Lichen striatus (LS) is an acquired, benign, linear inflammatory dermatosis characterized by a sudden eruption of asymptomatic small, flat-topped, lichenoid, scaly papules along Blaschko’s lines. The skin lesions are frequently localized on the limbs, distributed as a continuous or interrupted linear band of pink, red, tan, or skin-colored papules.^1,2 It often occurs in children, most commonly in 2- to 3-year-old, although it is infrequently observed also in adults.²

Digital involvement may lead to onycholysis, longitudinal ridging, splitting, and nail loss.³ Although LS is not associated with specific etiologic agents, it could be triggered by infections, trauma, hypersensitivity reactions, vaccines, medications, and pregnancy.¹ In most cases, LS is a self-limited dermatosis and resolves within 1 year, but it may relapse.

Topical steroids are first-line therapy for LS, but this treatment is not always effective and prolonged use of corticosteroids may be associated with adverse effects such as cutaneous atrophy.¹ Cases of LS unresponsive to topical steroids have been successfully treated with other therapies such as oral acitretin¹and photodynamic therapy.⁴ We describe the case of an atopic 45-year-old woman presented with a 1-year history of an asymptomatic linear skin eruption on the right limb (Figure 1). During this period of time, the lesions had been treated unsuccessfully with mometasone furoate cream 0.1% for three cycles of treatment (once daily for 2 weeks). Skin examination revealed erythematous and skin-colored papular lesions along the right lower limb following Blaschko’s lines.

No other lesions in any other site was observed. Histopathologic examination of one of these lesions revealed a predominant pattern of interface dermatitis consisting of a dense band-like perivascular inflammatory infiltrate, also round appendages (Figure 2), composed of histiocytes and T lymphocytes CD3 (PanT) and CD8. Hyperparakeratosis and focal spongiosis of epidermis were also observed.

On the basis of the histopathological findings, suggestive for LS,⁵ since little improvement had been obtained with mometasone furoate cream, and after receiving an informed consent by the patient, we decided to administer systemic therapy with cyclosporine (4 mg/kg/die).

The LS regressed completely after only 4 weeks of therapy. No drug side effects and no recurrence of LS were observed during the subsequent 1-year follow-up period.

Figure 1.

Asymptomatic linear skin eruption on the right lower limb of the patient.

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Figure 2.

(a) A dense perivascular inflammatory infiltrate focally with the features of the interface dermatitis (hematoxylin–eosin, 100× original magnification) and (b) most of the perivascular inflammatory cells show intense immunohistochemical expression of CD8 (100× original magnification).

LS is in most cases an asymptomatic and self-limited dermatosis but may resolve leaving post-inflammatory hyper or hypopigmentation causing significant psychological distress for the patient. Moreover, it can relapse and be resistant to topical corticosteroid therapy.⁶ In our case, the patient was resistant to topical steroid treatment while she had a complete response to oral cyclosporine. Although the pathogenesis of LS remains unclear, it has been considered a CD8+ T-cell-mediated inflammatory reaction with a cytotoxic reaction directed toward mutated post-zygotic skin cell.⁷ We may speculate that the therapeutic efficacy of cyclosporine is due to its immunomodulatory activity. This treatment approach could reduce morbidity and prevent complications of LS.

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