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Article: Statins were associated with a reduced gastric cancer risk in patients with eradicated Helicobacter pylori infection: a territory-wide propensity score matched study

TitleStatins were associated with a reduced gastric cancer risk in patients with eradicated Helicobacter pylori infection: a territory-wide propensity score matched study
Authors
Keywordsadult
cancer incidence
cancer risk
cohort analysis
comorbidity
Issue Date2020
PublisherAmerican Association for Cancer Research. The Journal's web site is located at http://cebp.aacrjournals.org/
Citation
Cancer Epidemiology, Biomarkers & Prevention, 2020, v. 29 n. 2, p. 493-499 How to Cite?
AbstractBackground: Individuals may still develop gastric cancer even after Helicobacter pylori eradication. We aimed to investigate statin effect on gastric cancer development in H. pylori–eradicated subjects. Methods: All adult subjects who were prescribed clarithromycin-based triple therapy between 2003 and 2012 were identified in this retrospective cohort study utilizing a territory-wide electronic healthcare database. Patients were observed from index date of H. pylori therapy, and censored at gastric cancer diagnosis, death, or December 2015 (study end date). Statin use was defined as ≥180-day use after index date. Exclusion criteria included gastric cancer diagnosed within the first year after index date, previous gastric cancer or gastrectomy, and H. pylori treatment failure. Subdistribution hazard ratio (SHR) of gastric cancer with statins was calculated by competing risk regression with propensity score (PS) analysis matching 19 variables (age, sex, comorbidities, and other drug usage, including proton pump inhibitors, nonsteroidal anti-inflammatory drugs, aspirin, cyclooxygenase-2 inhibitors, and metformin). Results: During a median follow-up of 7.6 years (interquartile range = 5.1–10.3), 169 (0.27%) of 63,605 patients developed gastric cancer at an incidence rate of 3.5 per 10,000 person-years. Among 22,870 PS-matched subjects, statins were associated with a lower gastric cancer risk (SHR = 0.34; 95% confidence interval, 0.19–0.61), in a duration– and dose–response manner (Ptrend < 0.05). Conclusions: Statins were associated with a lower gastric cancer risk in a duration– and dose–response manner among H. pylori–eradicated patients. Impact: This study provides evidence on the additional benefits of statins as chemopreventive agents against gastric cancer among H. pylori–eradicated patients.
Persistent Identifierhttp://hdl.handle.net/10722/284570
ISSN
2019 Impact Factor: 4.344
2015 SCImago Journal Rankings: 2.579

 

DC FieldValueLanguage
dc.contributor.authorCheung, KS-
dc.contributor.authorChan, EW-
dc.contributor.authorWong, AYS-
dc.contributor.authorChen, L-
dc.contributor.authorSeto, WK-
dc.contributor.authorWong, ICK-
dc.contributor.authorLeung, WK-
dc.date.accessioned2020-08-07T08:59:31Z-
dc.date.available2020-08-07T08:59:31Z-
dc.date.issued2020-
dc.identifier.citationCancer Epidemiology, Biomarkers & Prevention, 2020, v. 29 n. 2, p. 493-499-
dc.identifier.issn1055-9965-
dc.identifier.urihttp://hdl.handle.net/10722/284570-
dc.description.abstractBackground: Individuals may still develop gastric cancer even after Helicobacter pylori eradication. We aimed to investigate statin effect on gastric cancer development in H. pylori–eradicated subjects. Methods: All adult subjects who were prescribed clarithromycin-based triple therapy between 2003 and 2012 were identified in this retrospective cohort study utilizing a territory-wide electronic healthcare database. Patients were observed from index date of H. pylori therapy, and censored at gastric cancer diagnosis, death, or December 2015 (study end date). Statin use was defined as ≥180-day use after index date. Exclusion criteria included gastric cancer diagnosed within the first year after index date, previous gastric cancer or gastrectomy, and H. pylori treatment failure. Subdistribution hazard ratio (SHR) of gastric cancer with statins was calculated by competing risk regression with propensity score (PS) analysis matching 19 variables (age, sex, comorbidities, and other drug usage, including proton pump inhibitors, nonsteroidal anti-inflammatory drugs, aspirin, cyclooxygenase-2 inhibitors, and metformin). Results: During a median follow-up of 7.6 years (interquartile range = 5.1–10.3), 169 (0.27%) of 63,605 patients developed gastric cancer at an incidence rate of 3.5 per 10,000 person-years. Among 22,870 PS-matched subjects, statins were associated with a lower gastric cancer risk (SHR = 0.34; 95% confidence interval, 0.19–0.61), in a duration– and dose–response manner (Ptrend < 0.05). Conclusions: Statins were associated with a lower gastric cancer risk in a duration– and dose–response manner among H. pylori–eradicated patients. Impact: This study provides evidence on the additional benefits of statins as chemopreventive agents against gastric cancer among H. pylori–eradicated patients.-
dc.languageeng-
dc.publisherAmerican Association for Cancer Research. The Journal's web site is located at http://cebp.aacrjournals.org/-
dc.relation.ispartofCancer Epidemiology, Biomarkers & Prevention-
dc.subjectadult-
dc.subjectcancer incidence-
dc.subjectcancer risk-
dc.subjectcohort analysis-
dc.subjectcomorbidity-
dc.titleStatins were associated with a reduced gastric cancer risk in patients with eradicated Helicobacter pylori infection: a territory-wide propensity score matched study-
dc.typeArticle-
dc.identifier.emailCheung, KS: cks634@hku.hk-
dc.identifier.emailChan, EW: ewchan@hku.hk-
dc.identifier.emailSeto, WK: wkseto@hku.hk-
dc.identifier.emailWong, ICK: wongick@hku.hk-
dc.identifier.emailLeung, WK: waikleung@hku.hk-
dc.identifier.authorityCheung, KS=rp02532-
dc.identifier.authorityChan, EW=rp01587-
dc.identifier.authoritySeto, WK=rp01659-
dc.identifier.authorityWong, ICK=rp01480-
dc.identifier.authorityLeung, WK=rp01479-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1158/1055-9965.EPI-19-1044-
dc.identifier.pmid31792089-
dc.identifier.scopuseid_2-s2.0-85079079422-
dc.identifier.hkuros311614-
dc.identifier.volume29-
dc.identifier.issue2-
dc.identifier.spage493-
dc.identifier.epage499-
dc.publisher.placeUnited States-

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