Lichen Striatus Clinical Presentation

  • Author: June Kim, MD; Chief Editor: Dirk M Elston, MD   more...
 
Updated: May 11, 2012
 

History

Lichen striatus often appears as a sudden eruption of small papules on an extremity. The papules are usually asymptomatic, reaching maximum involvement within several days to weeks. When lichen striatus patients are symptomatic, the most common complaint is pruritus. Lichen striatus is self-limited, but it may resolve with postinflammatory hyper or hypopigmentation.

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Physical

Lichen striatus appears as a continuous or interrupted, linear band consisting of small (1- to 3-mm) pink, tan, or skin-colored lichenoid papules. The papules may be smooth, scaly, or flat topped. Occasionally, a vesicular component is present. The band may range from a few millimeters to 1-2 cm wide and extends from a few centimeters to the full length an extremity. The lesions are usually unilateral and single on an extremity along the lines of Blaschko.[4, 5] In rare cases, they may be bilateral or occur in multiple parallel bands.[6, 7, 8] The lesions are most commonly located on a proximal extremity and less commonly on the trunk, head, neck, or buttock. In darkly pigmented individuals, eruptions may appear as a bandlike area of hypopigmentation. Note the images below.

Extensive unilateral lichen striatus that affects 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. Lichen striatus over the inner thigh. Hypopigmented lichen striatus over the leg. Hypopigmented lichen striatus over the leg.

Nail involvement is uncommon in lichen striatus, with approximately 30 reported cases worldwide.[9] Nail lesions may occur before, after, or concurrently with the skin lesions. They may also be the only area of involvement. Often, only the medial or lateral portions are involved, and involvement is almost always restricted to one single nail. Nail changes may include longitudinal ridging, splitting, onycholysis, nail loss, hyperkeratosis of the nail bed, thinning or thickening of the nail plate, nail pitting, onychodystrophy, punctuate and striate leukonychia, and overcurvature of the nail plate.[10, 11] Dermoscopic examination may reveal sharply marginated, deep-white structures resembling Wickham striae and brown, keratotic, cerebriform structures with pinpoint red dots surrounded by a pale halo.[12]

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Causes

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.[13] Lichen striatus has also been reported after adalimumab administration.[14] Furthermore, one case was reported after an allogenic stem cell transplantation, and the authors suggest that this may be an unusual form of localized, chronic graft versus host disease.[15] Some reports simply suggest that lichen striatus is an inflammatory skin disease mediated by T cells.

An environmental (infectious or trauma[16] ) etiology has also been suggested. Familial cases,[17, 18] 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.[5] 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, after UV exposure from a tanning bed,[19] following a prick from a pineapple leaf, and after varicella infection.[20]

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.[5]

Lesions of lichen striatus follow the lines of Blaschko.[4, 5, 21, 22, 23] 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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Contributor Information and Disclosures
Author

June Kim, MD  Mohs Surgery Fellow, Department of Dermatologic Surgery, Yale Medical Center

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, and Women's Dermatologic Society

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

Disclosure: Nothing to disclose.

Specialty Editor Board

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, and Canadian Dermatology Association

Disclosure: Nothing to disclose.

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, Association of Military Dermatologists, Texas Dermatological Society, and Texas Medical Association

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, and Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Catherine M Quirk, MD  Clinical Assistant Professor, Department of Dermatology, University of Pennsylvania

Catherine M Quirk, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Dermatology

Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD  Director, Ackerman Academy of Dermatopathology, New York

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

Disclosure: Nothing to disclose.

Additional Contributors

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.

References

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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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