 9869610 DOI: 10.1016/s0016-5085(99)70236-2] [Citation(s) in RCA: 100] [Impact Index Per Article: 3.8] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/13/2022]
Abstract
BACKGROUND & AIMS Elevated hepatic iron concentration may affect the response to antiviral therapy in chronic hepatitis C. This study explored the contribution of genetic hemochromatosis to iron accumulation in chronic hepatitis C. METHODS HFE mutations (C282Y and H63D) were assessed in 184 patients with chronic hepatitis C virus and 487 controls. Liver biopsy specimens were available in 149 patients. Hepatic iron content was measured in 114 patients by atom-absorption spectrophotometry. RESULTS The C282Y and H63D allele frequencies were 7.06 and 11.6 in patients and 4.83 and 11.09 in controls, respectively. Eight patients were homozygotes (5 C282Y [2.7%] and 3 H63D [1.6%]), 2 compound heterozygotes (1%), and 49 heterozygotes (14 C282Y [7.6%] and 35 H63D [19%]). Biochemical evidence of iron overload was more common in patients with HFE mutations (28 of 47) than in those without (34 of 102; P = 0.0045). Histological iron grading and hepatic iron content overlapped among patients with or without mutations. A hepatic iron index of >1.9 was observed only in 1 of the 4 C282Y homozygotes and 1 of the 3 H63D homozygotes. CONCLUSIONS HFE mutations contribute to but do not fully explain hepatic iron accumulation in chronic hepatitis C. Furthermore, C282Y or H63D homozygosity in chronic hepatitis C is not necessarily associated with a high hepatic iron content.
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Affiliation(s)
- L Kazemi-Shirazi
- Department of Internal Medicine IV, University of Vienna, Vienna, Austria
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13
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Hepatotoxic iron storage in patients with chronic hepatitis C but no hepatic iron detectable histochemically. ACTA ACUST UNITED AC 1997. [DOI: 10.1007/bf01545084] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 10/25/2022]
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Beinker NK, Voigt MD, Arendse M, Smit J, Stander IA, Kirsch RE. Threshold effect of liver iron content on hepatic inflammation and fibrosis in hepatitis B and C. J Hepatol 1996; 25:633-8. [PMID: 8938538 DOI: 10.1016/s0168-8278(96)80231-5] [Citation(s) in RCA: 69] [Impact Index Per Article: 2.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/03/2023]
Abstract
BACKGROUND/AIMS In hepatitis C, iron depletion may improve serum aminotransferases and the response to interferon, but it is not known whether inflammation and fibrosis correlate with hepatic iron content. Our aim was to establish whether hepatic iron content correlates with histological and serum indices of hepatic inflammation and fibrosis in hepatitis B and C. METHODS Total hepatic iron was measured using computerized histomorphometry, and hepatic inflammation and fibrosis using a modified Knodell score, on histological slides from 31 patients with chronic hepatitis B and 38 with hepatitis C. RESULTS Total hepatic iron was similar in the hepatitis B and C groups (0.82 +/- 1.72% and 0.56 +/- 1.12%; mean +/- SD). No iron was detectable in 11 patients with hepatitis B and 13 with hepatitis C. Alanine aminotransferase (85.96 +/- 67.1 vs 44.2 +/- 39.7 p < 0.05), aspartate aminotransferase (93.8 +/- 75.6 vs 47 +/- 33.5 IU/ml p < 0.05) and histological inflammatory score (9.33 +/- 3.51 vs 7.79 +/- 3.3 p = 0.07) were increased in those with stainable hepatic iron compared to those without. However, where iron was present, no association was found between the amount of hepatic iron and inflammatory or fibrosis scores. In hepatitis C, fibrosis was minimal in 77% of patients if iron was absent vs 24% with iron present, while marked fibrosis was present in 56% with iron vs 15% without iron (p < 0.01, Fisher's exact test). CONCLUSION Hepatic iron is associated with increased hepatic inflammation in chronic hepatitis B and hepatitis C and with high fibrosis scores in hepatitis C. There is a threshold effect, and once present, increasing iron does not correlate with increasing inflammation or fibrosis.
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Affiliation(s)
- N K Beinker
- MRC/UCT Liver Research Centre, Groote Schuur Hospital, Cape Town, South Africa
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15
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Abstract
PURPOSE To report African Americans with primary iron overload diagnosed during life and to study iron stores in African Americans undergoing autopsy. PATIENTS AND METHODS We summarized information for 4 African-American patients diagnosed during life with iron overload not explainable by alcohol, blood transfusions, or ineffective erythropoiesis. We reviewed liver specimens and hospital records of 326 unselected adult African Americans who were autopsied, assessing Prussian blue-stained sections for hepatocellular iron and measuring iron quantitatively in specimens that stained positively. We calculated the hepatic iron index (the hepatic iron concentration in mumol/g dry weight divided by the age in years). In autopsy subjects we corrected the index to account for iron administered by blood transfusion (the adjusted hepatic iron index). The hepatic iron index is useful for distinguishing primary iron overload from the moderate siderosis that may accompany alcoholic liver disease. The normal index is < or = 1.0. An index > or = 1.7 cannot be explained by alcohol effects and an index > or = 1.9 indicates the magnitude of iron-loading found in Caucasian homozygous HLA-linked hemochromatosis. RESULTS The 4 living patients, all males and 27 to 50 years of age, had elevated body iron burdens and one or more of the following: hepatomegaly, cirrhosis, cardiomyopathy, diabetes mellitus, and impotence. Hepatic iron indices were 2.3, 11.5, and 20.2 in the 3 whose liver iron concentrations were measured. Among the autopsy subjects, 4 (1.2%), 2 men and 2 women aged 50 to 63 years, had adjusted hepatic iron indices > or = 1.9 (range 1.9 to 5.6). CONCLUSIONS Primary iron overload occurs in African Americans. Further studies are needed to define prevalence, pathophysiology and clinical consequences. Clinicians should look for this condition.
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Affiliation(s)
- R K Wurapa
- Department of Pathology, Case Western Reserve University, Cleveland, Ohio, USA
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Bayraktar Y, Koseoglu T, Somner C, Kayhan B, Temizer A, Uzunalimoglu B, De Maria N, Van Thiel DH. The use of deferoxamine infusions to enhance the response rate to interferon-alpha treatment of chronic viral hepatitis B. J Viral Hepat 1996; 3:129-35. [PMID: 8871871 DOI: 10.1111/j.1365-2893.1996.tb00003.x] [Citation(s) in RCA: 22] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/02/2023]
Abstract
An individual's iron status may affect the response rate achieved with the use of interferon (IFN) as therapy for chronic viral hepatitis. A total of 27 patients with chronic hepatitis B viral infection, who had elevated serum ferritin levels, were randomized to receive either IFN 5 MU, three times weekly by subcutaneous injection alone (n = 14) or in combination with cycles of deferoxamine at a dose od 80 mg kg-1 per cycle (n = 13) administered over 3 consecutive days, to reduce their iron and maintain a serum ferritin level less than 250 ng ml-1. All deferoxamine-treated patients were on a low iron-containing diet. An IFN response was defined as a normalization of the serum alanine aminotransferase (ALT) level and seroconversion from hepatitis B e antigen (HBeAg) positivity to hepatitis B e antibody (HBeAb) positivity. The deferoxamine-treated group experienced a reduction in their serum ferritin level to 226 +/- 73 ng ml-1 as a result of the deferoxamine treatment. Six of the 13 (46%) deferoxamine-treated patients and two of the 14 (14%) control patients normalized their ALT levels. Seven of the 13 (54%) deferoxamine but only 14% of the IFN-treated group seroconverted to HBeAb positivity. A greater rate of histological improvement and loss of hepatitis B virus (HBV) DNA was seen in the deferoxamine-treated group. Two of the deferoxamine-treated patients were treated only once, two were treated twice, seven were treated three times and two were treated four times to achieve a ferritin level below 250 ng ml-1. Based on these data, we conclude that deferoxamine infusion enhances the rate of response to IFN in subjects with chronic hepatitis B. The precise mechanism of this phenomenon is not clear.
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Affiliation(s)
- Y Bayraktar
- Gastroenterology Department, Hacettepe University, School of Medicine, Ankara, Turkey
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Doutre MS, Beylot C, Beylot-Barry M, Couzigou P, Beylot J. [Skin manifestations related to hepatitis C viruses]. Rev Med Interne 1995; 16:666-72. [PMID: 7481154 DOI: 10.1016/0248-8663(96)80769-7] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.1] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/25/2023]
Abstract
The hepatitis C virus causes both hepatic and extrahepatic disorders, particularly as regards dermatology. The link between essential mixed cryoglobulinemias and the C virus infection has been clearly evidenced., whereas its frequency seems low in other systemic vasculitis such as polyarteritis nodosa. Similarly, the link between C virus hepatopathy and porphyria cutanea tarda is now proven. Lichen planus is also described as being associated with this virus, but further epidemiological studies are required to determine the exact prevalence of lichen in C virus hepatopathy cases. Finally, various cutaneous disorders, such as urticaria, erythema multiforme, dermo-hypodermitis, etc, occasionally arise during acute or chronic hepatitis C.
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Affiliation(s)
- M S Doutre
- Service de dermatologie, hôpital du Haut-Lévêque, Pessac, France
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Fargion S, Piperno A, Cappellini MD, Sampietro M, Fracanzani AL, Romano R, Caldarelli R, Marcelli R, Vecchi L, Fiorelli G. Hepatitis C virus and porphyria cutanea tarda: evidence of a strong association. Hepatology 1992; 16:1322-6. [PMID: 1359994 DOI: 10.1002/hep.1840160603] [Citation(s) in RCA: 205] [Impact Index Per Article: 6.2] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/12/2022]
Abstract
Porphyria cutanea tarda in human beings is believed to be due to reduced hepatic uroporphyrinogen decarboxylase activity. However, extrinsic factors such as alcohol abuse and drug intake are required for clinical manifestation of the disease. In addition to typical cutaneous lesions, patients with porphyria cutanea tarda usually have chronic liver disease and moderate iron overload. Of 74 Italian patients with porphyria cutanea tarda, hepatitis C virus antibodies were detected in 76% by enzyme-linked immunoassay and in 82% by recombinant immunoblot assay. Viral genome, studied with nested polymerase chain reaction, was found in the sera of 49 subjects--47 positive and 2 indeterminate on recombinant immunoblot assay. Five percent of the patients were HBsAg-positive, and about 40% had had past hepatitis B contacts. Alcohol abuse was present in 38%. Liver biopsies performed in 42 patients showed chronic persistent hepatitis in 7 patients, chronic active hepatitis in 22 patients, fibrosis in three patients and cirrhosis in 10 patients. Hepatitis C virus antibody was detected in 100% of patients with chronic active hepatitis and in about 80% of all other groups. Alcohol abuse was more frequent in patients with cirrhosis (80%) than in the other groups. In Italian patients with porphyria cutanea tarda, the prevalence of hepatitis C virus infection was very high, comparable to that in non-A, non-B hepatitis and high-risk patient groups. Hepatitis C virus is probably the main pathogenetic factor of the liver disease of patients with porphyria cutanea tarda.
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Affiliation(s)
- S Fargion
- Institute of Internal Medicine and Medical Physiopathology, University of Milan, Italy
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19
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Piperno A, Fargion S, D'Alba R, Roffi L, Fracanzani AL, Vecchi L, Failla M, Fiorelli G. Liver damage in Italian patients with hereditary hemochromatosis is highly influenced by hepatitis B and C virus infection. J Hepatol 1992; 16:364-8. [PMID: 1487615 DOI: 10.1016/s0168-8278(05)80671-3] [Citation(s) in RCA: 50] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/27/2022]
Abstract
We evaluated the prevalence of hepatitis B virus (HBV) and hepatitis C virus (HCV) infection in 78 Italian patients with hereditary hemochromatosis as well as the relation between HCV antibody (anti-HCV) status, hepatitis B surface antigen (HBsAg) and liver histology. None of the patients had been transfused or ever consumed more than 60 g of alcohol per day. Eighteen showed histological signs of chronic hepatitis, active cirrhosis was present in 12, chronic active hepatitis in 4 and chronic persistent hepatitis in 2. Liver fibrosis or cirrhosis without inflammatory activity was observed in 31 subjects, whereas liver histology was normal except for iron overload in 18. The prevalence of HBsAg in the whole series was 5% and of anti-HCV was 20.5%. The prevalence of HBsAg and anti-HCV was significantly higher in the chronic hepatitis group than in the fibrosis/cirrhosis (p = 0.01) and the normal groups (p < 0.01). Fourteen of 18 hereditary hemochromatosis patients with chronic hepatitis were HBsAg (4) or anti-HCV (10) positive and all the latter subgroup had HCV-RNA in their serum as shown by the polymerase chain reaction. Although most of the patients with associated chronic hepatitis had cirrhosis, their serum ferritin levels and amount of mobilizable iron were significantly lower than those of the fibrosis/cirrhosis group (p < 0.01). This indicates that hepatitis viral infection acts synergistically with iron in accelerating the development of liver damage.
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Affiliation(s)
- A Piperno
- Institute of Biomedical Sciences S. Gerardo, Clinical Medicine, Monza, Italy
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