Polyarteritis Nodosa and Hepatitis B Association
Polyarteritis nodosa is associated with chronic hepatitis B infection, not acute hepatitis B. The disease typically develops shortly after initial HBV infection during the early chronic phase when active viral replication is occurring, characterized by the presence of HBeAg and high levels of HBV DNA 1, 2.
Timing and Pathophysiology
PAN develops within the first 6 months following HBV infection in most cases, during the transition from acute to chronic infection when viral replication is most active 3, 2.
The pathogenesis involves immune complex deposition with antigen excess during active viral replication, not the acute hepatitis phase itself 2.
Patients with HBV-related PAN are HBeAg-positive with actively replicating virus at diagnosis, indicating chronic infection with ongoing viral replication rather than acute self-limited infection 1, 4.
Clinical Context
Clinically evident hepatitis is present in only 19-29% of patients before PAN develops, meaning most patients do not have symptomatic acute hepatitis when vasculitis manifests 3.
Transaminases are frequently normal or only mildly elevated at PAN presentation, further supporting that this occurs during chronic infection rather than acute hepatitis 3.
The association is specifically with chronic HBV infection that progresses to persistent viremia, not with acute infection that resolves spontaneously 5, 2.
Treatment Implications
Treatment success correlates directly with achieving HBeAg to anti-HBe seroconversion, which represents control of chronic viral replication 1, 2, 4.
The therapeutic goal is to stop viral replication and facilitate seroconversion using antiviral agents (lamivudine or interferon-alpha), short-term corticosteroids, and plasma exchanges 6, 2.
Patients who achieve seroconversion obtain complete remission and do not relapse, confirming the disease is driven by ongoing chronic viral replication 2.
Key Distinction
Acute HBV infection resolves spontaneously in >95% of immunocompetent adults and does not cause PAN 5.
PAN is a complication of chronic HBV infection (defined by persistent HBsAg positivity beyond 6 months) with active replication, not acute infection 5, 2.
The frequency of HBV-related PAN has decreased dramatically due to vaccination and blood safety measures that prevent chronic HBV infection 2.