The Journal of dermatology最新文献

Previous research has highlighted a significant association between inflammatory proteins and the development and progression of hidradenitis suppurativa (HS). Nevertheless, the potential causative link between these factors remains to be definitively established. To investigate the genetic correlation between inflammatory proteins and HS, linkage disequilibrium score regression (LDSC) was employed. Mendelian randomization (MR) analysis, incorporating inverse variance weighted, MR-Egger, and weighted median methodologies, was utilized to evaluate the possible causal relationship between circulating inflammatory proteins (CIPs) and HS. Additionally, reverse MR analysis was carried out to explore reverse causality. The data set for 91 CIPs was derived from a genome-wide protein quantitative trait loci study, while HS-related data were acquired from the FinnGen study. Moreover, the stability of the causal relationships was assessed via sensitivity analyses, encompassing tests for pleiotropy, heterogeneity, and leave-one-out analysis. The LDSC analysis suggested the existence of genetic correlations between the levels of Fibroblast growth factor 21 (FGF-21), stem cell factor, and HS. The MR analysis identified a suggestive association of T-cell surface glycoprotein CD5 and C-X-C motif chemokine 11 with an elevated risk of HS. Conversely, C-C motif chemokine 4, Protein S100-A12, Interleukin-10 receptor subunit beta, and Programmed cell death 1 ligand 1 were associated with a diminished risk of HS. Moreover, HS was demonstrated to increase the levels of four CIPs: Interleukin-20, Leukemia inhibitory factor (LIF), LIF receptor, and Thymic stromal lymphopoietin. The findings of this investigation offer suggestive evidence for possible genetic correlations and causal links between various genetically predicted inflammatory proteins and HS. There exists a pressing requirement for additional studies to elucidate the fundamental processes driving these associations.

Although genetic, environmental, autoimmune, and psychological factors are believed to play a role in the onset of alopecia areata (AA), the exact cause remains unknown. This study aimed to investigate whether there are differences in traumatic experiences, dissociative symptoms, and alexithymia levels between groups. Fifty eight patients diagnosed with AA, 58 individuals with dermatological diseases thought to have a low psychosomatic component, and 58 individuals not diagnosed with any chronic disease were included in the study. All participants were assessed using the Childhood Trauma Questionnaire (CTQ-28), Dissociative Experiences Scale (DES), Posttraumatic Stress Disorder Checklist for DSM-5 (PCL-5), and Toronto Alexithymia Scale (TAS-20). A Structured Clinical Interview for DSM-5 (SCID-5-CV) form was used to exclude additional psychiatric diagnoses. Mean scores on the CTQ-28 scale revealed differences between groups in terms of physical neglect and emotional neglect scores (p < 0.001; p = 0.022; p < 0.001). There were no differences in DES scores between groups (p = 0.085). When compared in terms of TAS-20 and PCL-5 scores, differences were found (p = 0.016; p = 0.024). As a result of this study, it was concluded that physical neglect and emotional neglect could play a significant role in the onset of AA. Alexithymia and traumatic stress disorder symptoms might be more prevalent in patients with AA.

Generalized pustular psoriasis (GPP) is a severe autoinflammatory keratinization disease (AiKD) characterized by acute flares of widespread sterile pustules and high fever. GPP is potentially life-threatening. Recently clarified genetic predisposing factors for GPP suggest that the excessive activation of innate immune pathways in the skin, including of interleukin (IL)-1 and IL-36 signaling, plays a significant role in the GPP pathogenesis. IL36RN, CARD14, AP1S3, MPO, SERPINA3, BTN3A3, and MEFV have been identified as GPP-related genes. The pathogenesis of GPP provoked by variants in these seven genes is tightly associated with the excessive activation of innate immune pathways and the resulting autoinflammation in the skin. Various biologics, including inhibitors for the tumor necrosis factor, IL-17, and IL-23 pathways, are used as treatments for GPP. The new understanding of the genetic background of GPP, mentioned above, indicates that the genetic predisposing factors are predominantly related to the excessive activation of innate immunity and autoinflammation. In this context, inhibitors of inflammatory signaling, including of the IL-1 and IL-36 pathways, have been used in clinical practice and investigated as potential future therapies.