Early Diagnosis and Treatment of Discoid Lupus Erythematosus

Suresh Panjwani, MD, MSc, FRACGP

Disclosures

J Am Board Fam Med. 2009;22(2):206-213. 

In This Article

Clinical Features

Discoid lupus is by far the most common manifestation of LE.[6] It commonly presents with erythematous, scaly papules and plaques (Figure 1) occurring on sun-exposed areas, although 50% of discoid lupus lesions are found on areas of hair-bearing scalp that are presumably protected from the sun[6] (Figures 2 and 3). In the localized variety of discoid lupus the lesions tend to be confined to the head and neck and in the generalized variety they occur both above and below the neck. Patients with generalized discoid have significantly greater chances of having laboratory abnormalities and of progressing to systemic LE. Most people with DLE do not have any systemic or serologic abnormality although antinuclear antibodies may be present.

Figure 1.

Plaques on beard and scalp in patient with discoid lupus erythematosus.

Figure 2.

Critical alopecia on scalp caused by discoid lupus erythematosus.

Figure 3.

Extensive loss of scalp hair in a patient with discoid lupus.

Discoid lupus occurs at all ages and among all ethnic groups; it occurs more frequently in women than in men, but the predilection among women is not as marked as in systemic lupus. Discoid lupus starts as an erythematous papule or plaque, usually on the head or neck, with an adherent scale. The lesion tends to spread centrifugally and as it progresses there is follicular plugging and pigmentary changes, generally hyperpigmentation at the periphery, and hypopigmentation with atrophy, scarring, and telengiectasia at the center of the lesion (Figure 4).

Figure 4.

Close-up view of plaque in a patient with discoid lupus.

Involvement of the scalp commonly produces a scarring alopecia,[6] but there has been an increase in incidence of alopecia areata among patients with LE.[7] Scarring alopecia was present in 34% of 89 patients with DLE and was associated with a prolonged disease course. More than half of those patients had scalp disease at the onset.[7] There are no reliable predictors of scalp involvement. Histologically there is a perifollicular lymphocytic inflammation maximal around mid-follicle. The mid-follicle is in fact a very important structure becuase it contains the bulge that contains the follicular stem cells.

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