Background: Helicobacter pylori(HP) infection is considered to play a role in the pathogenesis of chronic spontaneous urticaria (CSU). However, the efficacy of HP eradication therapy on CSU symptom improvement has not been well established. This meta‐analysis was conducted to estimate the association between HP infection and CSU and to evaluate whether HP eradication therapy benefits patients with CSU.Material and Methods: In October 2018, we searched databases for studies investigating the efficacy of HP eradication therapy for patients with CSU. Risk ratios (RRs) and 95% confidence intervals (CIs) were pooled using random effects models.Results: The meta‐analysis included 22 studies with a total of 1385 patients with CSU. When comparing the spontaneous remission of urticarial symptom in patients with HP‐positive to HP‐negative patients, HP‐negative patients showed significantly higher spontaneous remission of urticarial symptoms. (risk ratio 0.39; 95% confidence interval: 0.19‐0.81). Among HP‐positive CSU patients, remission of CSU was more likely shown in HP eradication therapy group compared to untreated group, aside from achieving HP elimination (risk ratio 2.10; 95% confidence interval: 1.20‐3.68). However, there was no significant difference in the remission of CSU whether antibiotic therapy was successful in eradication of HP or not (risk ratio 1.00; 95% confidence interval: 0.65‐1.54).Conclusions: The results of this meta‐analysis show that HP might be associated with the occurrence and persistence of CSU. The effectiveness of HP eradication therapy in suppressing CSU symptoms was significant. Interestingly, we found that resolution of CSU was not associated with successful eradication of HP infection. CSU Patients who were undergone antibiotic therapy for HP eradication showed significant higher CSU remission with or without HP eradication. Further studies are recommended to evaluate the mechanisms associated with relation of HP with CSU.

Kim JE, et al. J Korean Med Sci. 2019 Apr;34(16):e126. https://doi.org/10.3346/jkms.2019.34.e126

Kim JE, et al. Ann Dermatol. 2021 Apr;33(2):138-146. https://doi.org/10.5021/ad.2021.33.2.138

Autophagy, one mechanism of programmed cell death, is fundamental to cellular homeostasis. Previous studies have identified autophagy as a novel mechanism by which cytokines control the immune response. However, its precise role in immune‐related inflammatory skin diseases such as psoriasis remains unclear. Thus, this study explored the functional role of autophagy in psoriatic inflammation of epidermal keratinocytes. Strong light chain 3 immunoreactivity was observed in epidermal keratinocytes of both human psoriatic lesions and imiquimod‐induced mice psoriatic model, and it was readily induced by polycytidylic acid (poly (I:C)), which stimulates Toll‐like receptor 3 (TLR3), in human epidermal keratinocytes in vitro. Rapamycin‐induced activation of autophagy significantly reduced poly (I:C)‐induced inflammatory reaction, whereas, inhibition of autophagy by 3‐methyladeine increased that. Our results indicate that the induction of autophagy may attenuate TLR3‐mediated immune responses in human epidermal keratinocytes, thus providing novel insights into the mechanisms underlying the development of inflammatory skin diseases including psoriasis.

Kim JE, et al. Ann Dermatol. 2019 Apr;31(2):196-200. https://doi.org/10.5021/ad.2019.31.2.196