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Evidence Levels: A Double-blind study B Clinical trial ≥ 20 subjects C Clinical trial < 20 subjects D Series ≥ 5 subjects E Anecdotal case reports
Discoid lupus erythematosus (DLE) is the most common type of chronic cutaneous lupus erythematosus (CCLE). Lesions typically occur on the scalp, face, and ears, although they can be generalized. The lesions are photodistributed and are scaly, erythematous plaques and papules, which can be hypertrophic/hyperkeratotic. Late-stage lesions result in atrophy and scarring accompanied by dyspigmentation and permanent alopecia.
Although the chance of progression of DLE to systemic lupus erythematosus (SLE) is low, a thorough workup is needed to rule out systemic disease. SLE is also more likely to occur with generalized DLE lesions. This includes inquiring about symptoms of systemic disease such as fever, fatigue, arthralgia, arthritis, myalgia, weight loss, and loss of appetite. Laboratory workup should include urinalysis, complement levels, CBC, and autoantibodies such as antinuclear antibodies (ANA) and double-stranded DNA (dsDNA). Primary counseling includes smoking cessation and sun avoidance and protection.
In localized disease, topical and intralesional steroids are first line. Intralesional injection of corticosteroids can also treat alopecia due to early-stage lesions on the scalp. However, if new lesions are appearing despite local treatment or are widespread, systemic treatment is warranted. Antimalarials are first-line systemic therapy and afford a measure of photoprotection and are highly effective, despite their relatively slow onset of action. Calcineurin inhibitors are also considered a first-line therapy and are important for use on delicate skin, where corticosteroids may not be used.
For refractory DLE, there is a lack of rigorous, randomized studies. However, immunosuppressive agents such as methotrexate (MTX) and mycophenolate mofetil (MMF) clear lesions and act as steroid-sparing agents for SLE. Retinoids are effective in hypertrophic DLE. Thalidomide, and its derivative lenalidomide, are also effective but can have serious adverse effects.
Garza-Mayers AC, McClurkin M, Smith GP. Dermatol Ther 2016; 29: 74–83.
Keyes E, Werth VP, Brod B. Int J Womens Dermatol 2019; 5: 227–32.
DLE can be precipitated and exacerbated by ultraviolet (UV) light exposure. Generous sunscreen use with regular reapplication has been shown to be efficacious in preventing UV-induced DLE lesions. A retrospective study confirmed that sunscreen prevented photoprovocation and pigment changes of lesions. Data suggests that higher sun protection factor (SPF 70 or greater) with broad-spectrum UVA and UVB coverage or physical blockers are effective in prevention of UV-induced DLE lesions. Although sunscreen usage is crucial in patients with autoimmune skin conditions, these patients have an increased risk of reaction to allergenic ingredients and developing contact dermatitis. Most sunscreens found on Amazon, Target, and CVS are not allergen-free, but many have no high-prevalence allergens.
Jessop S, Whitelaw DA, Grainge MJ, et al. Cochrane Database Syst Rev 2017; 5: CD002954.
Topical steroids can be used for localized DLE lesions. In a study comparing fluocinonide 0.05% (potent steroid) and hydrocortisone 1% (low-potency steroid) there was complete resolution of skin lesions in 27% of participants using fluocinonide and 10% using hydrocortisone. Side effects included skin irritation and burning.
Avgerinou G, Papafragkaki DK, Nasiopoulou A, et al. J Eur Acad Dermatol Venereol 2012; 26: 762–7.
Garza-Mayers AC, McClurkin M, Smith GP. Dermatol Ther 2016; 29: 74–83.
The macrolactam immunosuppressive agents, tacrolimus and pimecrolimus, are steroid-sparing agents that are effective in the topical treatment of lesions of DLE lesions. Tacrolimus 0.03% or 0.1% and pimecrolimus 1% cream are important in thin-skinned areas where corticosteroids are not appropriate, such as the eyelids and in areas of atrophy resulting from the disease itself. Hypertrophic lesions may not respond well to calcineurin inhibitors or to other topical therapies because of limited penetration. Topical calcineurin inhibitors can also be used in combination with systemic therapy (e.g., hydroxychloroquine).
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