Background:: Recent animal studies and clinical trials suggest that thiazolidinediones, a class of oral antidiabetic agents, are efficacious in reducing inflammation, yet no studies have evaluated their effectiveness in preventing flares. We examined the association between thiazolidinedione use and ulcerative colitis (UC)‐related flares.
Methods:: We conducted a retrospective cohort study using administrative data from 87 health plans across 33 states. Individuals with both UC and diabetes were identified using administrative definitions. Exposure to thiazolidinediones or other oral antidiabetic agents was ascertained through outpatient pharmacy claims. The primary outcome was occurrence of a UC flare defined by: 1) a new prescription for oral steroids, infliximab, or oral/rectal salicylates, or 2) a claim for colectomy. Secondary analyses analyzed outcomes separately. We estimated hazard ratios (HRs) and 95% confidence intervals (CIs) using Cox proportional hazards regression after matching each thiazolidinedione user to a comparable oral antidiabetic user on propensity score.
Results:: This study included 142 thiazolidinedione and 468 other oral antidiabetic users with a mean follow‐up of 7.3 and 6.2 months, respectively. Thiazolidinedione use was not associated with UC‐related flares as measured by the composite outcome (HR = 1.05, 95% CI: 0.66, 1.68). However, thiazolidinedione use was associated with a nonsignificant reduction in risk of oral steroid use when analyzed as a separate outcome (HR = 0.53, 95% CI: 0.20, 1.44).
Conclusions:: Thiazolidinediones do not provide any benefit over other oral antidiabetics in preventing UC‐related flares as measured by our primary composite outcome. However, thiazolidinedione use may reduce the risk of more significant disease flares requiring oral steroid treatment. (Inflamm Bowel Dis 2011;)
1Department of Epidemiology, University of North Carolina, Gillings School of Global Public Health, Chapel Hill, North Carolina
2Cecil G. Sheps Center for Health Services Research, University of North Carolina, Chapel Hill, North Carolina
3Department of Medicine, Division of Gastroenterology and Hepatology, University of North Carolina, School of Medicine, Chapel Hill, North Carolina
4Division of Pediatric Gastroenterology, Department of Pediatrics, University of North Carolina, School of Medicine, Chapel Hill, North Carolina
*Department of Epidemiology, Gillings School of Global Public Health, University of North Carolina at Chapel Hill, McGavran‐Greenberg Hall, CB# 7435, Chapel Hill, NC 27599‐7435
Received for publication February 21 2010; Accepted March 31 2010.
Grant sponsor: National Institutes of Health; Grant Numbers: T32 DK 07634, KL2 RR025746, P30 DK034987; Grant sponsor: UNC‐GSK Center of Excellence in Pharmacoepidemiology and Public Health; Grant sponsor: UNC; Grant sponsor: Pozen, Inc.; Grant sponsor: Centecor, Inc..
Grant support: National Institutes of Health (grant T32 DK 07634 to J.L.L); grants KL2 RR025746 (to M.D.K.), P30 DK034987 (to R.S.S.), the UNC‐GSK Center of Excellence in Pharmacoepidemiology and Public Health (to T.S.); unrestricted research grants from pharmaceutical companies to UNC (to T.S.); Robert Sandler serves as a consultant to Pozen, Inc.; Michael Kappelman receives research support from Centecor, Inc.
Additional supporting information may be found in the online version of this article.