Hepatitis B Annual

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Year : 2006  |  Volume : 3  |  Issue : 1  |  Page : 128-154

Extrahepatic manifestations of chronic hepatitis B

1 Division of Digestive Diseases, David Geffen School of Medicine at UCLA, Los Angels, CA, USA
2 Pfleger Liver Institute, David Geffen School of Medicine at UCLA, Los Angels, CA, USA

Correspondence Address:
Steven-Huy B Han
Pfleger Liver Institute, 200 Medical Plaza, Suite 214, Los Angeles, CA 90095-7302
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Source of Support: None, Conflict of Interest: None

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Hepatitis B virus (HBV) infection and its complications are global health problems. Approximately 400 million people are chronic HBV carriers worldwide. The spectrum of chronic HBV infection ranges from asymptomatic hepatitis B surface antigen (HBsAg) carrier state to chronic hepatitis with progression to cirrhosis and end-stage liver disease. It is estimated that 15% to 40% of people with chronic HBV will progress to cirrhosis. Several extrahepatic syndromes are associated with chronic HBV infection. These syndromes contribute significantly to morbidity and mortality. The mechanism of extrahepatic syndromes seen with chronic viral hepatitis appears to be immune-mediated. including deposition of circulating immune complexes, induction of local immune complex formation by viral antigens, reaction with tissue antigens by viral-induced autoantibodies, or a direct viral reaction to extrahepatic tissue sites. Polyarteritis nodosa (PAN) is a rare, but serious, systemic complication of chronic HBV infection affecting the small- and medium-sized vessels. PAN ultimately involves multiple organ systems, some with devastating consequences, though the hepatic manifestations are often more mild. HBV-associated glomerulonephritis (GN) occurs mainly in children, predominantly males, in HBV endemic areas of the world. In children, GN is usually self-limited with only rare progression to renal failure. In adults, course of GN may be more relentless, progressing slowly to renal failure. A serum-sickness like "arthritis-dermatitis" prodrome is also seen in some patients acquiring HBV infection. The joint and skin manifestations are varied, but the syndrome spontaneously resolves after the onset of clinical hepatitis without significant sequelae. Occasionally, the arthritis following the acute prodromal infection may persist; however, joint destruction is rare. The association between HBV and mixed essential cryoglobulinemia remains controversial. Finally, skin manifestations of HBV infection typically present as palpable purpura. Though papular acrodermatitis of childhood has been reported to be caused by chronic HBV, this association remains controversial.

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