Impact of Angiotensin II Signaling Blockade on Clinical Outcomes in Patients with Inflammatory Bowel Disease

  • Jeffrey D. Jacobs
  • Thomas Wagner
  • George Gulotta
  • Chuanhong Liao
  • Yan Chun Li
  • Marc Bissonnette
  • Joel PekowEmail author
Original Article



Preclinical data demonstrate that activation of the renin–angiotensin system (RAS) contributes to mucosal inflammation, and RAS inhibition by angiotensin-converting-enzyme inhibitors (ACEI) and angiotensin receptor blockers (ARB) improves colitis in animal models. Less is known regarding the effects of RAS inhibition on clinical outcomes in inflammatory bowel disease (IBD) patients.


Evaluate the impact of ACEI and ARB on clinical outcomes in IBD.


Rates of IBD-related hospitalizations, operations, and corticosteroid use were evaluated retrospectively in two groups. First, 111 IBD patients taking an ACEI or ARB were compared to nonusers matched 1:1 based on sex, age, diagnosis, disease location, and hypertension diagnosis. Second, outcomes in a cohort of 130 IBD patients were compared prior to and during ACEI/ARB exposure.


Compared to matched controls, all IBD patients together with ACEI/ARB exposure had fewer hospitalizations (OR 0.26, p < 0.01), operations (OR 0.08, p = 0.02), and corticosteroid prescriptions (OR 0.5, p = 0.01). Comparing outcomes before and during ACEI/ARB use, there were no differences in hospitalizations, operations, or corticosteroid use for all IBD patients together, but patients with UC had increased hospitalizations (0.08 pre- vs. 0.16 during ACEI/ARB exposure, p = 0.03) and decreased corticosteroid use (0.24 pre-ACEI/ARB vs. 0.12 during ACEI/ARB exposure, p < 0.01) during ACEI/ARB use.


IBD patients with ACEI/ARB exposure had fewer hospitalizations, operations, and corticosteroid use compared to matched controls. No differences in outcomes were observed in individuals on ACEI/ARB therapy when compared to a period of time prior to medication exposure.


RAS inhibition Angiotensin-converting-enzyme inhibitor Angiotensin receptor blocker Inflammatory bowel disease 


Grant support

National Institute of Diabetes and Digestive and Kidney Diseases, Grant Number P30 DK42086 and National Institutes of Health, Grant Number K08 DK090152 (JP).

Compliance with ethical standards

Conflict of interest

The authors declare that they have no conflict of interest.


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Copyright information

© Springer Science+Business Media, LLC, part of Springer Nature 2019

Authors and Affiliations

  • Jeffrey D. Jacobs
    • 1
  • Thomas Wagner
    • 2
  • George Gulotta
    • 3
  • Chuanhong Liao
    • 4
  • Yan Chun Li
    • 5
  • Marc Bissonnette
    • 5
  • Joel Pekow
    • 5
    Email author
  1. 1.Division of Gastroenterology, Department of MedicineUniversity of WashingtonSeattleUSA
  2. 2.Department of MedicineUniversity of ChicagoChicagoUSA
  3. 3.Center for Research InformaticsUniversity of ChicagoChicagoUSA
  4. 4.Department of Public Health SciencesUniversity of ChicagoChicagoUSA
  5. 5.Section of Gastroenterology, Hepatology, and Nutrition, Department of MedicineUniversity of ChicagoChicagoUSA

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