Dermatology · Papulosquamous Disorders
The facts most likely to be tested
Lichen planus presents clinically as the 6 Ps: planar, purple, polygonal, pruritic, papules, and plaques.
The surface of the lesions often displays a fine, white, lacy network of lines known as Wickham striae.
The condition exhibits the Koebner phenomenon, where new lesions develop at sites of localized skin trauma.
Oral involvement frequently manifests as reticular or erosive lesions on the buccal mucosa.
Histopathology reveals a dense band-like lymphocytic infiltrate at the dermo-epidermal junction with sawtooth rete ridges.
Lichen planus is strongly associated with Hepatitis C virus (HCV) infection, necessitating screening in affected patients.
First-line treatment for localized cutaneous disease is high-potency topical corticosteroids.
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A 45-year-old woman presents to the clinic complaining of intense itching on her wrists and ankles. Physical examination reveals multiple violaceous, flat-topped, polygonal papules distributed symmetrically on the flexor surfaces of the wrists. Close inspection of the lesions reveals a fine, white, lacy reticular pattern on the surface. The patient has no history of recent trauma, but she notes that new bumps appear where she scratches her skin. She has a history of chronic Hepatitis C infection.
What is the most likely diagnosis?
Lichen planus
The patient's presentation of the '6 Ps' and the presence of Wickham striae are pathognomonic for lichen planus, which is highly associated with Hepatitis C.
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Etiology / Epidemiology
Chronic inflammatory condition often linked to Hepatitis C and cell-mediated immunity.
Clinical Manifestations
Presents as 6 Ps: pruritic, planar, purple, polygonal, papules, plaques with Wickham striae.
Diagnosis
Clinical diagnosis confirmed by punch biopsy showing saw-tooth rete ridges.
Treatment
High-potency topical corticosteroids are first-line; avoid systemic steroids for long-term use.
Prognosis
Self-limiting in 50% of cases within 18 months; monitor for squamous cell carcinoma.
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Epidemiology & Etiology
Most common in adults aged 30–60 years. Strong association with Hepatitis C virus infection. Can be triggered by medications including thiazides, beta-blockers, and gold.
Pertinent Anatomy
Affects the skin, oral mucosa, scalp, and nails. Oral involvement often presents as reticular or erosive patterns on the buccal mucosa.
Pathophysiology
T-cell mediated autoimmune reaction against basal keratinocytes. Results in interface dermatitis and destruction of the basal layer. Chronic inflammation leads to the characteristic saw-tooth epidermal architecture.
Clinical Manifestations
Classic 6 Ps: pruritic, planar, purple, polygonal, papules, plaques. Look for Wickham striae (white lacy lines) on lesions. Erosive oral lesions carry a higher risk of malignant transformation.
Diagnosis
Punch biopsy is the gold standard. Histology reveals band-like lymphocytic infiltrate at the dermo-epidermal junction and saw-tooth rete ridges.
Treatment
High-potency topical corticosteroids (e.g., clobetasol) are the standard of care. For refractory cases, use narrow-band UVB or systemic agents like acitretin. Systemic corticosteroids should be avoided for chronic maintenance due to side effects.
Prognosis
Cutaneous lesions typically resolve within 18 months. Oral lichen planus is chronic and requires long-term monitoring for squamous cell carcinoma development.
Differential Diagnosis
Psoriasis: silvery scales, extensor surfaces
Lichen simplex chronicus: lichenification from chronic scratching
Leukoplakia: non-removable white patch, pre-malignant
Erythema multiforme: targetoid lesions, often drug-induced
Lupus erythematosus: photosensitive, positive ANA