Background: Atopic dermatitis (AD) is a chronic inflammatory skin disorder. It is often reported to be worsened by psychological stress. Objective: To explore the role of psychological stress and related triggers in AD, and its connection to worsening of this disease, focusing on patients’ perspectives. Methods: In total, 28 patients with AD were included in focus groups. Topics regarding psychological stress and psychological triggers were discussed. Results: The hypothesis that psychological stress may have impact on eczema and its pruritus was supported by all of the patients. Distinguishing the worsening effect of psychological stress from effects of physiological triggers, such as infection, climate and allergic factors, was claimed to be difficult by many patients. Most of the patients thought that chronic stress affected the AD more when compared to acute stress. Family problems, financial problems, work overload, school exam periods, lack of structure at work, and unforeseen events were identified as important psychological triggers. Conventional treatment/therapy with topical corticosteroids and emollients, UV light treatment, were suggested as possible treatments, as well as psychological intervention and physical exercise. Conclusion Psychological stress is an important factor to consider in the management of patients with AD. In particular, chronic stress tends to worsen AD. The type of stress can possibly also affect the quality of the pruritus experienced by the patients. Unforeseen events and decision making were frequently mentioned as important triggers. Furthermore, physical exercise was reported to provide beneficial effects.

Although genome-wide association studies have identified more than eighty genetic variants associated with non-small cell lung cancer (NSCLC) risk, biological mechanisms of these variants remain largely unknown. By integrating a large-scale genotype data of 15 581 lung adenocarcinoma (AD) cases, 8350 squamous cell carcinoma (SqCC) cases, and 27 355 controls, as well as multiple transcriptome and epigenomic databases, we conducted histology-specific meta-analyses and functional annotations of both reported and novel susceptibility variants. We identified 3064 credible risk variants for NSCLC, which were overrepresented in enhancer-like and promoter-like histone modification peaks as well as DNase I hypersensitive sites. Transcription factor enrichment analysis revealed that USF1 was AD-specific while CREB1 was SqCC-specific. Functional annotation and gene-based analysis implicated 894 target genes, including 274 specifics for AD and 123 for SqCC, which were overrepresented in somatic driver genes (ER = 1.95, P = 0.005). Pathway enrichment analysis and Gene-Set Enrichment Analysis revealed that AD genes were primarily involved in immune-related pathways, while SqCC genes were homologous recombination deficiency related. Our results illustrate the molecular basis of both well-studied and new susceptibility loci of NSCLC, providing not only novel insights into the genetic heterogeneity between AD and SqCC but also a set of plausible gene targets for post-GWAS functional experiments.
Adenocarcinoma of Lung/genetics* ; Carcinoma, Non-Small-Cell Lung/genetics* ; Carcinoma, Squamous Cell/genetics* ; Genetic Heterogeneity ; Genetic Predisposition to Disease ; Genome-Wide Association Study ; Humans ; Lung Neoplasms/genetics* ; Polymorphism, Single Nucleotide