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Article: Calcium channel blockers are associated with lower gastric cancer risk: a territory‐wide study with propensity score analysis

TitleCalcium channel blockers are associated with lower gastric cancer risk: a territory‐wide study with propensity score analysis
Authors
Keywordscalcium channel blockers
gastric cancer
H pylori
Issue Date2021
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/journal/29331/home
Citation
International Journal of Cancer, 2021, v. 148 n. 9, p. 2148-2157 How to Cite?
AbstractPrior studies showed that calcium channel blockers (CCBs) could modify cancer risk, but data on gastric cancer (GC) are limited. We aimed to investigate whether CCBs could modify GC risk in Helicobacter pylori-eradicated patients. H pylori-infected patients with hypertension who are aged ≥50 and had received clarithromycin-based triple therapy between 2003 and 2016 were identified from a territory-wide healthcare database. Patients with eradication failure, GC diagnosed within 6 months after HP eradication, and gastric ulcer were excluded. Time-fixed Cox model with one-to-one propensity score matching was used to calculate hazard ratio (HR) of GC with CCBs. Sensitivity analysis using time-dependent multivariable Cox model in which CCB use was treated as time-varying covariate was also performed to address immortal time bias. 17 622 (29.6%) H pylori-eradicated patients with hypertension were included. During a median follow-up of 8.6 years, 105 (0.6%) developed GC. After PS matching, CCBs were associated with a lower GC risk (HR: 0.56; 95% CI: 0.32-0.97). Time-dependent analysis showed consistent result (aHR: 0.50; 95% CI: 0.33-0.75). A longer duration of CCB use was associated with even lower GC risk (adjusted HR [aHR]: 0.69; 95% CI: 0.61-0.79 for every 1-year increase in use). Long-acting CCBs (aHR: 0.47; 95% CI: 0.29-0.76) and dihydropyridines (aHR: 0.49; 95% CI: 0.32-0.73) conferred greater benefit than short-acting ones (aHR: 0.60; 95% CI: 0.36-1.03) and nondihydropyridines (aHR: 0.76; 95% CI: 0.24-2.48). The aHR was 0.57 (95% CI: 0.34-0.97) for noncardia and 0.59 (95% CI: 0.27-1.31) for cardia cancer. Use of CCBs was associated with lower risk of GC development in H pylori-eradicated patients, in a duration- and dose-response manner.
Persistent Identifierhttp://hdl.handle.net/10722/294103
ISSN
2021 Impact Factor: 7.316
2020 SCImago Journal Rankings: 2.475
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorLi, B-
dc.contributor.authorCheung, KS-
dc.contributor.authorWong, IYH-
dc.contributor.authorLeung, WK-
dc.contributor.authorLaw, S-
dc.date.accessioned2020-11-23T08:26:21Z-
dc.date.available2020-11-23T08:26:21Z-
dc.date.issued2021-
dc.identifier.citationInternational Journal of Cancer, 2021, v. 148 n. 9, p. 2148-2157-
dc.identifier.issn0020-7136-
dc.identifier.urihttp://hdl.handle.net/10722/294103-
dc.description.abstractPrior studies showed that calcium channel blockers (CCBs) could modify cancer risk, but data on gastric cancer (GC) are limited. We aimed to investigate whether CCBs could modify GC risk in Helicobacter pylori-eradicated patients. H pylori-infected patients with hypertension who are aged ≥50 and had received clarithromycin-based triple therapy between 2003 and 2016 were identified from a territory-wide healthcare database. Patients with eradication failure, GC diagnosed within 6 months after HP eradication, and gastric ulcer were excluded. Time-fixed Cox model with one-to-one propensity score matching was used to calculate hazard ratio (HR) of GC with CCBs. Sensitivity analysis using time-dependent multivariable Cox model in which CCB use was treated as time-varying covariate was also performed to address immortal time bias. 17 622 (29.6%) H pylori-eradicated patients with hypertension were included. During a median follow-up of 8.6 years, 105 (0.6%) developed GC. After PS matching, CCBs were associated with a lower GC risk (HR: 0.56; 95% CI: 0.32-0.97). Time-dependent analysis showed consistent result (aHR: 0.50; 95% CI: 0.33-0.75). A longer duration of CCB use was associated with even lower GC risk (adjusted HR [aHR]: 0.69; 95% CI: 0.61-0.79 for every 1-year increase in use). Long-acting CCBs (aHR: 0.47; 95% CI: 0.29-0.76) and dihydropyridines (aHR: 0.49; 95% CI: 0.32-0.73) conferred greater benefit than short-acting ones (aHR: 0.60; 95% CI: 0.36-1.03) and nondihydropyridines (aHR: 0.76; 95% CI: 0.24-2.48). The aHR was 0.57 (95% CI: 0.34-0.97) for noncardia and 0.59 (95% CI: 0.27-1.31) for cardia cancer. Use of CCBs was associated with lower risk of GC development in H pylori-eradicated patients, in a duration- and dose-response manner.-
dc.languageeng-
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/journal/29331/home-
dc.relation.ispartofInternational Journal of Cancer-
dc.rightsSubmitted (preprint) Version This is the pre-peer reviewed version of the following article: [FULL CITE], which has been published in final form at [Link to final article using the DOI]. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Use of Self-Archived Versions. Accepted (peer-reviewed) Version This is the peer reviewed version of the following article: [FULL CITE], which has been published in final form at [Link to final article using the DOI]. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Use of Self-Archived Versions.-
dc.subjectcalcium channel blockers-
dc.subjectgastric cancer-
dc.subjectH pylori-
dc.titleCalcium channel blockers are associated with lower gastric cancer risk: a territory‐wide study with propensity score analysis-
dc.typeArticle-
dc.identifier.emailCheung, KS: cks634@hku.hk-
dc.identifier.emailWong, IYH: iyhwong@hku.hk-
dc.identifier.emailLeung, WK: waikleung@hku.hk-
dc.identifier.emailLaw, S: slaw@hku.hk-
dc.identifier.authorityCheung, KS=rp02532-
dc.identifier.authorityWong, IYH=rp02293-
dc.identifier.authorityLeung, WK=rp01479-
dc.identifier.authorityLaw, S=rp00437-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1002/ijc.33379-
dc.identifier.pmid33152125-
dc.identifier.scopuseid_2-s2.0-85096901993-
dc.identifier.hkuros319306-
dc.identifier.volume148-
dc.identifier.issue9-
dc.identifier.spage2148-
dc.identifier.epage2157-
dc.identifier.isiWOS:000594056900001-
dc.publisher.placeUnited States-

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