Bilateral Lichen Striatus: A Case Report with Review of Literature.

Lichen striatus is a self-limiting dermatosis presenting with sudden eruption of lichenoid papules along the lines of Blaschko. A 5-year-old girl presented with asymptomatic hypopigmented linear lesions over both upper limbs. The histopathological examination revealed spongiosis, vacuolar alteration of the basal layer and lymphocytic exocytosis with a mild-to-moderate perivascular mononuclear infiltrate in the dermis. Lichen striatus was diagnosed based upon the characteristic clinical and histopathological findings. The pathogenetic mechanism of bilateral lichen striatus is unknown at present, however, a somatic mutation in two different clones of cells can be a possibility.

Introduction

Lichen striatus is an uncommon, self-limiting linear dermatosis that predominantly affects children of 5–15 years of age. It is diagnosed based upon its appearance and morphological expression along the lines of Blaschko.[1] It usually appears as a sudden eruption of small skin-colored or pink lichenoid papules forming a continuous or interrupted, linear band on the limbs or trunk. The papules are usually asymptomatic, flat topped, smooth or scaly and evolve within several days to weeks. In dark-pigmented individuals, it may appear as a band-like area of hypopigmentation.[2] The lesions may extend from a few centimeters to involve the full length of an extremity. It is usually unilateral and single, although, bilateral or multiple parallel bands have been documented.[1234] To the best of our knowledge, only four cases of bilateral lichen striatus have been previously reported in the literature.

Case Report

A 5-year-old girl presented with a hypopigmented linear band on the left upper extremity since 1 month. The lesions first appeared on the inner aspect of the left forearm and later extended linearly to involve the posterior aspect of the arm and trunk on the same side [Figure 1]. Further, her parents had also noticed hypopigmented pin head-sized asymptomatic raised lesions on the contralateral forearm in the last 5 days [Figure 2]. The lesions were not itchy. Nails were uninvolved. There were no features suggestive of atopy. Skin biopsy from the right forearm showed mild hyperkeratosis, spongiosis, vacuolar alteration of basal layer and lymphocytic exocytosis with a mild-to-moderate perivascular mononuclear inflammatory infiltrate and melanin incontinence in the dermis [Figure 3]. A distinctive feature of lichen striatus is a dense infiltrate extending deep into the dermis around the hair follicles and eccrine sweat glands and ducts in some cases, which was absent in our case. It was diagnosed as a case of lichen striatus based upon the characteristic clinical and histopathological findings. Emollients were prescribed for treatment and the lesions resolved within 3 months leaving no sequelae.

Figure 1

Hypopigmented macules forming a linear band along the lines of Blaschko extending from the back to the left arm and forearm

Figure 2

Hypopigmented papules present linearly on the right forearm and hypopigmented linear macular lesion on the left forearm

Figure 3

Epidermis showing spongiosis, vacuolar alteration of basal layer and lymphocytic exocytosis with a mononuclear infiltrate in the dermis (H and E, ×100)

Discussion

The pathogenesis of lichen striatus is elusive, however, various etiological factors have been implicated. The most commonly accepted hypothesis is that of environmental stimuli acting in a genetically predisposed individual.[5] Linear dermatoses such as lichen striatus follow the lines of Blaschko, which are embryonic in origin. A somatic mutation in early embryogenesis results in formation of an abnormal clone of cells, which on subsequent exposure to an environmental stimulus results in formation of lichen striatus.

Others believe that it is secondary to an autoimmune response mediated by T cells.[6] Atopy has been reported to be a predisposing factor. Drugs, such as adalimumab and etanercept, BCG and hepatitis B vaccination, UV exposure from a tanning bed, minor trauma, insect bite, and viral infections, such as varicella, influenza, and human herpes viruses 6 and 7 have been reported as triggers.[789]

The histopathological findings are nonspecific and vary depending on the stage of evolution. Usually a superficial perivascular lymphohistiocytic infiltrate is seen, which may extend focally into the lower part of epidermis causing vacuolar alteration of basal layer with melanin incontinence. The epidermal reaction pattern may include spongiosis, focal parakeratosis, and lymphocyte exocytosis.[10]

The course of LS is self-limiting, usually regressing spontaneously within 3–12 months, thus requiring symptomatic treatment only. The patient should be reassured and emollients and topical steroids may be used to relieve dryness and pruritus. Post-inflammatory hypopigmentation or hyperpigmentation can develop as a sequelae.[1]

Our patient had lesions which corroborated with the clinical and histopathological findings in lichen striatus, however, they were distributed bilaterally. To the best of our knowledge, only four cases of bilateral LS have been described previously [Table 1].[12311] Although the pathogenesis is unknown at present, a somatic mutation in two different clones of keratinocytes can be a possibility.

Table 1

Review of cases of bilateral lichen striatus

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Conflicts of interest

There are no conflicts of interest.