Mucocutaneous manifestation mimicking vasculitis in chronic hepatitis B: A case report

Table 1 Extrahepatic manifestations of hepatitis B infection

Reported condition	Symptoms	Diagnosis	Treatment	Prognosis	Histology	Treatment response
Mixed cryoglobulinemia vasculitis	Arthralgia (non-deforming, bilateral, symmetrical); Palpable purpura; Raynaud’s phenomenon; sicca syndrome	Presence of serum cryoglobulin; low complement levels (especially C4)	Antiviral therapy; B-cell–depleting therapy (Rituximab); Corticosteroids; Plasma exchange; Removal of circulating cryoglobulins; Non-steroidal anti-inflammatory drugs	In rare cases, life-threatening, affecting; the central nervous system, the gastrointestinal tract, and the heart	Immune complex-mediated small-vessel vasculitis characterized by leukocytoclastic infiltration and complement deposition, typically involving the skin, kidneys, and peripheral nerves. C4 is markedly decreased	Antiviral therapy leads to improvement in vasculitic symptoms, though immunosuppressives (e.g., rituximab) may be necessary for refractory cases. Prognosis improves with viral suppression
Serum sickness-like syndrome	Fever (< 39°C); skin rash (erythematous, macular, maculopapular, urticarial, nodular, or petechial lesions), polyarthritis	Clinical diagnosis	Antiviral therapy	Occurs before the onset of acute HBV hepatitis symptoms and tends to regress with the onset of hepatitis symptoms	Immune complex–mediated hypersensitivity reaction involving IgM and complement deposition, mimicking type III hypersensitivity. Unlike classic serum sickness, cryoglobulins and hypocomplementemia are typically absent	Symptoms generally improve spontaneously or with supportive care. Antiviral therapy hastens resolution when associated with acute HBV
Non-rheumatoid arthritis	Asymmetric skin erythema within the first 3 months of hepatitis onset	Anti-CCP (5%); ANA (10%); RF (25%)	Non-steroidal anti-inflammatory drugs	Improvement within days of treatment	Transient arthritis without erosive joint changes, possibly immune-mediated in response to HBV antigens. Lacks autoantibodies seen in rheumatoid arthritis (e.g., anti-CCP)	Responds rapidly to NSAIDs. Symptoms resolve within days and rarely recur after viral clearance
Polyarteritis nodosa (PAN)	Polyarthritis, polyarthralgia, rash, fever, livedo reticularis, abdominal pain, diarrhea, weight loss, peripheral nervous system involvement, and hypertension	Biopsy (arteritis or aneurysms in medium-sized arteries); ANCA (−)	Combinations of antiviral drugs, corticosteroids, and plasma exchange	HBV-related PAN is characterized by fewer relapses but has higher mortality than the non-HBV form	Necrotizing inflammation of medium-sized arteries with transmural fibrinoid necrosis; biopsy confirms arteritis or microaneurysms. Often associated with HBV surface antigen–antibody immune complex deposition	Requires antiviral therapy combined with corticosteroids and/or plasma exchange. Prognosis improves significantly with viral suppression
Glomerulopathies (MN/MPGN)	Proteinuria; renal failure	Decreased of C3 and C4 Level; biopsy (microspherular substructures)	Antiviral treatment; corticosteroids	Renal involvement improves after HBsAg clearance, but the disease may progress to chronic renal failure in a small number of patients	Deposition of immune complexes (HBsAg-HBsAb) in glomerular basement membrane, leading to mesangial and subendothelial inflammation. Complement (C3/C4) often reduced	Antiviral therapy improves renal outcomes in most cases. Some progress to chronic kidney disease despite HBsAg clearance

HBsAg: Hepatitis B surface antigen; HBsAb: Hepatitis B surface antibody; HBV: Hepatitis B virus; C3: Complement component 3; C4: Complement component 4; ANCA: Anti-neutrophil cytoplasmic antibody; MN: Membranous nephropathy; MPGN: Membranoproliferative glomerulonephritis; anti-CCP: Anti-cyclic citrullinated peptide antibodies; ANA: Antinuclear antibody; RF: Rheumatoid factor; IgM: Immunoglobulin M; NSAIDs: Nonsteroidal anti-inflammatory drugs.