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已发表论文
乳糜泻作为疱疹样皮炎遗传易感因素的两样本孟德尔随机化分析
Authors Su Y, Xu P , Zhang M, Wen P, Xu K, Xie J, Wan X, Liu L, Yang Z, Yang M
Received 24 July 2025
Accepted for publication 28 October 2025
Published 7 December 2025 Volume 2025:18 Pages 3317—3329
DOI https://doi.org/10.2147/CCID.S556046
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 3
Editor who approved publication: Dr Jeffrey Weinberg
Yani Su,1,* Peng Xu,2,* Ming Zhang,3,* Pengfei Wen,2 Ke Xu,2 Jiale Xie,2 Xianjie Wan,2 Lin Liu,2 Zhi Yang,2 Mingyi Yang2
1Department of Radiotherapy, Tangdu Hospital, Fourth Military Medical University, Xi’an, Shaanxi, People’s Republic of China; 2Department of Joint Surgery, HongHui Hospital, Xi’an Jiaotong University, Xi’an, Shaanxi, People’s Republic of China; 3Department of General Practice, Honghui Hospital, Xi’an Jiaotong University, Xi’an, Shaanxi, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Mingyi Yang, Email ymy25808@163.com Zhi Yang, Email hhyy_yangzhi@163.com
Objective: Observational studies have consistently highlighted a robust clinical association between celiac disease (CD) and dermatitis herpetiformis (DH). Building on this foundation, the present study aims to investigate whether this observed relationship is underpinned by a causal genetic mechanism, providing insights into the potential hereditary basis of their connection.
Methods: This study employed bidirectional two-sample Mendelian randomization (MR) analysis to investigate the potential genetic causality between CD and DH, utilizing genome-wide association study (GWAS) summary data. To comprehensively examine the genetic relationship between CD and DH, we applied multiple MR methodologies. Furthermore, to enhance the robustness and credibility of our results, we conducted extensive sensitivity analyses.
Results: The fixed-effects inverse variance weighted (IVW) analysis revealed a significant positive genetic causal relationship between CD and DH (P = 0.001, odds ratio [OR] 95% confidence interval [CI]: 1.546 [1.195– 1.999]). In contrast, no significant genetic causality was found in the reverse direction, from DH to CD (P = 0.113, OR 95% CI: 1.039 [0.991– 1.090]). Notably, the MR analysis revealed no evidence of heterogeneity, further reinforcing the reliability of the fixed-effects IVW model. Additionally, sensitivity analyses confirmed the stability and robustness of the results, further validating the integrity of the conclusions drawn from the MR analysis.
Conclusion: The results of our study indicate that CD acts as a genetic susceptibility factor for the development of DH. Furthermore, the occurrence of DH in individuals with a history of CD appears to be attributed to a causal genetic relationship, suggesting that the genetic predisposition linked to CD may drive the manifestation of DH.
Keywords: celiac disease, dermatitis herpetiformis, mendelian randomization, causal, genetic
1Department of Radiotherapy, Tangdu Hospital, Fourth Military Medical University, Xi’an, Shaanxi, People’s Republic of China; 2Department of Joint Surgery, HongHui Hospital, Xi’an Jiaotong University, Xi’an, Shaanxi, People’s Republic of China; 3Department of General Practice, Honghui Hospital, Xi’an Jiaotong University, Xi’an, Shaanxi, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Mingyi Yang, Email ymy25808@163.com Zhi Yang, Email hhyy_yangzhi@163.com
Objective: Observational studies have consistently highlighted a robust clinical association between celiac disease (CD) and dermatitis herpetiformis (DH). Building on this foundation, the present study aims to investigate whether this observed relationship is underpinned by a causal genetic mechanism, providing insights into the potential hereditary basis of their connection.
Methods: This study employed bidirectional two-sample Mendelian randomization (MR) analysis to investigate the potential genetic causality between CD and DH, utilizing genome-wide association study (GWAS) summary data. To comprehensively examine the genetic relationship between CD and DH, we applied multiple MR methodologies. Furthermore, to enhance the robustness and credibility of our results, we conducted extensive sensitivity analyses.
Results: The fixed-effects inverse variance weighted (IVW) analysis revealed a significant positive genetic causal relationship between CD and DH (P = 0.001, odds ratio [OR] 95% confidence interval [CI]: 1.546 [1.195– 1.999]). In contrast, no significant genetic causality was found in the reverse direction, from DH to CD (P = 0.113, OR 95% CI: 1.039 [0.991– 1.090]). Notably, the MR analysis revealed no evidence of heterogeneity, further reinforcing the reliability of the fixed-effects IVW model. Additionally, sensitivity analyses confirmed the stability and robustness of the results, further validating the integrity of the conclusions drawn from the MR analysis.
Conclusion: The results of our study indicate that CD acts as a genetic susceptibility factor for the development of DH. Furthermore, the occurrence of DH in individuals with a history of CD appears to be attributed to a causal genetic relationship, suggesting that the genetic predisposition linked to CD may drive the manifestation of DH.
Keywords: celiac disease, dermatitis herpetiformis, mendelian randomization, causal, genetic