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 in | Frontiers in genetics Vol. 15; p. 1368915 |
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Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
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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 |
Author_xml | – sequence: 1 givenname: Yan surname: Zhang fullname: Zhang, Yan – sequence: 2 givenname: Yihong surname: Huang fullname: Huang, Yihong – sequence: 3 givenname: Yuyu surname: Wu fullname: Wu, Yuyu – sequence: 4 givenname: Jinying surname: Zhang fullname: Zhang, Jinying – sequence: 5 givenname: Wanzhu surname: Chen fullname: Chen, Wanzhu – sequence: 6 givenname: Danfeng surname: Xu fullname: Xu, Danfeng – sequence: 7 givenname: Maosheng surname: Guo fullname: Guo, Maosheng |
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Cites_doi | 10.1177/1745691610383505 10.1159/000330053 10.1001/jama.2021.18236 10.3389/fmicb.2023.1115014 10.1093/hmg/ddu328 10.1007/s00417-003-0779-5 10.2147/OPTH.S26659 10.1111/hel.12165 10.1093/ije/dyv080 10.3390/microorganisms8060894 10.1101/cshperspect.a041302 10.3389/fcvm.2023.1080252 10.1016/S0161-6420(03)00093-9 10.1001/archinte.162.11.1237 10.1097/MD.0000000000001578 10.1016/j.ophtha.2014.05.013 10.1016/j.mcna.2021.01.004 10.1016/s0161-6420(00)00598-4 10.1097/IJG.0b013e31815a34ac 10.1097/EDE.0000000000000699 10.1002/gepi.21965 10.3389/fpsyt.2023.1135923 |
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Keywords | pseudo-exfoliation glaucoma normal tension glaucoma Helicobacter pylori primary open-angle glaucoma mendelian randomization |
Language | English |
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Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 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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StartPage | 1368915 |
SubjectTerms | Genetics 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 |
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