Classifying discoid lupus erythematosus: background, gaps, and difficulties

Abstract

To inform our ongoing efforts to develop defining features to be incorporated into a novel set of classification criteria for discoid lupus erythematosus (DLE), we conducted a literature review using the Ovid MEDLINE database. A search was performed to identify studies reporting criteria used to distinguish DLE from other cutaneous lupus erythematosus subtypes. We examined which clinical, histopathologic, and serologic features have data to support their use as effective features in distinguishing DLE from other potential disease mimickers and cutaneous lupus subsets. Through our search, we were also able to identify gaps that exist in the literature which can inform future directions for research endeavors. We found that localization of lesions, characteristic features of damage, and the absence of high titer Ro/SSA antibody seem most effective in differentiating DLE from other cutaneous lupus erythematosus subtypes. Histopathologic features and class of immunoreactant deposition appear to be less helpful.

Histopathological Review on Discoid Lupus Erythematous Mimicking Granuloma Faciale

“…A clinical overview of spherical active DLE regarding areas exposed to sunlight and follicular plugging. 9 Granuloma faciale is a chronic benign vasculitis cutaneous disease with a typical morphological pattern and unknown etiologies. The clinical feature of granuloma faciale is brownish-red plaques on the face, especially on areas exposed to sunlight.…”

Treatments for disease damage in cutaneous lupus erythematosus: A narrative review

“…23 In DLE, deep lymphocytic inflammation likely leads to atrophy, as there is underlying tissue loss that remains after the inflammation subsides, leading to depressions in the skin (Figure 1). 4 Injectable fillers have been reported to improve the appearance of atrophic cutaneous lupus lesions (Table 3, Figure 2). Hyaluronic acid (HA), poly-L-lactic acid (PLLA), polymethylmethacrylate, and polyacrylamide fillers have all been reported to improve atrophy secondary to lupus panniculitis.…”

“…Specifically, in DLE, where dyspigmentation is an important feature of disease damage, intense inflammatory infiltrates can be observed in the deep dermis. 4 While the pathogenesis of hyperpigmentation in DLE is not fully known, inflammatory mediators, generated by this dense inflammation, are thought to stimulate melanocyte activity, leading to increased pigmentation. Leukotriene (LT)-C4, LT-D4, prostaglandins E2, F2α and D2, thromboxane-2, interleukin (IL)-1, IL-6, IL-18, IL-33, tumor necrosis factor (TNF)-α, epidermal growth factor, granulocyte-macrophage colony-stimulating factor and reactive oxygen species such as nitric oxide have all exhibited melanocyte stimulating properties.…”

JAK‐STAT signaling pathway inhibition: a role for treatment of discoid lupus erythematosus and dermatomyositis

“…There is a thickening of the basement membrane and destruction of sebaceous glands and elastic fibers throughout the reticular dermis. 4 Mucosal surfaces throughout the body can also be sites for discoid lesions, such as on the lips and oral nasal, conjunctival, and genital mucosa. 3 In addition, DLE of the scalp will result in hair loss, which may partially or completely recover with treatment, but cicatricial alopecia may be permanent.…”

“…Specific pathology involves interface dermatitis with vacuolar degeneration of the basal cell layer and necrotic keratinocytes. There is a thickening of the basement membrane and destruction of sebaceous glands and elastic fibers throughout the reticular dermis . Mucosal surfaces throughout the body can also be sites for discoid lesions, such as on the lips and oral nasal, conjunctival, and genital mucosa .…”