Discoid lupus erythematosus

Erythematous scaly plaques on scalp, causing scarring alopecia. Notice the hyperpigmented borders and atrophic (=thin, hypopigmented) central area

Typical site- Auricular and Pre-auricular area

Erythematous scaly plaques with adherent scale, causing scarring alopecia. Notice the variable pigmentation with depigmentation in occipital area and hyperpigmented border (on right side)

 

In Brief

• Lupus erythematosus (LE) is usually divided into two main types: DLE and SLE
• Discoid lupus erythematosus (DLE) generally occurs in young adults, with women outnumbering men 2:1 (Discoid= Disc-like)
• DLE can be subdivided into a localized form (localized DLE) in which lesions are confined to the face above the chin, the scalp and the ears, and a disseminated form (Disseminated DLE) in which lesions go below the neck.

Presentation

• Discoid lesions are usually localized above the neck. Favored sites are the scalp, bridge of the nose, malar areas, lower lip, and ears.
• Usually, lesions occur as well-defined erythematous plaques.
• There is adherent scale in many cases (as is seen in photo) and when this is removed its undersurface shows horny plugs which have occupied underlying dilated pilosebaceous canals (When not obscured by scaling, these dilated follicular openings may be seen clinically as well). This so-called ‘tin-tack’ sign or carpet tack sign or langue du chat (cat’s tongue) sign.-    MCQ
• Scarring alopecia ensues- (cause of scarring alopecia. SLE causes both scarring and Non-scarring alopecia) MCQ
• Itching and tenderness are common. 

Investigation

1) Histology- Investigation of choice MCQ - 2 out of 3 should be present

• Degenerative changes in the dermal connective tissue, consisting of hyalinization, oedema and fibrinoid change in upper dermis. Thickening of the basement membrane zone and dermal mucin deposition
• Liquefaction degeneration of the basal cell layer of the epidermis
• A patchy dermal lymphocytic infiltrate with a few plasma cells and histiocytes, particularly around the appendages, which may be atrophic

 

                                             (Ref: http://pixshark.com/discoid-lupus-erythematosus-histopathology.htm)

 (Ref: IJDVL)

2) ANA – Antinuclear antibodies are found in between 5-60% of cases depending on patient selection and laboratory techniques: the ‘homogeneous’ type of antinuclear factor being twice as frequent as the ‘speckled’ type. 

Treatment

Exposure to sunlight must be avoided, and a high sun-protection factor (SPF) sunscreen should be used daily

Treatment chart for DLE

Topical	Systemic
Steroids Potent or superpotent topical corticosteroids are beneficial. The single most effective local treatment is the injection of corticosteroids into the lesions. Triamcinolone acetonide, 2.5–10 mg/mL, is infiltrated into the lesion through a 30-gauge needle at intervals of 4–6 weeks.	1) Antimalarials The safest class 2) Acitretin Second-line agents and are particularly helpful in treating hypertrophic DLE

Complication

1)  Rate of progression to SLE- Extra edge point MCQ

- Localised DLE- 1.2% risk

- Disseminated DLE- 22% risk

- Females with DLE before< age of 40 years with HLA-B8, have an increased risk

- Patients with DLE showing signs of nephropathy, arthralgia and ANA titres of 1 : 320 or more should be carefully monitored

2) Rarely, aggressive squamous cell carcinoma arises in long-standing lesions of DLE.

Topical

Systemic

Steroids

Potent or superpotent topical corticosteroids are beneficial. The single most effective local treatment is the injection of corticosteroids into the lesions. Triamcinolone acetonide, 2.5–10 mg/mL, is infiltrated into the lesion through a 30-gauge needle at intervals of 4–6 weeks.

1) Antimalarials

The safest class

2) Acitretin

Second-line agents and are particularly helpful in treating hypertrophic DLE