Absence of causative genetic association between Helicobacter pylori infection and glaucoma: a bidirectional two-sample mendelian randomization study

Background: While clinical research has indicated a potential link between Helicobacter pylori infection and the onset of glaucoma, the causality of this association remains uncertain due to the susceptibility of observational studies to confounding factors and reverse causation. Methods: A comprehe...

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Published inFrontiers in genetics Vol. 15; p. 1368915
Main Authors Zhang, Yan, Huang, Yihong, Wu, Yuyu, Zhang, Jinying, Chen, Wanzhu, Xu, Danfeng, Guo, Maosheng
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LanguageEnglish
Published Switzerland Frontiers Media S.A 24.05.2024
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Abstract Background: While clinical research has indicated a potential link between Helicobacter pylori infection and the onset of glaucoma, the causality of this association remains uncertain due to the susceptibility of observational studies to confounding factors and reverse causation. Methods: A comprehensive two-sample bidirectional Mendelian randomization (MR) analysis was conducted to assess the causal connection between H. pylori infection and glaucoma. Glaucoma was categorized into primary open-angle glaucoma (POAG), normal tension glaucoma (NTG), and pseudo-exfoliation glaucoma (PEG). Various methods, including inverse variance weighted, MR-Egger regression, weighted median, and mode-based estimator, were employed for effect estimation and pleiotropy testing. To enhance result robustness, a sensitivity analysis was performed by excluding proxy single nucleotide polymorphisms. Results: Genetic predisposition for H. pylori infection has no causal effect on glaucoma: (OR 1.00; 95% CI 0.95–1.06, p = 0.980), (OR 0.97; 95% CI 0.86–1.09, p = 0.550), and (OR 0.99; 95% CI 0.90–1.08, p = 0.766) with POAG, NTG, and PEG, respectively. An inverse MR showed no causal effect of POAG, NTG, and PEG on H. pylori infection (OR 1.01; 95% CI 0.97–1.05, p = 0.693), (OR 1.00; 95% CI 0.98–1.03, p = 0.804), and (OR 0.99; 95% CI 0.96–1.01, p = 0.363), respectively. Heterogeneity ( p > 0.05) and pleiotropy ( p > 0.05) analysis confirmed the robustness of MR results. Conclusion: These results indicated that there was no genetic evidence for a causal link between H. pylori and glaucoma, suggesting that the eradication or prevention of H. pylori infection might not benefit glaucoma and vice versa .
AbstractList While clinical research has indicated a potential link between infection and the onset of glaucoma, the causality of this association remains uncertain due to the susceptibility of observational studies to confounding factors and reverse causation. A comprehensive two-sample bidirectional Mendelian randomization (MR) analysis was conducted to assess the causal connection between infection and glaucoma. Glaucoma was categorized into primary open-angle glaucoma (POAG), normal tension glaucoma (NTG), and pseudo-exfoliation glaucoma (PEG). Various methods, including inverse variance weighted, MR-Egger regression, weighted median, and mode-based estimator, were employed for effect estimation and pleiotropy testing. To enhance result robustness, a sensitivity analysis was performed by excluding proxy single nucleotide polymorphisms. Genetic predisposition for infection has no causal effect on glaucoma: (OR 1.00; 95% CI 0.95-1.06, = 0.980), (OR 0.97; 95% CI 0.86-1.09, = 0.550), and (OR 0.99; 95% CI 0.90-1.08, = 0.766) with POAG, NTG, and PEG, respectively. An inverse MR showed no causal effect of POAG, NTG, and PEG on infection (OR 1.01; 95% CI 0.97-1.05, = 0.693), (OR 1.00; 95% CI 0.98-1.03, = 0.804), and (OR 0.99; 95% CI 0.96-1.01, = 0.363), respectively. Heterogeneity ( > 0.05) and pleiotropy ( > 0.05) analysis confirmed the robustness of MR results. These results indicated that there was no genetic evidence for a causal link between and glaucoma, suggesting that the eradication or prevention of infection might not benefit glaucoma and .
Background: While clinical research has indicated a potential link between Helicobacter pylori infection and the onset of glaucoma, the causality of this association remains uncertain due to the susceptibility of observational studies to confounding factors and reverse causation.Methods: A comprehensive two-sample bidirectional Mendelian randomization (MR) analysis was conducted to assess the causal connection between H. pylori infection and glaucoma. Glaucoma was categorized into primary open-angle glaucoma (POAG), normal tension glaucoma (NTG), and pseudo-exfoliation glaucoma (PEG). Various methods, including inverse variance weighted, MR-Egger regression, weighted median, and mode-based estimator, were employed for effect estimation and pleiotropy testing. To enhance result robustness, a sensitivity analysis was performed by excluding proxy single nucleotide polymorphisms.Results: Genetic predisposition for H. pylori infection has no causal effect on glaucoma: (OR 1.00; 95% CI 0.95–1.06, p = 0.980), (OR 0.97; 95% CI 0.86–1.09, p = 0.550), and (OR 0.99; 95% CI 0.90–1.08, p = 0.766) with POAG, NTG, and PEG, respectively. An inverse MR showed no causal effect of POAG, NTG, and PEG on H. pylori infection (OR 1.01; 95% CI 0.97–1.05, p = 0.693), (OR 1.00; 95% CI 0.98–1.03, p = 0.804), and (OR 0.99; 95% CI 0.96–1.01, p = 0.363), respectively. Heterogeneity (p > 0.05) and pleiotropy (p > 0.05) analysis confirmed the robustness of MR results.Conclusion: These results indicated that there was no genetic evidence for a causal link between H. pylori and glaucoma, suggesting that the eradication or prevention of H. pylori infection might not benefit glaucoma and vice versa.
Background: While clinical research has indicated a potential link between Helicobacter pylori infection and the onset of glaucoma, the causality of this association remains uncertain due to the susceptibility of observational studies to confounding factors and reverse causation. Methods: A comprehensive two-sample bidirectional Mendelian randomization (MR) analysis was conducted to assess the causal connection between H. pylori infection and glaucoma. Glaucoma was categorized into primary open-angle glaucoma (POAG), normal tension glaucoma (NTG), and pseudo-exfoliation glaucoma (PEG). Various methods, including inverse variance weighted, MR-Egger regression, weighted median, and mode-based estimator, were employed for effect estimation and pleiotropy testing. To enhance result robustness, a sensitivity analysis was performed by excluding proxy single nucleotide polymorphisms. Results: Genetic predisposition for H. pylori infection has no causal effect on glaucoma: (OR 1.00; 95% CI 0.95–1.06, p = 0.980), (OR 0.97; 95% CI 0.86–1.09, p = 0.550), and (OR 0.99; 95% CI 0.90–1.08, p = 0.766) with POAG, NTG, and PEG, respectively. An inverse MR showed no causal effect of POAG, NTG, and PEG on H. pylori infection (OR 1.01; 95% CI 0.97–1.05, p = 0.693), (OR 1.00; 95% CI 0.98–1.03, p = 0.804), and (OR 0.99; 95% CI 0.96–1.01, p = 0.363), respectively. Heterogeneity ( p > 0.05) and pleiotropy ( p > 0.05) analysis confirmed the robustness of MR results. Conclusion: These results indicated that there was no genetic evidence for a causal link between H. pylori and glaucoma, suggesting that the eradication or prevention of H. pylori infection might not benefit glaucoma and vice versa .
Background: While clinical research has indicated a potential link between Helicobacter pylori infection and the onset of glaucoma, the causality of this association remains uncertain due to the susceptibility of observational studies to confounding factors and reverse causation. Methods: A comprehensive two-sample bidirectional Mendelian randomization (MR) analysis was conducted to assess the causal connection between H. pylori infection and glaucoma. Glaucoma was categorized into primary open-angle glaucoma (POAG), normal tension glaucoma (NTG), and pseudo-exfoliation glaucoma (PEG). Various methods, including inverse variance weighted, MR-Egger regression, weighted median, and mode-based estimator, were employed for effect estimation and pleiotropy testing. To enhance result robustness, a sensitivity analysis was performed by excluding proxy single nucleotide polymorphisms. Results: Genetic predisposition for H. pylori infection has no causal effect on glaucoma: (OR 1.00; 95% CI 0.95-1.06, p = 0.980), (OR 0.97; 95% CI 0.86-1.09, p = 0.550), and (OR 0.99; 95% CI 0.90-1.08, p = 0.766) with POAG, NTG, and PEG, respectively. An inverse MR showed no causal effect of POAG, NTG, and PEG on H. pylori infection (OR 1.01; 95% CI 0.97-1.05, p = 0.693), (OR 1.00; 95% CI 0.98-1.03, p = 0.804), and (OR 0.99; 95% CI 0.96-1.01, p = 0.363), respectively. Heterogeneity (p > 0.05) and pleiotropy (p > 0.05) analysis confirmed the robustness of MR results. Conclusion: These results indicated that there was no genetic evidence for a causal link between H. pylori and glaucoma, suggesting that the eradication or prevention of H. pylori infection might not benefit glaucoma and vice versa.Background: While clinical research has indicated a potential link between Helicobacter pylori infection and the onset of glaucoma, the causality of this association remains uncertain due to the susceptibility of observational studies to confounding factors and reverse causation. Methods: A comprehensive two-sample bidirectional Mendelian randomization (MR) analysis was conducted to assess the causal connection between H. pylori infection and glaucoma. Glaucoma was categorized into primary open-angle glaucoma (POAG), normal tension glaucoma (NTG), and pseudo-exfoliation glaucoma (PEG). Various methods, including inverse variance weighted, MR-Egger regression, weighted median, and mode-based estimator, were employed for effect estimation and pleiotropy testing. To enhance result robustness, a sensitivity analysis was performed by excluding proxy single nucleotide polymorphisms. Results: Genetic predisposition for H. pylori infection has no causal effect on glaucoma: (OR 1.00; 95% CI 0.95-1.06, p = 0.980), (OR 0.97; 95% CI 0.86-1.09, p = 0.550), and (OR 0.99; 95% CI 0.90-1.08, p = 0.766) with POAG, NTG, and PEG, respectively. An inverse MR showed no causal effect of POAG, NTG, and PEG on H. pylori infection (OR 1.01; 95% CI 0.97-1.05, p = 0.693), (OR 1.00; 95% CI 0.98-1.03, p = 0.804), and (OR 0.99; 95% CI 0.96-1.01, p = 0.363), respectively. Heterogeneity (p > 0.05) and pleiotropy (p > 0.05) analysis confirmed the robustness of MR results. Conclusion: These results indicated that there was no genetic evidence for a causal link between H. pylori and glaucoma, suggesting that the eradication or prevention of H. pylori infection might not benefit glaucoma and vice versa.
Author Zhang, Jinying
Chen, Wanzhu
Guo, Maosheng
Xu, Danfeng
Zhang, Yan
Wu, Yuyu
Huang, Yihong
AuthorAffiliation 2 Department of Neurology , Second Affiliated Hospital of Fujian Medical University , Quanzhou , Fujian , China
3 Department of Ultrasound , Second Affiliated Hospital of Fujian Medical University , Quanzhou , Fujian , China
1 Department of Ophthalmology , Second Affiliated Hospital of Fujian Medical University , Quanzhou , Fujian , China
AuthorAffiliation_xml – name: 2 Department of Neurology , Second Affiliated Hospital of Fujian Medical University , Quanzhou , Fujian , China
– name: 1 Department of Ophthalmology , Second Affiliated Hospital of Fujian Medical University , Quanzhou , Fujian , China
– name: 3 Department of Ultrasound , Second Affiliated Hospital of Fujian Medical University , Quanzhou , Fujian , China
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Keywords pseudo-exfoliation glaucoma
normal tension glaucoma
Helicobacter pylori
primary open-angle glaucoma
mendelian randomization
Language English
License Copyright © 2024 Zhang, Huang, Wu, Zhang, Chen, Xu and Guo.
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Edited by: Maria Oana Sasaran, Sciences and Technology of Târgu Mureș, Romania
These authors have contributed equally to this work
Youjie Zeng, Central South University, China
Reviewed by: Valeria Lo Faro, Uppsala University, Sweden
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Snippet Background: While clinical research has indicated a potential link between Helicobacter pylori infection and the onset of glaucoma, the causality of this...
While clinical research has indicated a potential link between infection and the onset of glaucoma, the causality of this association remains uncertain due to...
Background: While clinical research has indicated a potential link between Helicobacter pylori infection and the onset of glaucoma, the causality of this...
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Helicobacter pylori
mendelian randomization
normal tension glaucoma
primary open-angle glaucoma
pseudo-exfoliation glaucoma
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Title Absence of causative genetic association between Helicobacter pylori infection and glaucoma: a bidirectional two-sample mendelian randomization study
URI https://www.ncbi.nlm.nih.gov/pubmed/38854431
https://www.proquest.com/docview/3066336384
https://pubmed.ncbi.nlm.nih.gov/PMC11157063
https://doaj.org/article/07f94cc21b6e412e92f69b5228f1b259
Volume 15
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