A population-based case–control study on statin exposure and risk of acute diverticular disease

Abstract

Objective: A reduced risk of perforated diverticular disease among individuals with current statin exposure has been reported. The aim of the present study was to investigate whether statins reduce the risk of acute diverticular disease. Material and methods: A nation-wide population-based case–control study was performed, including 13,127 cases hospitalised during 2006–2010 with a first-time diagnosis of colonic diverticular disease, and 128,442 control subjects (matched for sex, age, county of residence and calendar year). Emergency surgery, assumed to be a proxy for complicated diverticulitis, was performed on 906 of the cases during the index admission, with 8818 matched controls. Statin exposure was classified as “current” or “former” if a statin prescription was last dispensed ≤125 days or >125 days before index date, respectively. The association between statin exposure and acute diverticular disease was investigated by conditional logistic regression, including models adjusting for country of birth, educational level, marital status, comorbidities, nonsteroidal anti-inflammatory drug/steroid exposure and healthcare utilisation. Results: A total of 1959 cases (14.9%) and 16,456 controls (12.8%) were current statin users (crude OR 1.23 [95% CI 1.17–1.30]; fully adjusted OR 1.00 [0.94–1.06]). One hundred and thirty-two of the cases subjected to surgery (14.6%), and 1441 of the corresponding controls (16.3%) were current statin users (crude OR 0.89 [95% CI 0.73–1.08]; fully adjusted OR 0.70 [0.55–0.89]). Conclusions: The results do not indicate that statins affect the development of symptomatic diverticular disease in general. However, current statin use was associated with a reduced risk of emergency surgery for diverticular disease.

Keywords:

• Case–control studies
• diverticulitis
• hydroxymethylglutaryl-CoA reductase inhibitors
• pharmacoepidemiology

Declaration of interest:

The study was supported by the Emil and Wera Cornell Foundation. Ola Olén was funded by the Swedish Medical Society and The Bengt Ihre Fellowship in gastroenterology when working on this project. None of the funding organisations has had any role in the design and conduct of the study; in the collection, management and analysis of the data; or in the preparation, review and approval of the manuscript.

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