Background: Evidence of T1/IFN-γ overactivation as a major pathogenic driver somewhat conflicts with data supporting robust allergic background in patients with alopecia areata (AA). Previous investigations of immunological dysregulations show that both T1- and T2-related markers are overexpressed in AA. Clinical correlations in large populations may shed light on the immune pathways most likely to result in the clinical phenotype of AA.
Objective: To investigate the atopic comorbidities among patients with AA in a large population-based study.
Methods: This is a cross-sectional retrospective study of patients with AA and a matched comparison group, analyzing the associations between AA and 4 atopic comorbidities: asthma, atopic dermatitis (AD), allergic rhinitis, and allergic conjunctivitis. χ and t tests were used for univariate analysis, and logistic regression model was used for multivariate analysis. The study was performed using the computerized database of the Clalit Health Services, encompassing more than 4.4 million subjects.
Results: The study population included 51,561 patients with AA and 51,410 matched control subjects. The prevalence of asthma (7.8% vs 6.5%; odds ratio [OR], 1.22; 95% CI, 1.17-1.28; P < .001), AD (3.9% vs 2.6%; OR, 1.55; 95% CI, 1.44-1.66; P < .001), allergic rhinitis (16.0% vs 12.8%; OR, 1.29; 95% CI, 1.25-1.34; P < .001), and allergic conjunctivitis (23.5% vs 19.6%; OR, 1.27; 95% CI, 1.23-1.30; P < .001) was significantly higher among patients with AA as compared with matched control subjects. Patients with AA also had a significantly higher probability of having more than 1 atopic comorbidity, with increasing OR as the number of concomitant atopic conditions increased.
Conclusions: Our analysis supports the previous literature and provides strong generalizability of significant atopy in patients with AA, suggesting T2 pathogenicity in AA, and challenging the traditional view of AA as a single-axis, T1-centered disease.
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http://dx.doi.org/10.1016/j.jaip.2020.01.052 | DOI Listing |
Dermatol Ther (Heidelb)
January 2025
Department of Dermatology, Institute of Medical Sciences, Medical College of Rzeszow University, Rzeszow, Poland.
Introduction: Ultraviolet-induced fluorescence dermoscopy (UVFD) is increasingly utilized in dermatooncology and general dermatology. The objective of the study was to characterize the ultraviolet-induced fluorescence trichoscopy (UVFT) findings in a wide range of hair and scalp conditions.
Methods: Consecutive patients with non-scarring alopecias (alopecia areata, AA, n = 40; androgenetic alopecia, AGA, n = 40), scarring alopecias (frontal fibrosing alopecia, FFA, n = 20; lichen planopilaris, LPP, n = 20; folliculitis decalvans, FD, n = 14; discoid lupus erythematosus, DLE, n = 23), and inflammatory scalp conditions (psoriasis, n = 30; seborrheic dermatitis, n = 14) were included.
Background: Alopecia areata (AA) is a T-cell-mediated autoimmune disease that significantly impacts patient quality of life. The breakdown of hair follicle immune privilege underlies AA pathogenesis. However, the precise mechanism of this breakdown remains unclear.
View Article and Find Full Text PDFJ Cosmet Dermatol
January 2025
Department of Dermatology, China-Japan Friendship Hospital, Beijing, China.
Background: Alopecia areata (AA) is a prevalent autoimmune disorder in dermatology, impacting 0.5%-2% of the general population worldwide. More and more scholars are focusing on the important role of micronutrients in the occurrence and development of AA.
View Article and Find Full Text PDFJ Dermatol
December 2024
Department of Ophthalmology, Otolaryngology, and Dermatology, Kyung Hee University College of Korean Medicine, Kyung Hee University Hospital at Gangdong, Seoul, Republic of Korea.
The long-term complications of coronavirus disease 2019 (COVID-19) continue to cause global concern. This study aimed to estimate the incidence and risk of chronic urticaria, vitiligo, alopecia areata, and herpes zoster following COVID-19 infection. Only participants confirmed by real-time reverse transcription-polymerase chain reaction tests to have COVID-19 were enrolled in the COVID-19 group.
View Article and Find Full Text PDFElife
December 2024
Linda Crnic Institute for Down Syndrome, University of Colorado Anschutz Medical Campus, Aurora, United States.
Background: Individuals with Down syndrome (DS), the genetic condition caused by trisomy 21 (T21), display clear signs of immune dysregulation, including high rates of autoimmunity and severe complications from infections. Although it is well established that T21 causes increased interferon responses and JAK/STAT signaling, elevated autoantibodies, global immune remodeling, and hypercytokinemia, the interplay between these processes, the clinical manifestations of DS, and potential therapeutic interventions remain ill defined.
Methods: We report a comprehensive analysis of immune dysregulation at the clinical, cellular, and molecular level in hundreds of individuals with DS, including autoantibody profiling, cytokine analysis, and deep immune mapping.
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