Manifestations and Treatment of Cutaneous Lupus Erythematosus
(Part II of II)
See Part I in Volume 10 Issue 10 (October 2011) of JDD.
All patients with CLE should be counseled on proper sun protection and smoking cessation. Treatment of local disease should start with a topical corticosteroid or calcineurin inhibitors. Severe or widespread disease may warrant short-term use of systemic corticosteroids and initiation of an antimalarial. In recalcitrant disease, methotrexate, retinoids, dapsone, thalidomide, mycophenolate mofetil, or a biologic therapy can be considered.24 In general, these therapies are effective for all forms of CLE, with a tendency for DLE to be the least responsive and SCLE to be most responsive to treatment. Laser therapy is an emerging option for treating active and quiescent lesions.
CLE lesions can be induced or exacerbated by ultraviolet (UV) A or B light.25 Effective UV protection comes from the use of broad spectrum sunscreens and UV protective clothing, as well as from limiting activity in the midday sun.
Cigarette smoking is more prevalent in patients with CLE27,28 and SLE28 than in the general population. Furthermore, smoking is associated with poor response to antimalarial drugs.29 Although the exact role of smoking is unknown, patients with LE derive benefit from smoking cessation.
Topical steroids are an effective treatment for all subtypes of CLE in a potency-dependent manner.30 Use is limited by side effects. However, in DLE, where scarring and atrophy are part of the natural history of the lesion, the side effects of topical steroids carry less weight. Ointments are preferable to creams because they are more hydrating and contain fewer potential irritants.31 Intralesional injections are effective in 80 percent of cases but should not be used more frequently than every 4-6 weeks.5
Hydroxycloroquine, chloroquine, and quinacrine were developed as antimalarial drugs. However, they have also been used in the treatment of inflammatory processes such as SLE, CLE, and sarcoidosis because of their anti-inflammatory properties. Antimalarials accumulate in lysosomes and inhibit lysosomal proteases in the treatment of malaria, and these drugs also inhibit protein MHC interactions in the lysosome. The end result is a decrease in the presentation of self antigens and a decrease in inflammatory mediators.40