Lupus Erythematosus
Jeffrey P. Callen
(ICD-9 695.4)
Signs and Symptoms
Cutaneous lupus erythematosus (LE) can be divided into chronic, subacute, and acute forms. Patients may complain of photosensitivity, mildly pruritic or painful skin lesions, and/or arthralgias.
Chronic cutaneous LE is most commonly manifest as discoid lupus erythematosus (DLE). Lesions of DLE are red with adherent scale, telangiectasia, follicular plugging, and dyspigmentation. Atrophy and scarring are characteristic (Fig. 13-1). Lesions most often occur on the head, neck, ears, scalp, arms, and upper chest and back. Less than 5% of patients with DLE have systemic manifestations of lupus.
Systemic lupus erythematosus (SLE) often presents as the classic, malar “butterfly” rash when the skin is involved (Fig. 13-2). The rash is exacerbated by sun exposure or exposure to ultraviolet B (UVB) or ultraviolet A (UVA) from artificial light sources. Almost all patients with a butterfly rash have active SLE. Subacute cutaneous lupus erythematosus (SCLE) lesions are of at least two types: annular or papulosquamous. Both forms begin as red papules or plaques on sun-exposed skin, which eventually expand and form either rings or psoriasiform lesions. Annular lesions have central clearing. Papulosquamous lesions are scaling. Approximately 50% of patients with
SCLE have evidence of systemic manifestations of lupus. SCLE is associated with Sjögren’s syndrome, idiopathic thrombocytopenic purpura, cutaneous vasculitis, or deficiency of the second component of complement (C2d). It may be induced by a variety of drugs, most commonly hydrochlorothiazide, other antihypertensive agents, and terbinafine.
SCLE have evidence of systemic manifestations of lupus. SCLE is associated with Sjögren’s syndrome, idiopathic thrombocytopenic purpura, cutaneous vasculitis, or deficiency of the second component of complement (C2d). It may be induced by a variety of drugs, most commonly hydrochlorothiazide, other antihypertensive agents, and terbinafine.