Lichen planus (LP) can be difficult to manage. Inconsistent response to therapy often frustrates patients and physicians. Many patients with LP will experience only mild symptoms, but for others, the disease causes severe discomfort. Therefore, an individualized approach to treatment is required, with careful consideration of disease burden as well as the risks and benefits of treatment options. A multidisciplinary approach involving dermatologists, dentists, otolaryngologists, gynecologists, gastroenterologists, and others may be necessary depending on disease distribution. Clinically relevant drugs known to exacerbate LP should be discontinued if possible. Patients should take precautions to minimize trauma to the skin and mucosal surfaces. Good oral hygiene, including regular professional dental care, should be encouraged.1 Contact reactions to metals can trigger LP, therefore patch testing is often beneficial for oral lichen planus (OLP).
Various pharmacologic and light-based treatments have been proposed for mucosal lichen planus (MLP), cutaneous lichen planus (CLP), and the related disorders lichen planopilaris (LPP) and frontal fibrosing alopecia (FFA). Evidence supporting most of these therapies is limited to small case series and anecdotes, and is at best inconclusive.2 Topical immunosuppressive agents have the highest level of evidence supporting their use as first-line therapies. Systemic immunosuppressive and anti-inflammatory agents are indicated for generalized, severe, and/or refractory disease.2 Systemic 5α-reductase inhibitors are recommended as first-line adjunctive therapy for hair loss secondary to frontal fibrosing alopecia (FFA).3 They should be used concomitantly with topical/intralesional corticosteroids or systemic immunosuppressants.4 See Table 12-1.
Table 12-1Lichen Planus Treatment Table ||Download (.pdf) Table 12-1 Lichen Planus Treatment Table
|MEDICATION NAME ||INDICATION ||MECHANISM OF ACTION ||DOSING ||ADVERSE EFFECTS ||SUGGESTED MONITORING ||LEVEL OF EVIDENCE (REFERENCE) |
|Local Therapy || || || || || || |
|Topical and/or intralesional corticosteroids || |
Topical: CLP, MLP, LPP
Intralesional: FFA; CLP, MLP, and LPP refractory to 8-12 wk of topical corticosteroids
|Anti-inflammatory via activation of corticosteroid receptor || |
Topical: for sensitive sites, 1%-2.5% hydrocortisone cream/ointment 1-2 times daily; transition to TCI if ineffective after 2 wk.
For nonsensitive sites, 0.1% triamcinolone cream/ointment (or similar mid-potency agent)
1-2 times daily; escalate to 0.05% clobetasol cream/ointment (or similar ultrapotent agent) if ineffective after 2 wk.
IL: triamcinolone 5-10 mg/mL once monthly
HEENT: Oral candidiasis (common)
Skin: atrophy, hypopigmentation
|None ||IA2,5-9 |
|Topical calcineurin inhibitors ||CLP, MLP ||Inhibits T cell-mediated immune responses ||Twice daily tacrolimus 0.03%-0.1% or pimecrolimus 1% ||Minimal ||None ||IA10-18 |
|Topical retinoids ||MLP ||Activates retinoic acid receptors; anti-inflammatory and promotes epithelial turnover/maturation ||Isotretinoin (0.05%-0.18%) or tretinoin (0.1%) mucoadhesive gel twice daily ||Localized irritation, especially for erosive lesions ||None ||IB2,19-21 |
|Topical ruxolitinib ||CLP ||Anti-inflammatory via JAK inhibition ||1.5% cream twice daily ||None ||None ||IIA22 |
|Systemic Therapy ||Reserved for severe or refractory disease || || || || || |
|Corticosteroids ||CLP, MLP, LPP ||Anti-inflammatory via activation of corticosteroid receptor ||Prednisone 0.3-1.0 mg/kg once daily for 4-6 wk ...|