Which of the following is true about polyarteritis nodosa?

Correct Answer: C. 30% is associated with Hepatitis B

Polyarteritis nodosa (PAN) is a systemic necrotizing vasculitis of medium-sized muscular arteries with a well-established association with Hepatitis B virus (HBV). The critical discriminating fact is that approximately 30% of PAN cases worldwide are seropositive for HBV, with even higher prevalence (up to 50%) in endemic regions like India and Southeast Asia. This association is pathophysiologically mediated by immune complex deposition (HBsAg-anti-HBs complexes) in vessel walls, triggering complement activation and necrotizing inflammation. In Indian clinical practice, HBV screening is mandatory in all PAN patients, and HBV-associated PAN often presents with more severe systemic manifestations and higher mortality if untreated. The mechanism differs from other vasculitides: PAN is NOT ANCA-associated (unlike GPA or MPA), and immune complexes—not ANCA—drive the pathology. Treatment of HBV-associated PAN includes antiviral therapy (lamivudine, tenofovir) alongside immunosuppression, making the HBV association clinically actionable. This 30% figure is the most commonly tested association in Indian medical curricula and represents a key distinguishing feature of PAN from other vasculitides.

Why the other options are wrong

A. Patient has hypogammaglobulinemia — This is wrong because PAN is NOT associated with hypogammaglobulinemia; in fact, patients often have elevated immunoglobulins (especially IgM) due to immune complex-mediated disease. Hypogammaglobulinemia is seen in primary immunodeficiencies or X-linked agammaglobulinemia, not in vasculitis. NBE may trap students who confuse PAN with immunodeficiency syndromes or conflate vasculitis with antibody deficiency. B. 90% is associated with ANCA positivity — This is wrong because PAN is ANCA-negative by definition—it is NOT an ANCA-associated vasculitis (AAV). ANCA positivity (c-ANCA/PR3 or p-ANCA/MPO) is characteristic of GPA and MPA, not PAN. The 90% figure is a distractor mimicking the high ANCA prevalence in GPA. NBE exploits confusion between PAN and ANCA-associated vasculitides, which are distinct pathophysiologically and clinically. D. Necrotising inflammation of large vessels — This is wrong because PAN affects medium-sized muscular arteries, not large vessels. Large vessel vasculitis (Takayasu arteritis, giant cell arteritis) involves the aorta and its major branches. PAN spares the lungs, glomeruli, and skin (superficial vessels), which is a key diagnostic criterion. This option confuses PAN with large vessel vasculitis, a common NBE trap for students unfamiliar with vessel size classification.

High-Yield Facts

Mnemonics

PAN vs ANCA-AAV PAN = Polyarteritis Nodosa = ANCA-Negative (immune complex-mediated). ANCA-AAV = GPA/MPA = ANCA-Positive (ANCA-mediated). PAN = medium vessels; GPA/MPA = small vessels. Use: When differentiating vasculitides on serology. HBV-PAN Association 30% PAN = HBV+ (immune complex deposition). Always screen HBV in PAN. Treat with antivirals + immunosuppression. Use: When managing PAN or seeing unexplained vasculitis in endemic regions.

NBE Trap

NBE pairs "ANCA positivity" with vasculitis to trap students who conflate PAN with ANCA-associated vasculitides (GPA/MPA). The 90% figure mimics the high ANCA prevalence in GPA, but PAN is fundamentally ANCA-negative and immune complex-mediated.

Clinical Pearl

In Indian practice, a patient presenting with fever, abdominal pain, and mononeuritis multiplex with negative ANCA should raise suspicion for PAN—and HBV serology (HBsAg, anti-HBc) is the next step. HBV-associated PAN often responds dramatically to antiviral therapy, making this association clinically transformative.

_Reference: Robbins Ch. 11 (Vasculitis); Harrison Ch. 378 (Vasculitis); KD Tripathi Ch. 18 (Immunosuppressants and vasculitis management)_