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Article: Metformin Use and Gastric Cancer Risk in Diabetic Patients After Helicobacter pylori Eradication

TitleMetformin Use and Gastric Cancer Risk in Diabetic Patients After Helicobacter pylori Eradication
Authors
Issue Date2019
PublisherOxford University Press. The Journal's web site is located at http://jncicancerspectrum.oxfordjournals.org/
Citation
JNCI: Journal of the National Cancer Institute, 2019, v. 111 n. 5, p. 484-489 How to Cite?
AbstractBackground Although prior studies showed metformin could reduce gastric cancer (GC) risk in patients with diabetes mellitus, they failed to adjust for Helicobacter pylori infection and glycemic control. We aimed to investigate whether metformin reduced GC risk in H. pylori-eradicated diabetic patients and its association with glycemic control. Methods This was a territory-wide cohort study using hospital registry database, recruiting all diabetic patients who were prescribed clarithromycin-based triple therapy for H. pylori infection from 2003 to 2012. Subjects were observed from H. pylori therapy prescription until GC diagnosis, death, or end of study (December 2015). Exclusion criteria included GC diagnosed within first year of H. pylori therapy, prior history of GC or gastrectomy, and failure of H. pylori eradication. The hazard ratio (HR) of GC with metformin (defined as at least 180-day use) was estimated by Cox model with propensity score adjustment for covariates (age, sex, comorbidities, medications [including insulin], and time-weighted average hemoglobin A1c [HbA1c]). All statistical tests were two-sided. Results During a median follow-up of 7.1 years (IQR = 4.7–9.8), 37 (0.51%) of 7266 diabetic patients developed GC at a median age of 76.4 years (IQR = 64.8–81.5 years). Metformin use was associated with a reduced GC risk (adjusted HR = 0.49, 95% CI = 0.24 to 0.98). There was a trend towards a lower GC risk with increasing duration (Ptrend = .01) and dose of metformin (Ptrend = .02). HbA1c level was not an independent risk factor for GC. Conclusions Metformin use was associated with a lower GC risk among H. pylori-eradicated diabetic patients in a duration- and dose-response manner, which was independent of HbA1c level.
Persistent Identifierhttp://hdl.handle.net/10722/269577
ISSN
2023 Impact Factor: 9.9
2023 SCImago Journal Rankings: 4.986
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorCheung, KSM-
dc.contributor.authorChan, EW-
dc.contributor.authorWong, AY-
dc.contributor.authorChen, L-
dc.contributor.authorSeto, WKW-
dc.contributor.authorWong, ICK-
dc.contributor.authorLeung, WK-
dc.date.accessioned2019-04-24T08:10:30Z-
dc.date.available2019-04-24T08:10:30Z-
dc.date.issued2019-
dc.identifier.citationJNCI: Journal of the National Cancer Institute, 2019, v. 111 n. 5, p. 484-489-
dc.identifier.issn0027-8874-
dc.identifier.urihttp://hdl.handle.net/10722/269577-
dc.description.abstractBackground Although prior studies showed metformin could reduce gastric cancer (GC) risk in patients with diabetes mellitus, they failed to adjust for Helicobacter pylori infection and glycemic control. We aimed to investigate whether metformin reduced GC risk in H. pylori-eradicated diabetic patients and its association with glycemic control. Methods This was a territory-wide cohort study using hospital registry database, recruiting all diabetic patients who were prescribed clarithromycin-based triple therapy for H. pylori infection from 2003 to 2012. Subjects were observed from H. pylori therapy prescription until GC diagnosis, death, or end of study (December 2015). Exclusion criteria included GC diagnosed within first year of H. pylori therapy, prior history of GC or gastrectomy, and failure of H. pylori eradication. The hazard ratio (HR) of GC with metformin (defined as at least 180-day use) was estimated by Cox model with propensity score adjustment for covariates (age, sex, comorbidities, medications [including insulin], and time-weighted average hemoglobin A1c [HbA1c]). All statistical tests were two-sided. Results During a median follow-up of 7.1 years (IQR = 4.7–9.8), 37 (0.51%) of 7266 diabetic patients developed GC at a median age of 76.4 years (IQR = 64.8–81.5 years). Metformin use was associated with a reduced GC risk (adjusted HR = 0.49, 95% CI = 0.24 to 0.98). There was a trend towards a lower GC risk with increasing duration (Ptrend = .01) and dose of metformin (Ptrend = .02). HbA1c level was not an independent risk factor for GC. Conclusions Metformin use was associated with a lower GC risk among H. pylori-eradicated diabetic patients in a duration- and dose-response manner, which was independent of HbA1c level.-
dc.languageeng-
dc.publisherOxford University Press. The Journal's web site is located at http://jncicancerspectrum.oxfordjournals.org/-
dc.relation.ispartofJNCI: Journal of the National Cancer Institute-
dc.rightsPre-print: Journal Title] ©: [year] [owner as specified on the article] Published by Oxford University Press [on behalf of xxxxxx]. All rights reserved. Pre-print (Once an article is published, preprint notice should be amended to): This is an electronic version of an article published in [include the complete citation information for the final version of the Article as published in the print edition of the Journal.] Post-print: This is a pre-copy-editing, author-produced PDF of an article accepted for publication in [insert journal title] following peer review. The definitive publisher-authenticated version [insert complete citation information here] is available online at: xxxxxxx [insert URL that the author will receive upon publication here].-
dc.titleMetformin Use and Gastric Cancer Risk in Diabetic Patients After Helicobacter pylori Eradication-
dc.typeArticle-
dc.identifier.emailCheung, KSM: cks634@hku.hk-
dc.identifier.emailChan, EW: ewchan@hku.hk-
dc.identifier.emailChen, L: equalclj@hku.hk-
dc.identifier.emailSeto, WKW: wkseto@hku.hk-
dc.identifier.emailWong, ICK: wongick@hku.hk-
dc.identifier.emailLeung, WK: waikleung@hku.hk-
dc.identifier.authorityCheung, KSM=rp02532-
dc.identifier.authorityChan, EW=rp01587-
dc.identifier.authoritySeto, WKW=rp01659-
dc.identifier.authorityWong, ICK=rp01480-
dc.identifier.authorityLeung, WK=rp01479-
dc.description.naturelink_to_subscribed_fulltext-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1093/jnci/djy144-
dc.identifier.scopuseid_2-s2.0-85062861861-
dc.identifier.hkuros297575-
dc.identifier.hkuros302430-
dc.identifier.volume111-
dc.identifier.issue5-
dc.identifier.spage484-
dc.identifier.epage489-
dc.identifier.isiWOS:000469779900008-
dc.publisher.placeUnited Kingdom-
dc.identifier.issnl0027-8874-

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