- Author: Tsu-Yi Chuang, MD, MPH, FAAD; Chief Editor: William D James, MD more...
Lichen planus is a cell-mediated immune response of unknown origin. It may be found with other diseases of altered immunity, such as ulcerative colitis, alopecia areata, vitiligo, dermatomyositis, morphea, lichen sclerosis, and myasthenia gravis. Lichen planus (see the image below) has been found to be associated with hepatitis C virus infection.[1, 2, 3, 4, 5]
Signs and symptoms
The following may be noted in the patient history:
Lesions initially developing on flexural surfaces of the limbs, with a generalized eruption developing after a week or more and maximal spreading within 2-16 weeks
Pruritus of varying severity, depending on the type of lesion and the extent of involvement
Oral lesions that may be asymptomatic, burning, or even painful
In cutaneous disease, lesions typically resolve within 6 months (>50%) to 18 months (85%); chronic disease is more likely oral lichen planus or with large, annular, hypertrophic lesions and mucous membrane involvement
In addition to the widespread cutaneous eruption, lichen planus can involve the following structures:
The clinical presentation of lichen planus has several variations, as follows:
Hypertrophic lichen planus
Atrophic lichen planus
Erosive/ulcerative lichen planus
Follicular lichen planus (lichen planopilaris)
Annular lichen planus
Linear lichen planus
Vesicular and bullous lichen planus
Actinic lichen planus
Lichen planus pigmentosus
Lichen planus pemphigoides
See Clinical Presentation for more detail.
Direct immunofluorescence study reveals globular deposits of immunoglobulin M (IgM) and complement mixed with apoptotic keratinocytes. No imaging studies are necessary.
Distinguishing histopathologic features of lichen planus include the following:
Hyperkeratotic epidermis with irregular acanthosis and focal thickening in the granular layer
Degenerative keratinocytes (colloid or Civatte bodies) in the lower epidermis; in addition to apoptotic keratinocytes, colloid bodies are composed of globular deposits of IgM (occasionally immunoglobulin G [IgG] or immunoglobulin A [IgA]) and complement
Linear or shaggy deposits of fibrin and fibrinogen in the basement membrane zone
In the upper dermis, a bandlike infiltrate of lymphocytic (primarily helper T) and histiocytic cells with many Langerhans cells
See Workup for more detail.
Lichen planus is a self-limited disease that usually resolves within 8-12 months. Mild cases can be treated with fluorinated topical steroids. More severe cases, especially those with scalp, nail, and mucous membrane involvement, may necessitate more intensive therapy.
Pharmacologic therapies include the following:
Cutaneous lichen planus: Topical steroids, particularly class I or II ointments (first-line treatment); systemic steroids; oral regimens like metronidazole, acitretin, methotrexate, hydroxychloroquine, griseofulvin, and sulfasalazine [6, 7, 8, 9] ; and other treatments with unproven efficacy (eg, mycophenolate mofetil)
Lichen planus of the oral mucosa: Topical steroids; topical calcineurin inhibitors; oral or topical retinoids (with close monitoring of lipid levels  )
Patients with widespread lichen planus may respond to the following:
Narrow-band or broadband UV-B radiation [11, 6, 7]
Psoralen with UV-A (PUVA) radiation; [6, 7] use of topical ointment at the time of UV-A treatment may decrease the effectiveness of PUVA; precautions should be taken for persons with a history of skin cancers or hepatic insufficiency
Lichen planus (LP) is a pruritic eruption commonly associated with hepatitis C. Lesions are characteristically papular, purple (violaceous color), polygonal, and peripherally located (eg. on the distal extremities). LP may also affect the genitalia or mucous membranes. It is most likely an immunologically mediated reaction, though the pathophysiology in unclear. See Oral Lichen Planus for more information on this variant of lichen planus.
Lichen planus is a cell-mediated immune response of unknown origin. It may be found with other diseases of altered immunity; these conditions include ulcerative colitis, alopecia areata, vitiligo, dermatomyositis, morphea, lichen sclerosis, and myasthenia gravis.
An association is noted between lichen planus and hepatitis C virus infection,[2, 3, 4, 5] chronic active hepatitis, and primary biliary cirrhosis. In one meta-analysis, 16% of patients with LP had hepatitis C infection. This association has been shown to exist in all regions of the world, including North America. A workup for hepatitis C should be considered in patients with widespread or unusual presentations of lichen planus. Onset or exacerbation of lichen planus has also been linked to stressful events.
Lichen planus is reported in approximately 1% of all new patients seen at health care clinics. Some areas have reported a higher incidence in December and January.
No significant geographical variation in frequency exists for lichen planus.
No racial predispositions have been noted for lichen planus.
No significant differences in incidence for lichen planus are noted between male and female patients, but in women, lichen planus may present as desquamative inflammatory vaginitis.
More than two thirds of lichen planus patients are aged 30-60 years; however, lichen planus can occur at any age.
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