Background Vitiligo is a frequent acquired depigmentation skin disease due to a loss of melanocytes. This study sought to characterize the expression pattern of microRNA (miRNA) in the peripheral blood mononuclear cells (PBMCs) of non‐segmental vitiligo (NSV) patients. We also screened for molecular markers that can be used to evaluate the clinical stages of NSV. Methods The miRNA expression profile in the PBMCs of four patients with progressive NSV and four healthy controls was determined using high‐throughput RNA sequencing. The divergently expressed miRNA was verified via qRT‐PCR in 26 progression, 26 stable NSV, and 26 healthy controls. Results Our findings posited that 323 miRNAs were differentially expressed in the PBMCs of NSV patients. The top 10 up‐regulated miRNAs in patients were hsa‐miR‐335‐5p, hsa‐miR‐20a‐5p, hsa‐miR‐514a‐3p, hsa‐miR‐144‐5p, hsa‐miR‐450b‐5p, hsa‐miR‐369‐3p, hsa‐miR‐101‐3p, hsa‐miR‐142‐5p, hsa‐miR‐19b‐3p, and hsa‐miR‐340‐5p. The top 10 down‐regulated miRNAs in patients were hsa‐miR‐4443, hsa‐miR‐1248, hsa‐miR‐6859‐3p, hsa‐miR‐668‐3p, hsa‐miR‐7704, hsa‐miR‐323a‐5p, hsa‐miR‐1237‐3p, hsa‐miR‐3127‐3p, hsa‐miR‐6735‐3p, and hsa‐miR‐127‐3p. The expressions of hsa‐miR‐20a‐5p in PBMCs of progressive and stable NSV were remarkably elevated relative to the healthy controls. In the characteristics curve analysis of hsa‐miR‐20a‐5p for differentiating progressive and stable NSV from normal subjects in PBMCs, the area under curve (AUC) was 0.92 and 0.81. Compared with patients in stable NSV, the hsa‐miR‐20a‐5p was markedly increased in PBMCs of progressive NSV patients, and the AUC was 0.81. Conclusion Our results showed that divergently expressed miRNAs contribute to the pathogenesis of NSV and that hsa‐miR‐20a‐5p can be applied as a biosignature for stage assessment in PBMCs of patients with NSV.
severe atopic dermatitis. JAK1 is involved in the signaling of γc receptor cytokines (IL-2, IL-4, IL-7, IL-9, IL-15, and IL-21) and IFNγ. 3 These cytokines are the main key factors in the pathogenesis of AA, so we use abrocitinib to treat AA, probably because it covers the cytokines in AA pathophysiology.This case suggests that axitinib may be an alternative treatment for children with refractory AA who fail to respond to conventional therapy. Further prospective studies are needed to evaluate its efficacy and safety.
Objective: We explored the patterns of long non-coding RNA (lncRNA) expression in peripheral blood mononuclear cells (PBMCs) from patients with non-segmental vitiligo. Methods: We used high-throughput RNA sequencing technology to generate sequence data from five patients with non-segmental vitiligo alongside five normal healthy individuals, and then performed bioinformatics analyses to detect the differential expression of lncRNA in PBMCs. Gene Ontology (GO) and pathway analyses were performed for functional annotation, and quantitative real-time polymerase chain reaction (qRT-PCR) was used to verify gene expression. Target miRNAs and mRNAs of differentially expressed lncRNAs were predicted using bioinformatics analysis. Results: A total of 292 lncRNAs were differentially expressed in non-segmental vitiligo (fold change ≥ 2.0, P < .05), of which 171 were upregulated and 121 were downregulated. Six differentially expressed lncRNAs were selected, namely ENST00000460164.1, ENST00000393264.2, NR - 046211.1, NR - 135491.1, NR - 135320.1, and ENST00000381108.3, for validation by qRT-PCR. The results showed that ENST00000460164.1 and NR - 046211.1 were highly expressed in PBMCs of non-segmental vitiligo. An lncRNA-miRNA-mRNA network containing two lncRNAs, 17 miRNAs, and 223 mRNAs was constructed. Conclusion: Our results revealed patterns of differentially expressed lncRNAs in the PBMCs of non-segmental vitiligo individuals. ENST00000460164.1, and NR - 046211.1 may be potential biomarkers and drug targets for the treatment of non-segmental vitiligo.
The prognostic nutritional index (PNI) and red blood cell distribution width-to-albumin ratio (RAR) are considered to be related to the prognosis of disease severity. However, the role of these biomarkers in predicting Stevens-Johnson syndrome/toxic epidermal necrolysis (SJS/TEN) severity and mortality is unclear. The aim of the current study was to investigate the association of PNI and RAR with severity and mortality in individuals with SJS/TEN. Clinical data were retrospectively collected from 74 individuals with SJS/ TEN and 74 healthy individuals, who were matched for age and sex during the same period. PNI, RAR, and other indicators were compared between individuals with SJS/ TEN and healthy controls. The association of PNI and RAR with SJS/TEN severity was assessed using Spearman or Pearson correlation analyses. Individuals with SJS/TEN were categorized into two groups, either survivors or nonsurvivors. The correlation between PNI, RAR, and SJS/TEN mortality was analyzed using univariate and multivariate logistic regression. The predictive value of the previously mentioned indicators on the mortality of patients with SJS/TEN was assessed using receiver operating characteristic curve analysis. The RAR level of patients with SJS/TEN was greater than that of the control group (p < 0.05), whereas PNI was lower. In compliance with correlation analysis, RAR was positively correlated with SCORTEN (Score of Toxic Epidermal Necrolysis) and ABCD-10 (age, bicarbonate, cancer, dialysis, 10% body surface area) (p < 0.05), and PNI was negatively correlated (p < 0.05). RAR is a risk factor for death in patients with SJS/TEN, but an elevated PNI level is a protective factor for mortality. The best cutoff values of PNI and RAR for predicting death in patients with SJS/TEN were 31.375 (sensitivity, 84.7%; specificity, 80%) and 0.486 (sensitivity, 73.3%; specificity, 84.7%). These results underscore the potential clinical value of PNI and RAR as appropriate and meaningful biomarkers to assess the severity of SJS/TEN and the mortality associated with it.
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