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Dipeptidyl‐peptidase‐4 inhibitors and pancreatic cancer: a cohort study
Author(s) -
Gokhale M.,
Buse J. B.,
Gray C. L.,
Pate V.,
Marquis M. A.,
Stürmer T.
Publication year - 2014
Publication title -
diabetes, obesity and metabolism
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.445
H-Index - 128
eISSN - 1463-1326
pISSN - 1462-8902
DOI - 10.1111/dom.12379
Subject(s) - medicine , hazard ratio , pancreatic cancer , dipeptidyl peptidase 4 inhibitor , dipeptidyl peptidase 4 , gastroenterology , interquartile range , cancer , confidence interval , propensity score matching , cohort , proportional hazards model , oncology , diabetes mellitus , type 2 diabetes , endocrinology
Aim To compare pancreatic cancer incidence and diagnostic evaluation among patients initiating dipeptidyl‐peptidase‐4 (DPP‐4) inhibitor treatment with those initiating sulfonylureas (SU) and thiazolidinediones (TZD). Methods Medicare claims data were examined in a new‐user active‐comparator cohort study. Patients >65 years with no prescriptions for DPP‐4 inhibitors, SU or TZD at baseline were included if they had at least two claims for the same drug within 180 days. Using an as‐treated approach and propensity score‐adjusted Cox models, we estimated the hazard ratios (HRs) and 95% confidence intervals (CIs) for pancreatic cancer. Diagnostic evaluations were compared using risk ratios. Results In the DPP‐4 inhibitor versus SU comparison, there were 18 179 patients who initiated treatment with DPP‐4 inhibitors, of whom 26 developed pancreatic cancer (interquartile range follow‐up 5–18 months). In the DPP‐4 inhibitor versus TZD comparison there were 29 366 people initiating DPP‐4 inhibitor treatment and 52 of these developed pancreatic cancer. The risk of pancreatic cancer with DPP‐4 inhibitor treatment was lower relative to SU treatment (HR: 0.6, CI: 0.4–0.9) and similar to TZD treatment (HR: 1.0, 95% CI: 0.7–1.4). After the first 6 months of follow‐up were excluded to reduce the potential for reverse causality, the results were not altered. The probability of diagnostic evaluation after commencing DPP‐4 inhibitor treatment (79.3%) was similar to that for TZD (74.1%, risk ratio 1.06, 95% CI: 1.05–1.07) and SU (74.6%) (risk ratio 1.06, 95% CI: 1.05–1.07). The probability of diagnostic evaluation before the index date (date of initiating treatment) was ∼80% for all cohorts. Conclusion Although the present study was limited by sample size and the observed duration of treatment in the USA, our well‐controlled population‐based study suggests there is no higher short‐term pancreatic cancer risk with DPP‐4 inhibitor treatment relative to SU or TZD treatment.