The expanding therapeutic landscape for inflammatory skin diseases, combined with rising healthcare costs, has increased the need for a comprehensive method to assess and compare treatment performance in daily practice care. In this context, drug survival—the time a patient remains on a given treatment—has gained increasing attention in dermatology because it comprehensively reflects treatment effectiveness, safety, and patient and clinician preferences. However, methodological approaches and reporting practices vary considerably across drug survival studies in dermatology. In this article, we aim to provide an updated and comprehensive guide for clinical researchers on drug survival methodology, offering recommendations for performing, reporting, and interpreting drug survival analyses in a standardized manner, while highlighting best practices within dermatology. We provide guidance on fundamental concepts of drug survival analysis, including Kaplan–Meier curves, reporting standards, censoring, stratification, regression analyses, and sample size calculations. In addition, to further enhance the quality of analyses, we discuss advanced topics such as restricted mean survival time, competing risks, time-dependent effects and covariates, and meta-analyses of drug survival data. Key concepts will be illustrated using a synthetic dataset, comprising patients with psoriasis treated with biologics, complemented by references to published studies that clarify relevant methodological concepts and provide real-world dermatological examples.
Solar UVR significantly influences human health, yet the early molecular effects of everyday low-dose exposure remain poorly understood. This study investigated acute molecular events in human skin after single and repeated low-dose UVR exposure, providing insights into early regulatory networks underlying cutaneous UVR responses. Healthy volunteers (n = 6, 5 female, aged 28–65 years, skin types II–III) received low-dose solar-simulated UVR to upper buttock skin on 3 consecutive days, with biopsies collected 30 minutes, 3 hours, and 24 hours after the 1st exposure; 24 hours after the 3rd exposure; and from unexposed skin. Biopsies were assessed by immunostaining and RNA sequencing. Whereas a single exposure induced few transcriptomic changes, repeated UVR exposure elicited a robust response with 1498 differentially expressed genes compared with those in unexposed skin. This included numerous long noncoding RNAs and showed pathway enrichment related to cell-cycle activation, inflammation, and IFN signaling. Accompanying this was the activation of upstream regulators, including IFNs, GFs, and proinflammatory molecules. Immunostaining suggested an apparent (nonsignificant) increase in epidermal cell proliferation and immune infiltration after 3 low-dose UVR challenges. The findings demonstrate that even brief repeated UVR exposures can induce cumulative effects, evoking molecular responses relevant to skin physiology.
UVR is a major environmental trigger of cutaneous inflammation. Although DNA damage has long been considered the main mediator of UV pathology, a growing body of evidence indicates that RNA is a primary driver of UV-induced inflammation. UV exposure induces RNA damage and dysregulates RNA metabolism, activating the ribotoxic stress response and promoting the generation and accumulation of immunostimulatory self-RNAs. RNA metabolism also plays a role in UV-related dermatologic pathologies, including photosensitive inflammatory skin disorders and skin carcinogenesis. In this review, we summarize the current knowledge and new advances on the role of RNA in UV-induced inflammation, with an emphasis on both mechanisms and translational implications. Together, these insights suggest that targeting RNA pathways may represent a new approach for treating or preventing UV-induced skin inflammation and inflammatory skin diseases.
