Hepatitis B-Related Autoimmune Manifestations

Cacoub, Patrice; Terrier, Benjamin

doi:10.1016/j.rdc.2009.03.006

Cited by 80 publications

(68 citation statements)

References 69 publications

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“…20,35-37 In addition, HBV-PAN has a greater frequency of gastrointestinal disorders, orchitis-like testicular disorders, severe arterial hypertension, and renal infarction compared with classic PAN and occurs more often in individuals younger than 40 years. 3,38 Hepatitis is rarely diagnosed first, because it remains mostly silent before PAN becomes clinically apparent. 3 HCV seropositivity has been reported in patients with PAN, and in an international study of more than 1000 patients with hepatitis C, 7.6% were found to have PAN.…”

Section: Viral-associated Panmentioning

confidence: 99%

Polyarteritis Nodosa

Forbess¹,

Bannykh²

2015

Rheumatic Disease Clinics of North America

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Polyarteritis nodosa (PAN) is a systemic disease, but variants are cutaneous PAN and single-organ disease. Histologic confirmation of vasculitis in medium-sized arteries is desirable, and biopsies should be obtained from the symptomatic and least invasive sites. Angiography can show multiple microaneurysms in the viscera. Treatment includes high-dose corticosteroids, which are combined with immunosuppressive agents when internal organs are involved and with life-threatening disease. Once remission is achieved, maintenance agents are initiated. PAN is becoming a rare disease. International collaborative efforts are under way to establish better diagnostic and classification for all vasculitides, including PAN.

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Section: Viral-associated Panmentioning

confidence: 99%

Polyarteritis Nodosa

Forbess¹,

Bannykh²

2015

Rheumatic Disease Clinics of North America

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“…Extrahepatic manifestations occur in up to 20% of HBVinfected individuals (30) and may involve the gastrointestinal, renal, and nervous systems (68). The mechanisms leading to extrahepatic manifestations of hepatitis B virus infection are poorly understood.…”

Section: Hbv Infection and Clinical Diseasementioning

confidence: 99%

“…Circulating immune complexes containing HBV have been demonstrated in patients with extrahepatic manifestations of chronic HBV infection (102,213). Circulating immune complexes and complement-mediated injury are implicated in extrahepatic manifestations of HBV infection, including arthralgia, serum sickness-like syndrome, polyarteritis nodosa, and glomerulonephritis (2,30,163,263). Chronic HBV infection is defined as the persistence of HBsAg for 6 months or longer.…”

Section: Hbv Infection and Clinical Diseasementioning

confidence: 99%

Molecular Mechanisms Underlying Occult Hepatitis B Virus Infection

2012

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SUMMARY Chronic hepatitis B virus (HBV) infection is a complex clinical entity frequently associated with cirrhosis and hepatocellular carcinoma (HCC). The persistence of HBV genomes in the absence of detectable surface antigenemia is termed occult HBV infection. Mutations in the surface gene rendering HBsAg undetectable by commercial assays and inhibition of HBV by suppression of viral replication and viral proteins represent two fundamentally different mechanisms that lead to occult HBV infections. The molecular mechanisms underlying occult HBV infections, including recently identified mechanisms associated with the suppression of HBV replication and inhibition of HBV proteins, are reviewed in detail. The availability of highly sensitive molecular methods has led to increased detection of occult HBV infections in various clinical settings. The clinical relevance of occult HBV infection and the utility of appropriate diagnostic methods to detect occult HBV infection are discussed. The need for specific guidelines on the diagnosis and management of occult HBV infection is being increasingly recognized; the aspects of mechanistic studies that warrant further investigation are discussed in the final section.

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“…Symptomatic hepatitis B is commonly accompanied by autoimmune phenomena clinically appearing as circulating organ non-specific and organ-specific autoantibodies. Although the pathogenic relevance of these responses to liver injury remains unclear in humans, it is generally accepted that their presence coincides with a more severe course of hepatitis (Poralla et al, 1991;Cacoub & Terrier, 2009). In the woodchuck model, WHV infection usually induces organ non-specific autoantibodies, such anti-smooth muscle antibodies (SMA) and anti-nuclear antibodies (ANA) , as well as liver-specific antibodies directed against hepatocyte asialoglycoprotein receptor (ASGPR) (Diao & Michalak, 1996.…”

Section: Symptomatic Serologically Evident Hepadnaviral Infectionmentioning

confidence: 99%