What causes lichen striatus?

Answer

The etiology of lichen striatus is unknown. Many etiologic or predisposing factors are suggested for lichen striatus. The most commonly accepted hypothesis is the combination of genetic predisposition with environmental stimuli.

Atopy may be a predisposing factor. One group reported that 85% of patients with lichen striatus have a family history of atopic dermatitis, asthma, or allergic rhinitis. However, another report disputes this claim, stating that the incidence of atopy is no greater than that of the general population.

An autoimmune response may also be involved in lichen striatus. A case of lichen striatus has been reported during pregnancy, and it has been postulated that the pregnancy may have triggered an autoimmune response leading to the appearance of the eruption.^[4]Lichen striatus has also been reported concurrently with vitiligo^{[5, 6]}and after adalimumab^[7]and etanercept.^[8]Some reports simply suggest that lichen striatus is an inflammatory skin disease mediated by T cells. It has been reported 17 months after allogenic peripheral blood stem cell transplantation.^[9]

An environmental (infectious or trauma^[10]) etiology has also been suggested. Familial cases,^{[11, 12, 13]}outbreaks among unrelated children in a shared living environment, and a possible seasonal variation suggest an environmental agent, such as a virus. Support of infectious involvement includes elevations of interleukin 1-beta in lichen striatus biopsy specimens.^[14]However, results of viral testing have not conclusively proven this association. In addition, familial episodes of lichen striatus are not always simultaneous, signifying a possible genetic predisposition as a second explanation. Lichen striatus has been reported to occur shortly following immunization with BCG and hepatitis B vaccination,^[15]after UV exposure from a tanning bed,^[16]following a prick from a pineapple leaf, after a sting by a bumblebee,^[17]and after varicella and influenza infection.^{[18, 19]}

One group of authors has suggested that epigenetic mosaicism may be involved. They hypothesize that lichen striatus is triggered by an immunologic reaction to an infection, which triggers methylation or demethylation of a partially silenced genomic element in predisposed patients.^[14]A report of concurrent pityriasis rosea and lichen striatus may lend support to this theory. Human herpes viruses 6 and 7 have been implicated in the etiology of pityriasis rosea. The concurrent lichen striatus eruption may have manifested after being triggered by this viral infection.^[20]

Lesions of lichen striatus follow the lines of Blaschko.^{[21, 14, 22, 23, 24]}Blaschko lines are thought to be embryologic in origin. They are believed to be the result of the segmental growth of clones of cutaneous cells or the mutation-induced mosaicism of cutaneous cells. In lichen striatus, an acquired event (eg, viral infection) may allow an aberrant clone of cutaneous cells to express a new antigen, resulting in the phenotypic skin changes.

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Media Gallery

Extensive unilateral lichen striatus that affects both the upper and lower extremities. Grouped keratotic lichenoid papules form plaques over the leg.
Lichen striatus over the inner thigh.
Hypopigmented lichen striatus over the leg.

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Author

June Kim, MD Mohs Surgeon/Dermatologist, Cascade Eye and Skin Center, PC

June Kim, MD is a member of the following medical societies: American Academy of Dermatology, American College of Mohs Surgery, American Medical Association, American Society for Dermatologic Surgery

Disclosure: Nothing to disclose.

Coauthor(s)

Wingfield Rehmus, MD, MPH Dermatologist, BC Children's Hospital, Vancouver, British Columbia

Wingfield Rehmus, MD, MPH is a member of the following medical societies: American Academy of Dermatology, Society for Pediatric Dermatology

Disclosure: Serve(d) as a speaker or a member of a speakers bureau for: Abbvie; Valeant Canada<br/> Received honoraria from Valeant Canada for advisory board; Received honoraria from Pierre Fabre for advisory board; Received honoraria from Mustella for advisory board; Received honoraria from Abbvie for advisory board.

Specialty Editor Board

Richard P Vinson, MD Assistant Clinical Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine; Consulting Staff, Mountain View Dermatology, PA

Richard P Vinson, MD is a member of the following medical societies: American Academy of Dermatology, Texas Medical Association, Association of Military Dermatologists, Texas Dermatological Society

Disclosure: Nothing to disclose.

Paul Krusinski, MD Director of Dermatology, Fletcher Allen Health Care; Professor, Department of Internal Medicine, University of Vermont College of Medicine

Paul Krusinski, MD is a member of the following medical societies: American Academy of Dermatology, American College of Physicians, Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD Professor and Chairman, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina College of Medicine

Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Additional Contributors

Daniel J Hogan, MD Clinical Professor of Internal Medicine (Dermatology), Nova Southeastern University College of Osteopathic Medicine; Investigator, Hill Top Research, Florida Research Center

Daniel J Hogan, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Contact Dermatitis Society, Canadian Dermatology Association

Disclosure: Nothing to disclose.

Acknowledgements

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous authors, Nelly Rubeiz, MD, and Amal Mehanna, MD, to the development and writing of this article.

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