INFLAMMATORY AND IMMUNE-MEDIATED SKIN DISORDERS

Lichen Planus

Classification: T-cell-mediated interface dermatitis targeting basal keratinocytes (Norris, 2020; Pincus & McCalmont, 2019).

Key diagnostic discriminator: Pruritic, purple, polygonal, planar papules/plaques with Wickham striae. Examine oral/genital mucosa, scalp, and nails because disease can scar or cause functional injury (Gohara et al., 2012; Pincus & McCalmont, 2019).

Clinical priority: Painful oral/genital erosions can impair intake or sexual/urinary function. Ocular or laryngeal disease and scarring alopecia require specialist care (Gohara et al., 2012; Pincus & McCalmont, 2019).

Etiology and risk factors

  • Often idiopathic. Cell-mediated autoimmunity targets basal keratinocytes after an incompletely defined trigger (Gohara et al., 2012; Norris, 2020; Pincus & McCalmont, 2019).
  • Associated contexts include hepatitis C in some populations and lichenoid drug reactions from selected antihypertensives, NSAIDs, antimalarials, and other agents. Association strength varies geographically (Gohara et al., 2012; Norris, 2020; Pincus & McCalmont, 2019).

Pathophysiology

  • Cytotoxic T cells injure basal keratinocytes at the dermoepidermal junction, producing a dense band-like lymphocytic infiltrate and interface change (Norris, 2020; Pincus & McCalmont, 2019).
  • Hypergranulosis creates Wickham striae; pigment incontinence and dermal melanophages contribute to violaceous lesions and residual hyperpigmentation (Norris, 2020; Pincus & McCalmont, 2019).

Clinical manifestations

  • Intensely pruritic, flat-topped, violaceous polygonal papules, often on flexor wrists/forearms, ankles, lower back, and genital skin. Koebner phenomenon may occur (Gohara et al., 2012; Pincus & McCalmont, 2019).
  • Fine white reticular lines are Wickham striae. Oral disease may be reticular and asymptomatic or erosive/painful. Scalp disease may scar; nail disease may cause ridging, thinning, or pterygium (Gohara et al., 2012; Pincus & McCalmont, 2019).

Findings that argue against or redirect

  • Wipeable white oral plaques favor candidiasis. Scale with fungal elements favors tinea (Gohara et al., 2012; Pincus & McCalmont, 2019).
  • A photodistributed or symmetric eruption beginning after a medication favors a lichenoid drug eruption, although biopsy can resemble idiopathic disease (Gohara et al., 2012; Pincus & McCalmont, 2019).
  • Lack of classic morphology does not exclude oral, hypertrophic, erosive, follicular, or nail variants (Gohara et al., 2012; Pincus & McCalmont, 2019).

Diagnostic evaluation

  • Diagnose clinically when classic; perform punch biopsy for atypical, erosive, hypertrophic, scarring, or diagnostically uncertain disease (Gohara et al., 2012; Pincus & McCalmont, 2019).
  • Review medications and examine skin, oral/genital mucosa, scalp, and nails. Test for hepatitis C when epidemiology, risk, or local practice supports it (Gohara et al., 2012; Pincus & McCalmont, 2019).

Expected diagnostic and laboratory findings

  • Histology: hyperkeratosis, wedge-shaped hypergranulosis, irregular sawtooth rete ridges, basal-cell degeneration, Civatte bodies, and a band-like lymphocytic infiltrate at the interface (Gohara et al., 2012; Pincus & McCalmont, 2019).
  • No routine blood test confirms lichen planus. Hepatitis testing identifies an associated condition, not the rash mechanism itself (Gohara et al., 2012; Pincus & McCalmont, 2019).

Differential diagnosis

  • Lichenoid drug eruption: medication timeline, often more generalized/symmetric or photodistributed; eosinophils/parakeratosis may support drug cause (Gohara et al., 2012; Pincus & McCalmont, 2019).
  • Psoriasis: silvery extensor plaques and psoriasiform rather than interface histology (Gohara et al., 2012; Pincus & McCalmont, 2019).
  • Secondary syphilis: palm/sole or systemic findings and positive serology (Gohara et al., 2012; Pincus & McCalmont, 2019).
  • Oral candidiasis or leukoplakia: wipeability, culture/clinical context, or biopsy distinguishes (Gohara et al., 2012; Pincus & McCalmont, 2019).

Treatment and management

  • High-potency topical corticosteroids are first line for limited cutaneous disease; use site-appropriate topical therapy for oral/genital disease (Norris, 2020; Pincus & McCalmont, 2019).
  • Phototherapy or systemic anti-inflammatory/immunomodulatory therapy may be required for widespread, erosive, hypertrophic, follicular, scarring, or refractory disease. Stop a likely culprit medication when clinically safe (Norris, 2020; Pincus & McCalmont, 2019).

Additional complications and red flags

  • Long-standing erosive mucosal disease has a small squamous-cell carcinoma risk and requires surveillance (Gohara et al., 2012; Pincus & McCalmont, 2019).

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References

Gohara, M. A., Schaffer, J. V., Abbasi, N. R., Kingsley, M. M., Sheehan, J. M., & Arndt, K. A. (2012). Inflammatory dermatoses (rashes). In M. C. Henderson, L. M. Tierney, Jr., & G. W. Smetana (Eds.), The patient history: An evidence-based approach to differential diagnosis (2nd ed.). McGraw-Hill.

Norris, T. L. (2020). Porth’s essentials of pathophysiology (5th ed.). Wolters Kluwer.

Pincus, L. B., & McCalmont, T. H. (2019). Diseases of the skin. In G. D. Hammer & S. J. McPhee (Eds.), Pathophysiology of disease: An introduction to clinical medicine (8th ed.). McGraw-Hill Education.