1. Malar (butterfly) in some cases (see Photo 18, Fig. 3).
2. Photoaccentuation in some cases, less pronounced than in other forms of LE.
Discoid in a small number of cases.
Skin biopsy is indicated when it assists in establishing a diagnosis of SLE or is needed to identify the skin lesion as part of an already established diagnosis of SLE. If the patient has established SLE and has cutaneous manifestations characteristic of LE, biopsy is unnecessary.
Direct immunofluorescence of lesional skin is indicated under the same circumstances as skin biopsy.
If associated features suggest SLE, and other serologic tests are inconclusive, positive direct immunofluorescence of nonlesional sun-protected skin supports a diagnosis of SLE.
CBC, multichemistry panel, urinalysis, ESR, complement screen (specifically C3, C4, and CH50), lupus antibody screen, and rheumatoid factor are always indicated.
With active vascular lesions (infarcts and ulcerations) or with CNS involvement, screen for lupus anticoagulant and antiphospholipid antibodies.
See Therapy in DLE section above.
Common Skin Conditions That May Simulate DLE, SCLE, and SLE
Seborrhea can simulate DLE, SCLE: Onset of seborrhea is gradual, and tends to wax and wane. Diffuse erythema occurs with very loose white or greasy yellow scale. Atrophy, scarring, telangectasia, and pigment change are absent. "Carpet-tack" sign is negative. The macrodistribution may overlap and cause confusion. No photosensitivity is present.
Rosacea can simulate DLE, SLE: Erythematous telangiectatic rosacea can simulate the facial erythema of early DLE and SLE. Onset is usually gradual with a long history of ease of flushing. Scale is absent, as are atrophy, scarring, and pigment change. The macrodistribution and prominent telangectasia can cause confusion. Dusky papules and pustules help with the differential diagnosis. Photosensitivity is common.
Psoriasis vulgaris can simulate DLE, SCLE: The onset, lesions, and distribution can be strikingly similar to DLE and SCLE. Only a biopsy and serologic tests will distinguish them. Generally, the lesions of LE have a deeper more violaceous hue, and telangec-tasia is not a feature of psoriasis. Although uncommon, sun sensitivity can occur in psoriasis vulgaris.
Pityriasis rosea (PR) can simulate early SCLE: Early papulosquamous lesions of SCLE can simulate PR. The persistence of SCLE, the telangectasia, and eventually the differences in macrodistribution should separate the two. In addition, PR improves rather than flaring with light therapy.
Tinea faciale can simulate DLE: Early DLE on the facial area can be clinically indistinguishable from tinea. When present, indolent follicular pustules should suggest the diagnosis of tinea faciale. A KOH preparation can prevent an embarrassing mistake.
Annular tinea corporis can simulate SCLE: Annular SCLE can simulate an active inflammatory annular tinea. Telangectasia and dark violaceous color help to distinguish them. A KOH prep is usually definitive.
Parvovirus B-19 can simulate SLE: Parvovirus B-19 infection, a cause of the common childhood exanthem called "fifth" disease, has been reported to exacerbate established SLE and to produce temporary symptoms in some patients that meet the criteria for SLE. Malar rash, arthralgias, fatigue, and low-titer positive ANAs are reported. History of exposure to affected children, or occurrence during epidemics of parvovirus B-19 infection, should lead to suspicion. Symptoms and serologies usually revert to normal within 1 to 3 months in patients who do not have SLE. Parvovirus arthritis may last beyond 3 months. Discoid lesions, alopecia, renal lesions, and cardiac lesions are not reported. Neurologic findings and serositis are uncommon with parvovirus B-19 infection. The anemia seen with the infection is usually associated with low reticulocyte counts, whereas reticulocytes are usually elevated in the hemolytic anemia of SLE. Parvovirus B-19 antibody titers may be helpful.
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