Dermatology MCQ - Viral Infections - Hepatitis B

A 35-year-old man presents with a sudden onset of urticarial lesions, arthralgia, and fever. Physical examination reveals non-blanching, palpable purpura on his lower extremities. Laboratory studies show elevated transaminases (AST 250 U/L, ALT 300 U/L) and a positive hepatitis B surface antigen (HBsAg). Skin biopsy demonstrates leukocytoclastic vasculitis with deposition of immune complexes. Which of the following is the most likely underlying immunologic mechanism for this cutaneous manifestation?

A) Direct viral infection of endothelial cells
B) Type I hypersensitivity reaction
C) Immune complex-mediated vasculitis
D) Autoantibodies targeting skin antigens
E) Cryoglobulin precipitation

Correct Answer: C) Immune complex-mediated vasculitis

Explanation

This presentation is classic for hepatitis B virus (HBV)-associated polyarteritis nodosa (PAN), a systemic vasculitis that commonly involves the skin.

Key Clinical Features:

• Constitutional Symptoms: Fever, arthralgia, myalgia.

• Cutaneous Findings: Palpable purpura (due to vasculitis), livedo reticularis, subcutaneous nodules, and ulcerations.

• Hepatitis B Serology: Positive HBsAg indicates active HBV infection.

• Systemic Involvement: Can affect nerves (mononeuritis multiplex), kidneys, gastrointestinal tract, and cardiovascular system.

Pathogenesis:

• Immune Complex Deposition: HBV infection leads to formation of antigen-antibody complexes (HBsAg-anti-HBs). These complexes deposit in small- to medium-sized arteries, activating complement and attracting neutrophils.

• Leukocytoclastic Vasculitis: The biopsy finding of neutrophilic infiltration, fibrinoid necrosis, and leukocytoclasis is characteristic of immune complex-mediated vasculitis.

• Timing: Typically occurs in the early stages of HBV infection (within first 6 months).

Why Not the Other Options?

• (A) Direct viral infection of endothelial cells: HBV does not directly infect endothelial cells; vasculitis is immune-mediated.

• (B) Type I hypersensitivity: Involves IgE and mast cells (e.g., urticaria, anaphylaxis), not purpura or vasculitis.

• (D) Autoantibodies targeting skin antigens: Seen in autoimmune blistering diseases (e.g., pemphigus), not HBV-associated vasculitis.

• (E) Cryoglobulin precipitation: HBV can cause cryoglobulinemic vasculitis (type III cryoglobulinemia), which may present similarly. However, the classic description here (systemic symptoms, HBsAg positivity, biopsy findings) is more specific for PAN. Cryoglobulinemia typically involves type II/III cryoglobulins and may have rheumatoid factor positivity.

Management:

• Antiviral therapy: Entecavir or tenofovir to control HBV replication.

• Immunosuppression: Corticosteroids ± cyclophosphamide for severe vasculitis, but must be combined with antivirals to prevent HBV flare.

• Plasma exchange: For severe cases to remove immune complexes.

Prognosis:
With antiviral therapy, outcomes have improved significantly. Without treatment, HBV-PAN has high mortality due to renal, gastrointestinal, or cardiac involvement.

Note: HBV can also cause other skin manifestations, including:

• Urticaria (in prodromal phase of acute hepatitis).

• Gianotti-Crosti syndrome (papular acrodermatitis of childhood).

• Lichen planus (associated with chronic HBV).

• Cryoglobulinemic vasculitis (less common than PAN).