Lichen Striatus

Etiology

The exact cause of this condition is unknown, although genetic factors and environmental triggers are believed to play a role in its development. One theory associates lichen striatus with atopy, a genetic predisposition to allergic responses. A study found that 85% of individuals with lichen striatus had a family history of allergy-related conditions, such as atopic dermatitis, asthma, and allergic rhinitis. However, conflicting research offered no similar statistical conclusion. Another study suggests an autoimmune response triggered by pregnancy. Possible connections include vitiligo, characterized by depigmented skin patches, or treatment with drugs like adalimumab and etanercept. Some reports describe lichen striatus as a T-cell-mediated inflammatory disorder.[4][5][6]

Another theory regarding the etiology of lichen striatus involves environmental triggers. For example, outbreaks have been reported among unrelated children sharing the same living environment. A potential viral link has also been suggested, supported by elevated interleukin 1β levels in biopsy samples from affected patients. However, no conclusive evidence fully supports this finding.[7]

Outbreaks have been reported in individuals exposed to UV rays via tanning beds following Bacille Calmette-Guerin (BCG) and hepatitis B vaccinations, as well as after picking a pineapple leaf, sustaining a bumblebee bite, and receiving varicella or influenza infections.[8] Evidence also suggests lichen striatus may result from epigenetic mosaicism, where populations of cells with different genotypes exist. A study proposed a genetic predisposition in affected individuals, with the condition triggered by an immunologic reaction to an infection. This process involves events like methylation or demethylation of a partially silenced genomic element. Reports have also linked lichen striatus to herpesvirus 6 and 7 infections.[9]

Epidemiology

More than 50% of the diagnosed lichen striatus cases involve children aged 5 to 15 years. This skin disorder is rarely seen in adults.[10] No racial predilection has been observed for lichen striatus. Some studies indicate that the condition occurs 2 to 3 times more often in girls than in boys, while others show an equal sex distribution. No consensus exists regarding sex predilection for this skin disorder.

Pathophysiology

The lesions of lichen striatus begin as small pink, flesh-colored, or red spots that may appear raised. These spots begin to coalesce to form a dull, red, linear band for approximately 1 to 2 weeks. The linear lesions can be lightly scaly. The band itself is often about 2 mm to 2 cm in width and a few centimeters in length or as long as the limb it affects. Occasionally, 2 parallel bands can be seen side by side. Typically, these bands are observed in 1 of the major extremities, such as an arm or a leg, but may also be seen in the neck, buttock, or trunk region. Pruritus is the most frequently accompanying symptom, ranging from mild to intense. Though less common, nails may also be affected, with or without the presence of skin lesions, and may thicken, become ridged, split, or possibly fall off.

Histopathology

Histopathological analysis of lichen striatus reveals features characteristic of a lichenoid inflammatory reaction, with distinct involvement of adnexal structures. Epidermal changes include focal hyperkeratosis, parakeratosis, mild acanthosis, basal cell vacuolization, and apoptotic keratinocytes (Civatte bodies), reflecting damage to the basal layer. Spongiosis is seen occasionally, particularly in early lesions. In the dermis, a dense, band-like lymphocytic infiltrate at the dermoepidermal junction is prominent, resembling lichen planus, but often accompanied by perivascular and periappendageal inflammatory infiltrates. These infiltrates frequently target eccrine glands and ducts (eccrine hidradenitis), a hallmark feature that helps distinguish lichen striatus from other lichenoid dermatoses.

Additional findings may include melanophages in the upper dermis, correlating with postinflammatory hyperpigmentation. The combination of lichenoid inflammation with adnexal involvement along Blaschko lines supports the diagnosis, emphasizing the importance of clinical and histopathological correlation.

History and Physical

Lichen striatus presents as a spontaneous eruption of a pink rash characterized by papules that merge to form 1 or more dull-red, potentially scaly, linear bands following the Blaschko lines. These lines are distinct cutaneous patterns and do not originate from nervous or vascular tissue. The condition typically affects the extremities but may also appear on the buttocks, neck, and trunk. Lichen striatus is often asymptomatic but may cause pruritus in some cases.[11] Lesions usually resolve on their own, though postinflammatory hyperpigmentation or hypopigmentation can occur in some individuals.[12][13][14]

Evaluation

Lichen striatus is diagnosed based on its specific clinical appearance and histopathological patterns through skin biopsies. Dermoscopy may also aid in the diagnosis, typically revealing linear white scales corresponding to clinical scaling, often arranged in a pattern following Blaschko lines. The background may show erythema, indicating underlying inflammation, interspersed with brownish pigmentation, suggesting melanin incontinence and postinflammatory hyperpigmentation. Vascular structures, such as dotted vessels, may be visible within erythematous areas, representing dilated capillaries in the inflamed dermis.

In lesions with significant pigmentary alteration, dermoscopy may show blue-gray granules or globules corresponding to dermal melanophages. These findings, along with the linear distribution and clinical presentation, support the diagnosis and help differentiate lichen striatus from other linear dermatoses, such as inflammatory linear verrucous epidermal nevus (ILVEN) or linear psoriasis.[15]

Treatment / Management

No treatment is necessary due to the self-limiting nature of the condition. However, patients seeking treatment may be prescribed emollients, low-dose systemic corticosteroids, a short course of acitretin, or topical steroids to address dryness or pruritus. Other therapies include photodynamic treatment with aminolevulinic acid. Tacrolimus and pimecrolimus can treat persistent, pruritic lesions on the face, arms, and legs. Nail abnormalities may be treated with tacrolimus.

Differential Diagnosis

The clinical presentation aids in the differential diagnosis. Lichen striatus must be distinguished from lichen planus or lichen planus-like keratosis, where apoptotic keratinocytes are confined to the basal epidermis rather than extending through all levels. The infiltrate typically does not involve eccrine glands.

The following conditions should be properly ruled out:

• Nevus unius lateris
• Annular lichenoid dermatitis
• Unilateral laterothoracic exanthema
• Tinea corporis
• Inflammatory linear verrucous epidermal nevus
• Linear Darier disease
• Lichen nitidus
• Lichen planus
• Lichen simplex chronicus
• Nongenital warts
• Plaque psoriasis
• Porokeratosis

Differentiating lichen striatus from other conditions requires a thorough clinical evaluation and careful consideration of histopathological features. Correct diagnosis helps guide treatment and avoid unnecessary interventions.

Prognosis

The prognosis of lichen striatus is excellent due to its self-limiting nature, with a complete recovery expected. This skin condition typically completely resolves spontaneously within a year, though the disease duration ranges from 4 weeks to 3 years. Relapses are uncommon. The nail component of lichen striatus usually resolves on its own but can last from 6 months to 5 years. Nail changes disappear without any remaining deformity.

Complications

Lichen striatus is generally benign and self-limiting, and complications are rare. However, secondary complications can arise in some cases. Persistent pruritus associated with the condition may lead to excoriation, increasing the risk of secondary bacterial infection. Postinflammatory pigmentary changes, such as hyperpigmentation or, less commonly, hypopigmentation, may occur, particularly in individuals with darker skin tones. These changes can take months to resolve, even after the primary lesions have healed.

Rarely, extensive or atypical presentations of lichen striatus may prompt unnecessary diagnostic procedures or treatments due to concern for other linear dermatoses. Delayed resolution or atypical evolution of lesions may occur in immunocompromised individuals. Overall, complications are minimal, and patient reassurance and monitoring are typically sufficient for management.[16]