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, β-blockers, sulfonylureas, antimalarials, penicillamine, gold salts, angiotensin-converting enzyme inhibitors, NSAIDs, isoniazid, tetracyclines, and allopurinol

Commonly Associated Conditions

• Hepatitis C virus infection, particularly in certain geographic regions (Asia, South America, the Middle East, Europe). Hepatitis should be considered in patients with widespread presentations of LP and those with primarily oral disease.
• Chronic active hepatitis, lichen nitidus, and primary biliary cirrhosis
• Dyslipidemia
• Others:
  • Bullous pemphigoid
  • Alopecia areata
  • Myasthenia gravis
  • Vitiligo
  • Ulcerative colitis
  • Graft-versus-host reaction
  • Lupus erythematosus (lupus erythematosus–LP overlap syndrome)
  • Morphea and lichen sclerosus et atrophicus