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Introduction: Ranitidine has been shown to contain the carcinogen N-nitrosodimethylamine and increase urinary N-nitrosodimethylamine in humans. We investigated whether ranitidine use is associated with increased bladder cancer risk., Methods: A nested case-control study was conducted within the Primary Care Clinical Informatics Unit Research database which contains general practice records from Scotland. Bladder cancer cases, diagnosed between 1999 and 2011, were identified and matched with up to 5 controls (based on age, sex, general practice, and date of registration). Ranitidine, other histamine-2 receptor agonists, and proton pump inhibitors were identified from prescribing records. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated using conditional logistic regression after adjusting for comorbidities and smoking., Results: There were 3,260 cases and 14,037 controls. There was evidence of an increased risk of bladder cancer in ranitidine users, compared with nonusers (fully adjusted OR = 1.22; 95% CI 1.06-1.40), which was more marked with use for over 3 years of ranitidine (fully adjusted OR = 1.43; 95% CI 1.05-1.94). By contrast, there was little evidence of any association between proton pump inhibitor use and bladder cancer risk based on any use (fully adjusted OR = 0.98; 95% CI 0.88-1.11) or over 3 years of use (fully adjusted OR = 0.98; 95% CI 0.80-1.20)., Discussion: In this large population-based study, the use of ranitidine particularly long-term use was associated with an increased risk of bladder cancer. Further studies are necessary to attempt to replicate this finding in other settings., (Copyright © 2021 by The American College of Gastroenterology.)

Background: Inflammation plays a role in pancreatic cancer. Many medications cause pancreatic inflammation, with some leading to a diagnosis of drug-induced pancreatitis (DIP), but few studies have examined these medications and pancreatic cancer risk. We therefore investigated the associations between pancreatic cancer risk and commonly-prescribed medicines for which there is strongest evidence of DIP., Methods: A nested case-control study was undertaken using the Primary Care Clinical Informatics Unit Research database containing general practice (GP) records from Scotland. Pancreatic cancer cases, diagnosed between 1999 and 2011, were identified and matched with up to five controls (based on age, gender, GP practice and date of registration). Medicines in the highest category of evidence for DIP, based on a recent systematic review, and used by more than 2 % of controls were identified. Odds ratios (OR) and 95 % confidence intervals (CI) for associations with pancreatic cancer were calculated using conditional logistic regression after adjusting for comorbidities., Results: There were 1,069 cases and 4,729 controls. Thirteen medicines in the highest category of evidence for DIP were investigated. There was little evidence of an association between any of these medications and pancreatic cancer risk apart from metronidazole (adjusted OR 1.69, 95 % CI 1.18, 2.41) and ranitidine (adjusted OR 1.37, 95 %CI 1.10, 1.70). However, no definitive exposure-response relationships between these medicines and cancer risk were observed., Conclusions: There is little evidence that commonly-prescribed medicines associated with inflammation of the pancreas are also associated with pancreatic cancer. These findings should provide reassurance to patients and prescribing clinicians., (Copyright © 2020 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Purpose: Preclinical studies show statins inhibit pathways involved in gastric cancer progression, with observational studies demonstrating reduced gastric cancer risk in statin users. However, few studies have investigated statin use and survival in gastric cancer. We investigated statin use and survival in two large population-based gastric cancer cohorts., Methods: Patients diagnosed with gastric cancer from 1998 to 2012 were identified from English and Scottish cancer registries. Statin prescriptions were identified from linkages to the UK Clinical Practice Research Datalink in England and the Prescribing Information System in Scotland, and deaths identified from national mortality records. Time-dependent Cox regression models were used to calculate hazard ratios (HR) and 95% confidence intervals (CIs) for cancer-specific mortality by statin use in multivariate analysis. Meta-analysis techniques pooled results across the cohorts., Results: The combined cohorts contained 3833 patients with gastric cancer and 2392 cancer-specific deaths. Statin use after diagnosis was associated with reduced cancer-specific mortality (adjusted HR 0.83; 95% CI, 0.74-0.92). HRs for less than 1 year and over 1 year of statin use were similar (adjusted HR 0.83; 95% CI, 0.73-0.94 and adjusted HR 0.83; 95% CI, 0.64-1.01, respectively). Statin use prior to diagnosis was also associated with reduced cancer-specific mortality (adjusted HR 0.91; 95% CI, 0.84-0.98)., Conclusions: In two independent UK cohorts, there was some evidence that statin use was associated with reduced cancer-specific mortality. However, these associations were weak in magnitude and did not follow a clear dose response, and we cannot rule out confounding by stage., (© 2018 John Wiley & Sons, Ltd.)