{"title":"Revisiting the Association Between Beta-blockers and Psoriasis: Evidence from Real-World Data.","authors":"Xiulan Zheng, Jian Sun, Zhen Wang, Kai Cao, Chen Feng, Rundong Lv","doi":"10.2174/0118715303383036250807095142","DOIUrl":null,"url":null,"abstract":"<p><strong>Introduction: </strong>Some cases report that beta-blockers may induce or exacerbate psoriasis. However, pharmacoepidemiology studies have yielded conflicting results. This study aims to investigate whether there is a potential association between beta-blockers and psoriasis.</p><p><strong>Methods: </strong>An observational study was conducted on the U.S. population from the National Health and Nutrition Examination Survey (NHANES) database using propensity score matching and multivariable logistic regression models. Subsequently, a disproportionality analysis was performed based on the FDA Adverse Event Reporting System (FAERS) database, and a two-sample Mendelian randomization (MR) study was conducted to assess the association between beta-blockers and the risk of developing psoriasis.</p><p><strong>Results: </strong>Based on the NHANES database, logistic regression analysis, adjusted for relevant confounders, showed no significant association between beta-blocker use and the risk of psoriasis (OR: 1.49, 95% CI: 0.76-2.92, p = 0.250). FAERS analysis identified 300 psoriasis-related reports for beta-blockers, but no robust safety signals were detected (ROR: 0.34, 95% CI: 0.30-0.38), even after false-negative analysis. The meta-analysis of MR results demonstrated a statistically significant association between beta-blocker use and reduced risk of psoriasis (OR: 0.9985, 95% CI: 0.9978-0.9991, p < 0.001).</p><p><strong>Discussion: </strong>The observed epidemiological association likely stems from confounding by cardiovascular indications for beta-blockers, rather than a direct causal effect. Neuroimmune pathways (sympathetic activity, β1/β2 receptor effects on immune cells/keratinocytes) present biologically plausible but complex and potentially opposing mechanisms, requiring further investigation.</p><p><strong>Conclusions: </strong>We found that beta-blockers did not significantly elevate the risk of psoriasis. In clinical practice, labeling beta-blockers as drug-induced psoriasis may be inappropriate.</p>","PeriodicalId":94316,"journal":{"name":"Endocrine, metabolic & immune disorders drug targets","volume":" ","pages":""},"PeriodicalIF":2.0000,"publicationDate":"2025-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Endocrine, metabolic & immune disorders drug targets","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.2174/0118715303383036250807095142","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Introduction: Some cases report that beta-blockers may induce or exacerbate psoriasis. However, pharmacoepidemiology studies have yielded conflicting results. This study aims to investigate whether there is a potential association between beta-blockers and psoriasis.
Methods: An observational study was conducted on the U.S. population from the National Health and Nutrition Examination Survey (NHANES) database using propensity score matching and multivariable logistic regression models. Subsequently, a disproportionality analysis was performed based on the FDA Adverse Event Reporting System (FAERS) database, and a two-sample Mendelian randomization (MR) study was conducted to assess the association between beta-blockers and the risk of developing psoriasis.
Results: Based on the NHANES database, logistic regression analysis, adjusted for relevant confounders, showed no significant association between beta-blocker use and the risk of psoriasis (OR: 1.49, 95% CI: 0.76-2.92, p = 0.250). FAERS analysis identified 300 psoriasis-related reports for beta-blockers, but no robust safety signals were detected (ROR: 0.34, 95% CI: 0.30-0.38), even after false-negative analysis. The meta-analysis of MR results demonstrated a statistically significant association between beta-blocker use and reduced risk of psoriasis (OR: 0.9985, 95% CI: 0.9978-0.9991, p < 0.001).
Discussion: The observed epidemiological association likely stems from confounding by cardiovascular indications for beta-blockers, rather than a direct causal effect. Neuroimmune pathways (sympathetic activity, β1/β2 receptor effects on immune cells/keratinocytes) present biologically plausible but complex and potentially opposing mechanisms, requiring further investigation.
Conclusions: We found that beta-blockers did not significantly elevate the risk of psoriasis. In clinical practice, labeling beta-blockers as drug-induced psoriasis may be inappropriate.