bubble_chart Overview

Lupus erythematosus (LE) is generally classified into discoid lupus erythematosus (DLE) and systemic lupus erythematosus (SLE), with subtypes such as subacute cutaneous lupus and lupus profundus in between. This article focuses solely on discoid lupus erythematosus.

bubble_chart Etiology

Currently, lupus erythematosus is considered an autoimmune disease, and its onset is associated with genetic factors, viral infections, photosensitivity, drug allergies, endocrine changes, and other factors.

bubble_chart Pathological Changes

Hyperkeratosis, keratin plugs in hair follicle openings, thickening of the granular layer, atrophy of the spinous layer, flattening of the rete ridges, liquefaction degeneration of the basal layer, edema in the upper dermis, fibrinoid degeneration of the superficial dermal connective tissue, vascular dilation and extravasation of red blood cells, pigment incontinence, and focal lymphocytic infiltrates around blood vessels and appendages.

bubble_chart Clinical Manifestations

The skin lesions initially appear as one or several papules or light red to purplish-red patches the size of a soybean, gradually expanding into well-defined, slightly raised-edged annular or irregular patches. The surface is covered with grayish-white adherent scales, and upon removal of the scales, enlarged follicular openings can be seen at the base, with agnail (keratotic plugs) on the undersurface of the scales. Over time, the center becomes atrophic and depressed, often accompanied by telangiectasia and hypopigmentation, while the peripheral area becomes slightly raised and surrounded by hyperpigmentation, hence the name discoid lupus erythematosus (Figure 12). When hypopigmentation is prominent, differentiation from vitiligo should be considered.

The rash commonly occurs on exposed areas, particularly the central bridge of the nose and both malar regions of the face, presenting a classic butterfly-shaped appearance. Other common sites include the lips, ears, scalp, and dorsum of the hands. When the scalp is involved, long-term lesions may lead to atrophic scarring and hair loss. Approximately one-third of patients have oral mucosal involvement, with the lower lip being the most frequently affected. A small number of patients exhibit only lip lesions without skin involvement, presenting as well-defined red or purplish-red patches with grayish-white scales, often developing erosions or shallow ulcers, with central atrophy over time. Symptoms are generally mild, though some patients may experience varying degrees of cutaneous pruritus or a burning sensation.

The disease is more common in middle-aged individuals, with a higher prevalence in women than in men. The course is chronic, and the prognosis is generally favorable. Most patients have lesions limited to the head and face (referred to as localized discoid lupus erythematosus), with few or no systemic symptoms. A minority of patients may have lesions extending beyond the head and face to the limbs and trunk (referred to as disseminated discoid lupus erythematosus), possibly accompanied by grade I systemic symptoms such as lack of strength, low-grade fever, and joint pain. Sun exposure can exacerbate or trigger recurrence. Approximately 2–5% of DLE patients may progress to SLE during the course of the disease. Rarely, DLE lesions may undergo malignant transformation.

bubble_chart Diagnosis

Based on the aforementioned rash characteristics and its predilection for exposed areas, the diagnosis is straightforward when combined with pathological examination.

bubble_chart Treatment Measures

For localized DLE, the main focus is on local treatment, while for disseminated cases and those with systemic symptoms, internal medications should be combined. At the same time, exposure to intense sunlight, ultraviolet radiation, cold stimulation, and excessive fatigue should be avoided. Photosensitizing drugs such as sulfonamides and tar preparations should not be used.

(1) Local Treatment

Topical sunscreens such as 5% quinine ointment; corticosteroid emulsions applied externally with occlusion; corticosteroid intralesional injections such as triamcinolone acetonide suspension or prednisolone suspension can also be used, administered once every 1–2 weeks.

(2) Internal Medications

Chloroquine 0.125–0.25g, twice daily, generally not exceeding 0.375g per day, with dosage reduced after improvement. Regular eye fundus and white blood cell examinations are required. Thalidomide can also be taken, 0.1g each time, twice daily, reduced to 0.1g daily after improvement, and continued for 3–6 months. Nicotinamide 0.1g, three times daily. Vitamin B12 0.25–0.5mg, intramuscular injection once daily; Vitamin E 50mg, taken orally three times daily, can all be used in combination.

Chinese medicinals may include Six-Ingredient Rehmannia Pill, Root Leaf or Flower of Common Threewingnut, or Tripterygium hypoglaucum, Artemisinin, etc. For patients with widespread rashes and systemic symptoms who do not respond to the above treatments, oral prednisone may be administered.