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Published on: March 13, 2015
[Extrahepatic manifestations of HBV and HCV infection]
1Abteilung Gastroenterologie und Endokrinologie, Georg-August-Universität Göttingen.
Insights
Hepatitis B (HBV) and Hepatitis C (HCV) infections can cause extrahepatic diseases like glomerulonephritis and cryoglobulinemia. Interferon therapy shows promise for treating these viral-related conditions.
Area of Science:
- Hepatology
- Immunology
- Infectious Diseases
Context:
- Hepatitis B virus (HBV) and Hepatitis C virus (HCV) infections are linked to various extrahepatic diseases.
- These manifestations can be non-specific, similar to those seen in liver cirrhosis, or specific to viral etiology.
Purpose:
- To review distinct clinical conditions associated with HBV and HCV infections.
- To discuss the pathogenesis and treatment of specific extrahepatic manifestations.
Summary:
- Chronic HBV infection is associated with glomerulonephritis and polyarteritis nodosa, driven by immune complex deposition. Interferon therapy may be beneficial.
- Chronic HCV infection frequently presents with mixed cryoglobulinemia and systemic vasculitis, potentially linked to lymphoma. Interferon alpha shows efficacy, with antiviral activity correlating to treatment benefits.
Impact:
- Highlights specific extrahepatic conditions linked to HBV and HCV, aiding in diagnosis and management.
- Underscores the role of immune complexes in pathogenesis and the therapeutic potential of interferon, particularly in HCV-related cryoglobulinemia.
Abstract:
Acute as well as chronic infections by HBV and HCV can be associated with extrahepatic disease. As in liver disease of non-viral etiology, several extrahepatic manifestations can be observed that are non-specific for HBV or HCV, e.g. those clinical signs and symptoms frequently encountered when cirrhosis of the liver is present. In addition, distinct clinical conditions have been described in which the unterlying liver disease is specifically due to HBV or HCV infection. In chronic HBV infection, glomerulonephritis (of the membranous and of the membranoproliferative type) and polyarteritis nodosa have been observed. The pathogenesis of both conditions involves the deposition of circulating immune complexes. Although controlled trials are lacking, interferon therapy appears to be beneficial. The use of immunosuppressive drugs and of plasmapheresis should probably be limited to the initial phase of treatment. In chronic HCV infection, mixed cryoglobulinemia (and ensuing systemic vasculitis) is a frequent extrahepatic manifestation. The clinical presentation might include the presence of purpura, arthralgias, weakness and renal involvement. Nowadays, HCV can be regarded as the etiological agent of a form of mixed cryoglobulinemia formerly considered to be 'essential'. In addition, an association to lymphoma has been postulated recently. Interferon alpha has been used for treatment with similar response rates as those observed in HCV-infected patients without cryoglobulinemia. Interestingly, the antiviral activity of interferon, e.g. normalization of transaminases and loss of serum HCV RNA, was closely related to the beneficial effect on cryoglobulinemia. An association of Sjögren's syndrome and of porphyria cutanea tarda to HCV infection (though claimed before) remains questionable. Serological markers of autoimmunity, e.g. antinuclear antibodies or anti-LKM-1, are present in many patients with chronic HCV infection. The clinical relevance of this latter observation appears low however, particularly since the decision for interferon treatment is hardly influenced by their presence.
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