- Deepti Gupta, MD
Deepti Gupta, MD
- Assistant Professor of Pediatrics (Dermatology)
- Department of Pediatrics and Division of Dermatology
- Seattle Children's Hospital
- University of Washington School of Medicine
- Erin Mathes, MD
Erin Mathes, MD
- Assistant Professor of Dermatology - Departments of Dermatology and Pediatrics
- University of California, San Francisco
Lichen striatus is an acquired, asymptomatic, and self-limited linear inflammatory skin disorder that predominantly affects children . The eruption is typically unilateral, involves most often the extremities, and follows the lines of Blaschko in a continuous or interrupted pattern. The onset is sudden, with full progression over a few weeks and resolution typically within 6 to 12 months.
This topic will discuss the pathogenesis, clinical manifestations, diagnosis, and treatment of lichen striatus.
Lichen striatus is a relatively uncommon disease that most frequently occurs in children 5 to 15 years of age. However, it may occur at any age, from early infancy to adulthood [2-7]. Lichen striatus has been reported in all ethnic groups and appears to be more common in females [3,5-7]. There are a few reports of familial cases [3,8-12].
The precise etiology of lichen striatus is unknown. Viral infections, trauma, hypersensitivity reactions, vaccines, medications, and pregnancy have been proposed as triggering factors [13-17]. A positive personal or family history of asthma, atopic dermatitis, or allergic rhinitis has been reported in 60 to 85 percent of individuals with lichen striatus, suggesting that atopy may be a predisposing factor [5,18].
The distribution of lichen striatus along the lines of Blaschko (lines corresponding to the direction of growth of cutaneous cells during embryogenesis (figure 1)) suggests that lichen striatus is a condition of cutaneous mosaicism, due to somatic (postzygotic) mutations that produce abnormal keratinocyte clones during early embryogenesis. These aberrant clones may remain silent until a triggering event causes a break in immunologic tolerance and initiates an autoimmune response [4,19]. Potential triggers include viral infections, vaccines, trauma, pregnancy, hypersensitivity reactions, and medications [5,9,13-16,20-22].
Subscribers log in hereLiterature review current through: Aug 2017. | This topic last updated: Jun 02, 2016.References
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