Tamoxifen use and acute pancreatitis: A population-based cohort study

PLoS One. 2017 Mar 14;12(3):e0173089. doi: 10.1371/journal.pone.0173089. eCollection 2017.

Abstract

Background: Several case reports have indicated that tamoxifen induced acute pancreatitis (AP); but no pharmacoepidemiological data support the claim. Therefore, we investigated whether tamoxifen use is correlated with the risk of AP in patients with breast cancer.

Methods: This population-based cohort study used the Taiwan National Health Insurance Research Database. A cohort of 22 005 patients aged ≥20 years with breast cancer from January 1, 2000 to December 31, 2009 was identified and the date of cancer diagnosis was set as the index date. The end point was developing AP during the follow-up. Hazard ratios (HRs) and 95% confidence intervals (CIs) were evaluated to determine the correlation between the risk of AP and tamoxifen use. Because the drug use varied over time, it was measured as a time-dependent covariate in the Cox proportional hazard model. The same approaches were applied in PS-matched cohorts.

Results: After adjustment for covariates and medication use including fluorouracil and doxorubicin, the risk of AP was not significant between tamoxifen users and tamoxifen nonusers (adjusted HR = 0.94, 95% CI = 0.74-1.19) in the non-matching cohorts. The results revealed no dose-response trend between tamoxifen use and the risk of AP (adjusted HR = 0.98, 95% CI = 0.96-1.00). The comorbidities DM and gallstones were associated with a significantly increased risk of AP. Similar trends were observed in PS-matched cohorts.

Conclusions: No significant correlation was observed between tamoxifen use and the risk of AP in patients with breast cancer.

MeSH terms

  • Acute Disease
  • Aged
  • Breast Neoplasms / drug therapy*
  • Cohort Studies
  • Female
  • Humans
  • Middle Aged
  • Pancreatitis / chemically induced*
  • Taiwan
  • Tamoxifen / adverse effects*
  • Tamoxifen / therapeutic use

Substances

  • Tamoxifen

Grants and funding

This study is supported in part by Taiwan Ministry of Health and Welfare Clinical Trial and Research Center of Excellence (MOHW104-TDU-B-212-113002, MOHW105-TDUB-212-133019); China Medical University Hospital, Academia Sinica Taiwan Biobank, Stroke Biosignature Project (BM104010092); NRPB Stroke Clinical Trial Consortium (MOST 103-2325-B-039-006, MOST 104-2325-B-039-005); Tseng-Lien Lin Foundation, Taichung, Taiwan; Taiwan Brain Disease Foundation, Taipei, Taiwan; Katsuzo and Kiyo Aoshima Memorial Funds, Japan; and CMU under the Aim for Top University Plan of the Ministry of Education, Taiwan. We appreciate the financial support by grants from the Ministry of Science and Technology (MOST103-2314-B-715-001-MY2, and MOST104-2314-B-715-003-MY3), Mackay Medical College (RD1040109), and Mackay Memorial Hospital (MMH-MM-10304, MMH-MM-10405). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. No additional external funding received for this study.