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Lichen Planus
Mercedes E. Gonzalez, MD, FAAD
Herbert P. Goodheart, MD
image BASICS
Lichen planus (LP) is an idiopathic eruption with characteristic shiny, flat-topped (Latin: planus, “flat”) purple (violaceous) papules and plaques on the skin, often accompanied by characteristic mucous membrane lesions. Itching may be severe.
DESCRIPTION
  • Classic (typical) LP is a relatively uncommon inflammatory disorder of the skin and mucous membranes; hair and nails may also be affected.
    • Skin lesions are small, flat, angular, red-to-violaceous, shiny, pruritic papules and/or plaques with overlying fine, white lines (called Wickham striae), or gray-white puncta; most commonly seen on the flexor surfaces of the upper extremities, extensor surfaces of the lower extremities, the genitalia, and on the mucous membranes
    • On the oral mucosa, lesions typically appear as raised white lines in a lacelike pattern seen most often on the buccal mucosa.
    • Onset is abrupt or gradual. Course is unpredictable; may resolve spontaneously, recur intermittently, or persist for many years
  • Drug-induced LP
    • Clinical and histopathologic findings may mimic those of classic LP. Lesions usually lack Wickham striae (see in the following text) and oral involvement is rare.
    • There is generally a latent period of months from drug introduction until lesions appear.
    • Lesions resolve when the inciting agent is discontinued, often after a prolonged period.
  • LP variants
    • Follicular: also called lichen planopilaris; typically seen on the scalp, can lead to scarring alopecia
    • Annular: Papules spread centrifugally as central area resolves; occur on glans penis, axillae, and oral mucosa
    • Linear: may be an isolated finding
    • Hypertrophic: itchy, hyperkeratotic, thick plaques on dorsal legs and feet
    • Atrophic: rare, most often the result of resolved lesions
    • Bullous LP: Intense inflammation in the dermis leads to blistering of epidermis.
    • LP pemphigoides: a combination of LP and bullous pemphigoid (IgG autoantibodies to collagen 17)
    • Nail LP: affects the nail matrix, lateral thinning, longitudinal ridging, and fissuring
  • System(s) affected: skin/exocrine
  • Synonym(s): lichenoid eruptions
EPIDEMIOLOGY
  • Predominant age: 30 to 60 years old; rare in children and the geriatric population
  • Predominant sex: female > male
Prevalence
In the United States, 450/100,000
ETIOLOGY AND PATHOPHYSIOLOGY
LP is considered to be a T-cell-mediated autoimmune response to self-antigens on damaged keratinocytes.
RISK FACTORS
Exposure to certain drugs or chemicals
  • Thiazides, furosemide, &bgr;-blockers, sulfonylureas, antimalarials, penicillamine, gold salts, and angiotensin-converting enzyme inhibitors
  • Rarely: photo-developing chemicals, dental materials, tattoo pigments
COMMONLY ASSOCIATED CONDITIONS
  • An association has been noted between LP and hepatitis C virus infection, particularly in certain geographic regions (Asia, South America, the Middle East, Europe) (1). Hepatitis should be considered in patients with widespread presentations of LP and those with primarily oral disease.
  • In addition, chronic active hepatitis, lichen nitidus, and primary biliary cirrhosis have been noted to coexist with LP.
  • Association with dyslipidemia has been reported (2)[B].
  • LP has also been reported in association with other diseases of altered immunity, more often than would be expected by chance.
    • Bullous pemphigoid
    • Alopecia areata
    • Myasthenia gravis
    • Vitiligo
    • Ulcerative colitis
    • Graft-versus-host reaction
    • Lupus erythematosus (lupus erythematosus-LP overlap syndrome)
    • Morphea and lichen sclerosis et atrophicus
image DIAGNOSIS
LP is most commonly diagnosed by its appearance despite its range of clinical presentations. A skin biopsy should be performed if the diagnosis is in doubt.
PHYSICAL EXAM
  • Skin (often severe pruritus)
    • Papules: 1 to 10 mm, shiny, flat-topped (planar) lesions that occur in crops; lesions may have a fine scale.
    • Evidence of scratching (i.e., crusts and excoriations) is usually absent.
    • Color: violaceous, with white lacelike pattern (Wickham striae) on surface of papules. Wickham striae are best seen after topical application of mineral oil and, if present, are virtually pathognomonic for LP.
    • Shape: polygonal or oval. Annular lesions may appear on trunk and mucous membranes. Various shapes and sizes may be noted (polymorphic).
    • Arrangement: may be grouped, linear, or scattered individual lesions
    • Koebner phenomenon (isomorphic response): New lesions may be noted at sites of minor injuries, such as scratches or burns.
    • Distribution: ventral surface of wrists and forearms, dorsa hands, glans penis, dorsa feet, groin, sacrum, shins, and scalp. Hypertrophic (verrucous) lesions may occur on lower legs and may be generalized.
    • Postinflammatory hyperpigmentation: Lesions typically heal, leaving darkly pigmented macules in their wake.
  • Mucous membranes (40-60% of patients with skin lesions; 20% have mucous membrane lesions without skin involvement)
    • Most commonly asymptomatic, nonerosive, milkywhite lines with an elegant, lacy, netlike streaked pattern
    • Usually seen on buccal mucosa but may appear on tongue, gingiva, palate, or lips
    • Less commonly, LP may be erosive; rarely bullous
    • Painful, especially if ulcers present
    • Lesions may develop into squamous cell carcinoma (1-3%).
    • Glans penis, labia minora, vaginal vault, and perianal areas may be involved.
  • Hair/scalp
    • LP of the hair follicle (lichen planopilaris) presents with keratotic plugs at the follicle orifice with a violaceous rim; may result in atrophy and permanent destruction of hair follicles (scarring alopecia)
  • Nails (10%)
    • Involvement of nail matrix may cause proximalto-distal linear grooves and partial or complete destruction of nail bed with pterygium formation.
DIFFERENTIAL DIAGNOSIS
  • Skin
    • Lichen simplex chronicus
    • Eczematous dermatitis
    • Psoriasis
    • Discoid lupus erythematosus
    • Other lichenoid eruptions (those that resemble LP)
    • Pityriasis rosea
    • Lichen nitidus
  • Oral mucous membranes
    • Leukoplakia
    • Oral hairy leukoplakia
    • Candidiasis
    • Squamous cell carcinoma (particularly in ulcerative lesions)
    • Aphthous ulcers
    • Herpetic stomatitis
    • Secondary syphilis
  • Genital mucous membranes
    • Psoriasis (penis and labia)
    • Nonspecific balanitis, Zoon balanitis
    • Fixed drug eruption (penis)
    • Candidiasis (penis and labia)
    • Pemphigus vulgaris, bullous pemphigoid, and Behçet disease (all rare)
  • Hair and scalp
    • Scarring alopecia (central centrifugal cicatricial alopecia)
DIAGNOSTIC TESTS & INTERPRETATION
If suggested by history
  • Serology for hepatitis
  • Liver function tests
P.609

Diagnostic Procedures/Other
  • Skin biopsy
  • Direct immunofluorescence helps to distinguish LP from discoid lupus erythematosus.
Test Interpretation
  • Dense, bandlike (lichenoid) lymphocytic infiltrate of the upper dermis
  • Vacuolar degeneration of the basal layer
  • Hyperkeratosis and irregular acanthosis, increased granular layer
  • Basement membrane thinning with “saw-toothing”
  • Degenerative keratinocytes, known as colloid or Civatte bodies, are found in the lower epidermis.
  • Melanin pigment in macrophages
image TREATMENT
Although LP can resolve spontaneously, treatment is usually requested by patients who may be severely symptomatic or troubled by its cosmetic appearance.
GENERAL MEASURES
  • Goal is to relieve itching and resolve lesions.
  • Asymptomatic oral lesions require no treatment.
MEDICATION
First Line
  • Skin
  • Superpotent topical steroids (e.g., 0.05% clobetasol propionate) twice daily.
    • Potent topical steroids such as triamcinolone acetonide 0.1% or fluocinonide 0.05% under occlusion
    • Intralesional corticosteroids (e.g., triamcinolone [Kenalog] 5 to 10 mg/mL) for recalcitrant and hypertrophic lesions
    • Antihistamines (e.g., hydroxyzine, 25 mg PO q6h) have limited benefit for itching but may be helpful for sedation at bedtime.
    • “Soak and smear” technique: can lead to a rapid improvement of symptoms in even 1 to 2 days and may obviate the need for systemic steroids. Soaking allows water to hydrate the stratum corneum and allows the anti-inflammatory steroid in the ointment to penetrate more deeply into the skin. Smearing of the ointment traps the water in the skin because water cannot move out through greasy materials.
      • Soaking is done in a bathtub using lukewarm plain water for 20 minutes, then, without drying the skin, the affected area is immediately smeared with a thin film of the steroid ointment containing clobetasol or another superpotent topical steroid.
      • Soak and smear may be done for 4 to 5 days or longer, if necessary. The treatments are best done at night because the greasy ointment applied to the skin gets on pajamas (instead of on daytime clothes) and the ointment is on the skin during sleep. A topical steroid cream is applied thereafter during the daytime hours, if necessary.
  • Mucous membranes
    • For oral, erosive, painful LP, a Cochrane review found at best weak evidence for the effectiveness of any intervention (3)[A].
      • Topical corticosteroids (0.1% triamcinolone [Kenalog] in Orabase) or 0.05% clobetasol propionate ointment BID
      • Intralesional corticosteroids
      • Topical 0.1% tacrolimus (Protopic ointment) BID or 1% pimecrolimus (Elidel) cream BID. A Cochrane review found no evidence that calcineurin inhibitors are better than placebo (4)[A].
      • Topical retinoids (e.g., 0.05% tretinoin [retinoic acid] in Orabase)
Pediatric Considerations
Children may absorb a proportionally larger amount of topical steroid because of larger skin surface-toweight ratio.
Second Line
Skin and mucous membranes
  • Intralesional corticosteroids
  • Topical 0.1% tacrolimus (Protopic ointment) BID or topical 1% pimecrolimus (Elidel) cream BID
  • Oral prednisone: used only for a short course (e.g., 30 to 60 mg/day for 2 to 4 weeks) or IM triamcinolone (Kenalog) 40 to 80 mg every 6 to 8 weeks
    • Precautions with systemic steroids
      • Systemic absorption of steroids may result in hypothalamic-pituitary-adrenal axis suppression, Cushing syndrome, hyperglycemia, or glucosuria.
      • Increased risk with high-potency topical steroids (i.e., use over large surface area, prolonged use, occlusive dressings)
      • In pregnancy: usually safe, but benefits must outweigh the risks
  • Oral retinoids: Isotretinoin in doses of 10 mg PO daily for 2 months, acitretin 30 mg, or alitretinoin 30 mg PO daily have resulted in improvement in some refractory cases. Observe carefully for resultant dyslipidemia.
  • Oral metronidazole 500 mg BID for 20 to 60 days can be given as a safer alternative to systemic corticosteroids.
  • Cyclosporine may be used in severe cases, but cost and potential toxicity limit its use; topical use for severe oral involvement refractory to other treatments
  • Thalidomide
  • Psoralen ultraviolet-A (PUVA), broad- or narrowband ultraviolet B (UVB) (5)[A]
  • Griseofulvin (5)[A]
  • Azathioprine
  • Mycophenolate mofetil
  • Metronidazole
INPATIENT CONSIDERATIONS
Admission Criteria/Initial Stabilization
Outpatient care
image ONGOING CARE
FOLLOW-UP RECOMMENDATIONS
Patient Monitoring
Serial oral examinations for erosive/ulcerative lesions
PATIENT EDUCATION
  • Oral, erosive, or ulcerative LP: annual follow-up to screen for malignancy (6)[A]
  • Avoid spicy foods, cigarettes, and excessive alcohol.
  • Avoid dry crispy foods such as corn chips, pretzels, and toast.
PROGNOSIS
  • Spontaneous resolution in weeks is possible, but disease may persist for years, especially oral lesions and hypertrophic lesions on the shins.
  • There is a tendency toward relapse.
  • Recurrence in 12-20%, especially in those with generalized involvement
REFERENCES
1. Shengyuan L, Songpo Y, Wen W, et al. Hepatitis C virus and lichen planus: a reciprocal association determined by a meta-analysis. Arch Dermatol. 2009;145(9):1040-1047.
2. Arias-Santiago S, Buendía-Eisman A, Aneiros-Fernández J, et al. Cardiovascular risk factors in patients with lichen planus. Am J Med. 2011;124(6):543-548.
3. Cheng S, Kirtschig G, Cooper S, et al. Interventions for erosive lichen planus affecting mucosal sites. Cochrane Database Syst Rev. 2012;(2):CD008092.
4. Thongprasom K, Carrozzo M, Furness S, et al. Interventions for treating oral lichen planus. Cochrane Database Syst Rev. 2011;(7):CD001168.
5. Atzmony L, Reiter O, Hodak E, et al. Treatments for cutaneous lichen planus: a systematic review and meta-analysis. Am J Clin Dermatol. 2016;17(1):11-22.
6. Fitzpatrick SG, Hirsch SA, Gordon SC. The malignant transformation of oral lichen planus and oral lichenoid lesions: a systematic review. J Am Dent Assoc. 2014;145(1):45-56.
Additional Reading
&NA;
  • Fazel N. Cutaneous lichen planus: a systematic review of treatments. J Dermatolog Treat. 2015;26(3):280-283.
  • Kolios AG, Marques Maggio E, Gubler C, et al. Oral, esophageal and cutaneous lichen ruber planus controlled with alitretinoin: case report and review of the literature. Dermatology. 2013;226(4):302-310.
Codes
&NA;
ICD10
  • L43.9 Lichen planus, unspecified
  • L43.0 Hypertrophic lichen planus
  • L43.1 Bullous lichen planus
Clinical Pearls
&NA;
  • Remember the 7 P's of LP: purple, planar, polygonal, polymorphic, pruritic (not always), papules that heal with postinflammatory hyperpigmentation.
  • Serial oral or genital exams are indicated for erosive/ulcerative LP lesions to monitor for the development of squamous cell carcinoma.
  • An association has been noted between LP and hepatitis C virus infection, chronic active hepatitis, and primary biliary cirrhosis.
  • The “soak and smear” technique can lead to a rapid improvement of symptoms in 1 to 2 days and may obviate the need for systemic steroids.