SCLE is highly associated with anti-Ro/SSA autoantibodies. Upon resolution, SCLE can leave dyspigmentation but no permanent scarring.

When active, it typically presents as papulosquamous lesions and/or annular plaques (psorasiform) with central clearing and raised erythematous scaly edges. SCLE most often occurs on the photo-exposed areas of the upper chest, back, and external upper extremities ( Figure 1). Lesions of SCLE last longer than the malar rash of ACLE, but systemic lupus occurs in a significantly lower percentage of the affected individuals. Histologically, ACLE manifests as lymphoplasmacytic interface dermatitis with vacuolar changes at the DEJ associated with mucin deposition.

Up to 80% of SLE patients experience malar rash, which typically flares with UV exposure but does not leave any scar or dyspigmentation. ACLE can affect the entire body in some patients with bad flares, and is considered a criterion for the diagnosis of SLE. This helps to distinguish it from other clinical mimickers such as rosacea and seborrheic dermatitis. A well-known example of ACLE is the malar rash, or butterfly rash, that classically crosses both cheeks but spares the nasolabial folds. All CLE subtypes are characterized histopathologically by interface dermatitis (with the exception of tumid lupus and lupus panniculitis) and lupus band reaction, which consist of infiltration of immune cells and deposition of autoantibodies at the dermal-epidermal junction (DEJ) ( 17).ĪCLE presents as transient erythematous patches that correspond to flares in SLE patients. It is typically classified into three main subtypes based on the disease chronicity, clinical morphology and distribution: acute (ACLE), subacute (SCLE), and chronic (CCLE) ( 15, 16).

CLE encompasses a heterogeneous group of photodermatoses with varying degrees of association with systemic disease (SLE).

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