Urticaria is a type of skin disease characterized by rapid onset of hives (superficial dermis edema, erythema, pruritus, or burning sensation). According to whether the natural course exceeds 6 weeks, urticaria can be divided into acute and chronic urticaria (CU). At present, the evaluation of CU activity mainly depends on the Urticaria Activity Score (UAS), but the evaluation indicators are relatively single, and we need more reliable experimental data for evaluation. We typically summarize advanced biomarkers and several related pathogenic pathways discovered in recent years on urticaria, including the cell adhesion/chemotaxis pathway, interleukin (IL)-6/Janus tyrosine kinase/STAT pathway, IL-17/IL-23 pathway, basophil- and mast cell-related pathway, coagulation/fibrinolysis-related pathways, single-nucleotide polymorphism, and some other pathways. This review aims to find appropriate biomarkers so that we can evaluate disease activity, discover novel therapeutic targets, and predict the patients’ response more accurately to therapeutic agents.

Background: Acanthosis nigricans (AN) involves skin hyperpigmentation in body folds and creases. Obesity-associated AN (OB_AN) is the most common type of AN. The skin condition of obese patients with AN can be improved through bariatric surgery, such as laparoscopic sleeve gastrectomy (LSG), after weight loss. However, the contributing factors to the remission of AN after surgery are still not fully determined. The authors aimed to assess the metabolic and pathological factors associated with remission of AN following LSG in obese individuals. Methods: The study included 319 obese patients who underwent LSG at our hospital. The subjects were divided into obesity (OB) only (OB, n=178) or OB with AN (OB_AN, n=141) groups. The basic clinical and metabolic indices and the dermatological features via reflectance confocal microscopy and histology were collected from patients prior to and after LSG. Results: OB_AN patients had higher fasting plasma glucose, homeostatic model assessment for insulin resistance, and testosterone levels than OB patients. LSG could significantly improve the biochemical and histopathological features of OB_AN patients. The remissive rate of OB_AN patients was about 86.5% (122 out of 141) after surgery. The remission of OB_AN skin lesions was positively correlated with testosterone levels (P<0.01). In addition, there was a significant positive correlation between changes in AN scores and epidermal thickness and skin pigmentation scores after surgery (P<0.01). Conclusion: The remissive rate of OB_AN after LSG is associated with improved testosterone levels and reduced epidermal thickness and skin pigmentation levels.

Frailty, a marker of biological ageing and reduced physiological reserve, is linked to many chronic conditions, yet its role in the development of systemic lupus erythematosus (SLE) remains unclear. To examine the association between frailty and incident SLE and to investigate potential inflammatory and genetic mechanisms underlying this relationship. We conducted a prospective cohort study among 462,762 participants from the UK Biobank to examine the associations of physical frailty and frailty index with incident SLE. Cox proportional hazards models were used to estimate hazard ratios and 95% confidence intervals, with further analyses assessing the interaction and joint effects of frailty and polygenic risk. Gene-level overlap between frailty and SLE was evaluated using MAGMA. In addition, we integrated circulating inflammatory markers and plasma proteomic profiles to identify potential mediating pathways and candidate biomarkers. During a median follow-up of 13.2 years, 309 of 462,762 participants (0.07%) developed incident SLE. Compared to non-frail individuals, both pre-frail and frail participants had a higher risk of developing SLE, with stronger associations observed in those with higher polygenic risk scores. Gene analysis identified 39 shared genes that were significantly correlated with both frailty and SLE. Circulating inflammatory markers, including C-reactive protein, were found to partially mediate the frailty-SLE relationship. Proteomic analyses identified ANGPTL3, CST3 and TNFSF8 as the candidate risk-related biomarkers associated with future incident SLE. Frailty is associated with an increased long-term risk of incident SLE, particularly in genetically susceptible individuals. Inflammatory cell measures and circulating proteins, including ANGPTL3, CST3 and TNFSF8, may help identify elevated SLE risk in pre-frail and frail populations.