Treatment of Leukocytoclastic Vasculitis
Immediate First Step: Identify and Remove Triggers
The cornerstone of treatment is immediate discontinuation of any offending medication, which alone often induces prompt resolution without requiring immunosuppressive therapy 1. Common culprit drugs include hydralazine, propylthiouracil, levamisole-adulterated cocaine, minocycline, levetiracetam, and warfarin 1. Additionally, identify and treat any underlying infections or systemic diseases that may be triggering the vasculitis 2.
Mild, Self-Limited Disease (Most Common Presentation)
For patients with isolated cutaneous involvement without systemic symptoms or impending necrosis:
- Conservative management is sufficient - the disease typically resolves spontaneously within weeks 2, 3
- Use compression stockings to reduce purpura and leg edema 2
- Provide symptomatic treatment only (elevation, rest, NSAIDs for pain if tolerated) 2
- Monitor closely for progression to skin necrosis or systemic involvement 2
When to Escalate: Signs of Incipient Skin Necrosis
Add systemic corticosteroids (prednisolone 1 mg/kg/day, maximum 60 mg/day) only when hemorrhagic blisters or signs of incipient skin necrosis appear 1, 2. This is the critical threshold for escalation - do not wait for frank necrosis to develop 2, 4.
Chronic or Relapsing Disease (>3 Months Duration)
For patients with persistent or recurrent lesions despite trigger removal:
First-line: Colchicine 2, 4, 5
- Effective in most patients with chronic disease
- Better safety profile than long-term corticosteroids
- Typical dosing: 0.6 mg twice daily
- Use when colchicine fails or is contraindicated
- Requires screening for G6PD deficiency before initiation 3
- Monitor blood counts regularly due to risk of blood dyscrasia, neuropathy, and hypersensitivity syndrome 3
- Topical dapsone may be considered for localized disease with fewer systemic side effects 3
Third-line: Azathioprine 5
- Reserve for refractory cases
- Requires monitoring for bone marrow suppression
Critical Pitfall: Do NOT Confuse with ANCA-Associated Vasculitis
Never treat drug-induced or isolated cutaneous leukocytoclastic vasculitis with cyclophosphamide or rituximab 1. These aggressive immunosuppressants are reserved for true ANCA-associated systemic vasculitis (granulomatosis with polyangiitis, microscopic polyangiitis) and carry significant toxicity including bladder cancer risk, infection, and infertility 6, 1.
Diagnostic clues that suggest drug-induced (not systemic AAV):
- High-titer MPO-ANCA or dual MPO/PR3 positivity 1
- Discordance between ANCA immunofluorescence and ELISA results 1
- Positive ANA and antihistone antibodies 1
- Isolated cutaneous involvement without glomerulonephritis or pulmonary hemorrhage 1
Special Considerations
Henoch-Schönlein Purpura (IgA-dominant): More likely to have systemic involvement including glomerulonephritis 2, 4. In adults with severe glomerulonephritis, evidence for corticosteroid efficacy is insufficient; consider ACE inhibitors for renal protection instead 4.
Cryoglobulinemic vasculitis: Treat the underlying disease (often hepatitis C or plasma cell disorder), sometimes supplemented by plasmapheresis 4.
Urticarial vasculitis: Start with dapsone or colchicine as first-line agents 4.
What NOT to Use
The following have shown only sporadic effectiveness and should not be first-line choices: