Morphea is an inflammatory fibrotic disorder of the skin that has been likened to systemic sclerosis (SSc). We sought to examine the molecular landscape of morphea by examining lesional skin gene expression and blood biomarkers and comparing the gene expression profiles with those from site-matched nonlesional and SSc lesional skin. We found the morphea transcriptome is dominated by IFN-γ-mediated T helper 1 immune dysregulation, with a relative paucity of fibrosis pathways.
View Article and Find Full Text PDFThis cross-sectional analysis compares clinical assessment with magnetic resonance imaging (MRI) findings in determining the extent of disease in patients with morphea.
View Article and Find Full Text PDFImportance: Prospective studies of the disease course in patients with morphea are lacking, particularly those comparing adults and children.
Objective: To investigate the disease course in patients with morphea treated with standard-of-care therapy using validated clinical outcome measures.
Design, Setting, And Participants: Prospective cohort study of 130 adults and children from the Morphea in Adults and Children cohort with at least 2 years of clinical follow-up and Localized Scleroderma Cutaneous Assessment Tool scores recorded at each study visit.
J Investig Dermatol Symp Proc
October 2017
Cutaneous lupus erythematosus, specifically discoid lupus erythematosus, disproportionately affects those with skin of color and may result in greater dyspigmentation and scarring in darker skin types. In this article, we review investigations relevant to cutaneous lupus patients with skin of color at University of Texas Southwestern Medical Center, associations and risk of progression to systemic lupus, and recommendations for monitoring for systemic disease spread. Between 5% and 25% of patients with cutaneous lupus can develop systemic lupus.
View Article and Find Full Text PDFIFN-related pathways have not been studied in morphea, and biomarkers are needed. We sought to characterize morphea serum cytokine imbalance and IFN-related gene expression in blood and skin to address this gap by performing a case-control study of 87 participants with morphea and 26 healthy control subjects. We used multiplexed immunoassays to determine serum cytokine concentrations, performed transcriptional profiling of whole blood and lesional morphea skin, and used double-staining immunohistochemistry to determine the cutaneous cellular source of CXCL9.
View Article and Find Full Text PDFA quantitative method to assess hip synovitis in Legg-Calvé-Perthes disease (LCPD) is not currently available. To develop this method, the areas of synovial enhancement on gadolinium-enhanced MRI (Gd-MRI) were measured by two independent observers. The volume of synovial enhancement was significantly increased in the initial and the fragmentation stages of LCPD (Waldenström stages I and II), with a persistence of synovitis into the reossification stage (stage III).
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