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Morphea is a rare autoimmune condition causing inflammation and sclerosis of the skin and underlying soft tissue. It is characterized by periods of activity (inflammation admixed with fibrosis), ultimately resulting in permanent damage (pigment change and tissue loss). Damage resulting from unchecked activity can lead to devastating, permanent cosmetic and functional sequelae including hair loss; cutaneous, soft tissue and bony atrophy; joint contractures; and growth restriction of the affected body site in children. This makes the early identification of activity and initiation of appropriate treatment crucial to limiting damage in morphea. To this end, recent investigative work has focused on validation of clinical, biomarker, imaging, and histologic outcomes aimed at accurately quantifying activity and damage.Despite promising results, further work is needed to better validate these measures before they can be used in the clinic and research settings. Although there has been recent approval of less toxic, targeted therapies for many inflammatory skin conditions, none have been systematically investigated in morphea.The mainstays of treatment for active morphea are corticosteroids and methotrexate. These are often limited by substantial toxicity. The paucity of new treatments for morphea is the result of a lack of studies examining its pathogenesis, with many reviews extrapolating from research in systemic sclerosis. Recent studies have demonstrated the role of dysregulated immune and fibrotic pathways in the pathogenesis of morphea, particularly interferon (IFN) gamma related pathways. Active morphea lesions have been foundto display an inflammatory morphea signature with CXCR3 receptor ligands, as well as a distinct fibrotic signature reflecting fibroblast activation and collagen production. CXCL9 and 10 have been associated with increased measures of disease activity. While immune dysfunction is thought to play the primary role in morphea pathogenesis, there are other factors that may also contribute, including genetic predisposition, environmental factors, and vascular dysregulation. There remains an essential need for further research to elucidate the pathogenesis of morphea and the mode of action of dysregulated upstream and downstream immune and fibrotic pathways. These studies will allow for the discovery of novel biomarkers and targets for therapeutic development.

ObjectiveEpidemiological studies have shown that discoid lupus erythematosus (DLE) has a higher incidence and prevalence in racial/ethnic minority groups, particularly Black individuals. The objective of this retrospective cohort study was to identify the differences in DLE lesion distribution and characteristics in Black individuals compared with non-Black individuals.Methods183 patients with DLE (112 Black patients and 71 non-Black patients) with a reported race/ethnicity and Cutaneous Lupus Erythematosus Disease Area and Severity Index (CLASI) scores were included in this retrospective cohort study. Univariate analysis was performed to determine significant differences in demographic data, clinical characteristics, DLE lesion distribution and DLE lesion characteristics in Black and non-Black patients with DLE. Multivariable logistic regression was preformed to determine significant predictors of DLE lesion location and characteristics.ResultsBlack patients with DLE had worse baseline CLASI damage scores compared with non-Black patients with DLE (median (IQR): 10.0 (6.0–14.5) vs 6.0 (3.0–10.0), p<0.001) and had 48.9 greater odds of dyspigmentation in any anatomical location (p<0.001). Black patients had 2.54 greater odds of having scalp involvement (p=0.015) and 1.97 greater odds of having ear involvement (p=0.032) compared with non-Black patients. Black patients also had greater odds of scalp dyspigmentation (OR=5.85, p<0.001), ear dyspigmentation (OR=2.89, p=0.001) and scarring alopecia (OR=3.00, p=0.001) compared with non-Black patients.ConclusionsSigns of disease damage, particularly ear dyspigmentation, scalp dyspigmentation and scarring alopecia, can more frequently affect Black patients with DLE. Recognising differences in clinical presentation of DLE among Black patients can assist future efforts with understanding biological, cultural, psychosocial and systemic factors that influence DLE presentation and outcomes in Black patients and may guide clinicians when counselling Black patients.

Background Cutaneous lupus erythematosus (CLE) is an autoimmune photosensitive skin condition. The impact of income on quality of life has been incompletely characterized in CLE. Objectives We aimed to assess how annual income affects quality of life among CLE patients. Methods In this cross-sectional study of 238 patients with CLE, relationships between predictor variables including annual income and each SKINDEX-29 + 3 subdomain were identified using univariate and multivariable analyses. In addition, answers to individual SKINDEX-29 + 3 questions were compared across income groups. Clinical factors in patients making less than <10,000 USD (N = 85) with worse SKINDEX-29 + 3 scores were also identified by univariate and multivariable analyses. Results Patients making <10,000 USD annually experienced worse quality of life across multiple SKINDEX-29 + 3 subdomains (p < 0.05). These patients specifically experienced poorer quality of life relating to social isolation and self-consciousness. (p < 0.001). Among those making <10,000 USD, predictors for worse quality of life included females, smokers, and those with higher skin disease activity were identified (p < 0.05). Limitations: This is a single center study. Income was also self-reported and could not be verified. Conclusions Lower income is related to poorer quality of life in patients with CLE. Specifically, patients experience limitations regarding social isolation and self-consciousness.

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