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Published on: February 16, 2024
Calcium channel blockers are associated with lower gastric cancer risk: A territory-wide study with propensity score
Bofei Li1, Ka Shing Cheung2,3, Ian Yu-Hong Wong1
1Department of Surgery, The University of Hong Kong, Queen Mary Hospital, Pokfulam Road, Hong Kong.
Insights
Calcium channel blockers (CCBs) may lower gastric cancer (GC) risk in patients previously treated for Helicobacter pylori. Longer CCB use and specific types, like long-acting and dihydropyridine CCBs, showed greater risk reduction.
Area of Science:
- Cardiovascular Pharmacology
- Gastroenterology
- Oncology
Background:
- Limited data exist on calcium channel blockers (CCBs) and gastric cancer (GC) risk.
- Investigating CCB effects in Helicobacter pylori-eradicated patients is crucial due to potential shared risk factors.
Purpose of the Study:
- To determine if CCBs modify GC risk in patients successfully treated for H. pylori infection.
- To explore the relationship between CCB use duration, type, and GC risk.
Main Methods:
- Retrospective cohort study using a territory-wide healthcare database.
- Included H. pylori-eradicated hypertensive patients aged ≥50, excluding those with eradication failure, early GC diagnosis, or gastric ulcers.
- Propensity score matching and time-dependent Cox models analyzed GC risk associated with CCB use.
Main Results:
- CCB use was associated with a significantly reduced risk of GC (HR: 0.56; 95% CI: 0.32-0.97).
- Time-dependent analysis confirmed this protective effect (aHR: 0.50; 95% CI: 0.33-0.75).
- Longer CCB duration, long-acting CCBs, and dihydropyridines demonstrated greater risk reduction, indicating a dose-response relationship.
Conclusions:
- CCB use is linked to a lower risk of developing gastric cancer in H. pylori-eradicated patients.
- The protective effect appears to be duration-dependent and more pronounced with specific CCB formulations.
Abstract:
Prior 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.
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