Abstract 1119
Background
Pancreatic cancer is the 4th leading cause of cancer death in the United States. With its anti-inflammatory property, soluble receptor for advanced glycation end-product (sRAGE) has been associated with lower risk of pancreatic cancer. Anti-hypertensive (anti-HT) medications were shown to modulate sRAGE levels and AGE/RAGE signaling pathway. However, few large-scale population based study have evaluated the associations between antihypertensive medications and risk of pancreatic cancer.
Methods
A total of 145,551 postmenopausal women aged 50 to 79 years with no prevalent cancer from Women Health Initiative (WHI) were included with a mean follow-up of 13.8 year. Medication data including product and generic name, duration of use, and dosage form were collected at baseline recruitment (1993-98). We examined four anti-HT drugs including β-blockers, diuretics, angiotensin converting enzyme inhibitors (ACEi) and calcium channel blockers (CCBs). Serum levels of sRAGE were measured in a subset of 1,466 study participants using immunoassay. Cox proportional hazard regression model was performed to obtain hazard ratio (HR) and its 95% confidence interval (CI) for each anti-HT medication use and its duration of use in association with risk of pancreatic cancer.
Results
By August 29, 2014, a total of 841 incident pancreatic cancer cases were ascertained through annual self-administered questionnaires and confirmed by central adjudication. Increased risk of incident pancreatic cancer was found among ever users of short-acting CCB (HR = 1.66, 95% CI: 1.20-2.29) and long-term (> 3 years) users of short-acting CCB (HR = 2.07, 95% CI: 1.42-3.02) compared to ever users of other anti-HT medications. Average sRAGE levels were lower in short-acting CCB ever users than those who took other anti-HT medication (1,158 pg/ml versus 1,446 pg/ml, P = 0.032).
Conclusions
We found a positive association between short-acting CCB use and risk of incident pancreatic cancer in postmenopausal women. Future studies are warranted to confirm these findings and elucidate potential mechanisms by which short-acting CCBs may influence development of pancreatic cancer, such as modulating RAGE signaling pathway.
Clinical trial identification
Legal entity responsible for the study
Li Jiao.
Funding
National Cancer Institute.
Editorial Acknowledgement
Disclosure
All authors have declared no conflicts of interest.