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Background: Alopecia areata (AA) and atopic dermatitis (AD) are chronic skin diseases where the suboptimal medication adherence (MA) may result in poor clinical outcomes. Objective: To assess the impact of AA on MA among adults compared to AD. Methods: Patient reported MA of adults with AA were compared with AD. Patients were identified from the Danish Skin Cohort, a nationwide prospective cohort of dermatological patients in Denmark. We used the Medication Adherence Report Scale- 5, a self-reporting questionnaire, to assess MA. Demographic and disease characteristics were collected. Logistic regression was conducted. Results: Patients with AA reported higher MA than AD (mean 21.81 vs 18.29). Logistic regression analyses showed AA diagnosis had a statistically significant positive effect on MA (odds ratio = 3.94, 95% CI 2.01-8.89). Men reported significantly higher MA (odds ratio = 1.49, 95% CI 1.14-1.94). Current disease severity did not impact MA. Limitations: Data were self-reported by patients. Data regarding the specific treatment undergone by patients were not available. Conclusion: Patients with AA have significantly higher MA compared to patients with AD. The stability of AA patients' symptoms may lead to higher MA due to a desire for disease control. Conversely, the sporadicity of AD symptoms could negatively affect adherence, causing fluctuations in medication use.
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Introduction: Ultraviolet (UV) light is a known trigger of both cutaneous and systemic disease manifestations in lupus patients. Lupus skin has elevated expression of type I interferons (IFNs) that promote increased keratinocyte (KC) death after UV exposure. The mechanisms by which KC cell death is increased by type I IFNs are unknown. Methods: Here, we examine the specific cell death pathways that are activated in KCs by type I IFN priming and UVB exposure using a variety of pharmacological and genetic approaches. Mice that overexpress Ifnk in the epidermis were exposed to UVB light and cell death was measured. RNA-sequencing from IFN-treated KCs was analyzed to identify candidate genes for further analysis that could drive enhanced cell death responses after UVB exposure. Results: We identify enhanced activation of caspase-8 dependent apoptosis, but not other cell death pathways, in type I IFN and UVB-exposed KCs. In vivo, overexpression of epidermal Ifnk resulted in increased apoptosis in murine skin after UVB treatment. This increase in KC apoptosis was not dependent on known death ligands but rather dependent on type I IFN-upregulation of interferon regulatory factor 1 (IRF1). Discussion: These data suggest that enhanced sensitivity to UV light exhibited by lupus patients results from type I IFN priming of KCs that drives IRF1 expression resulting in caspase-8 activation and increased apoptosis after minimal exposures to UVB.