Lichen striatus successfully treated with oral cyclosporine.

Lichen striatus is an acquired, benign, linear inflammatory dermatosis characterized by a sudden skin eruption along Blaschko's lines that usually is not associated with specific etiologic agents. In most cases, it is a self-limited dermatosis, but may relapse. Topical steroids are its first-line therapy, but this treatment is not always effective. We describe the case of a 45-year-old woman affected by a lichen striatus on her right limb resistant to topical corticosteroid therapy. The patient was successfully treated with cyclosporine (4 mg/kg/die) for 4 weeks with no recurrence of the dermatitis during the subsequent 1-year follow-up period.

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 acitretin[1] and 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.

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.