Diagnosis: Discoid lupus erythematosus
Discoid lupus erythematosus (DLE) is an autoimmune inflammatory disorder of the skin that often leads to scarring and alopecia. It may be localized to sun-exposed areas such as the face, ears, and scalp but occasionally is much more extensive, involving the trunk and extremities. Most patients are otherwise healthy, and DLE may be the only clinical finding.
Although its prevalence is not known, DLE is not uncommon. It affects females twice as often as males, and patients fall between the ages of 25 to 45 years, with no racial predilection. While about 15% to 20% of patients with systemic lupus erythematosus (SLE) manifest DLE lesions, only about 5% to 10% of patients with DLE go on to develop SLE.1
Like SLE, DLE is believed to be an autoimmune disorder. Unlike SLE, however, DLE patients do not have similar serologic abnormalities. Skin trauma and ultraviolet light exposure have been reported to induce or exacerbate the lesions of DLE. Sex hormones may also play a role: exacerbation may occur during pregnancy, during menstrual or premenstrual periods, or while taking oral contraceptives. Drugs such as procainamide, hydralazine, isoniazid, diphenylhydantoin, methyldopa, penicillamine, guanides, and lithium may also precipitate DLE lesions.2
DLE usually begins as dull red macules with adherent scales on sun-exposed areas. If the overlying scales are removed, an undersurface of horny plugs is revealed. These plugs fill the follicles and resemble carpet tacks or a cat’s tongue (langue au chat). The macules slowly expand to form large plaques.
Usually only a mild pruritus and tenderness is seen with DLE lesions. As the lesions progress, the scale may thicken and pigmentary changes become evident. The lesions heal with atrophy, scarring, telangiectasias, and changes in pigmentation. Morphological appearance of older lesions may vary from erythematous plaques to hyperkeratotic, dark gray plaques with centrally depressed scars.3 Scalp involvement in DLE results in more sclerotic and depressed scars with subsequent scarring alopecia.4
Differential diagnosis is wide. The differential diagnosis of DLE is extensive and includes actinic keratosis, dermatomyositis, granuloma annulare, granuloma faciale, keratoacanthoma, lichen planus, subacute cutaneous lupus erythematosus, psoriasis, rosacea, sarcoidosis, squamous cell carcinoma, syphilis, and nongenital warts.
Histopathology
Histopathological findings include hyperkeratosis, parakeratosis, follicular plugging, telangiectasias, and atrophy of the epidermis. Liquefaction or hydropic degeneration of the basal layer leads to pigmentary incontinence. A perivascular and perifollicular mononuclear inflammatory cell infiltrate is present in the superficial and deep dermis.5,6
Direct immunofluorescence demonstrates immunoglobulins and complement deposits at the dermoepidermal junction.5 This test was not recommended for this patient, as the diagnosis of DLE had already been confirmed on clinical and histopathologic grounds.