Current studies reporting on the risk of smoking and development of symptomatic diverticular disease have reported conflicting results.
The aim of this study was to investigate the association between smoking and symptomatic diverticular disease.
This is a cohort study
Information was derived from the Swedish Construction Workers Cohort 1971–1993.
Patients were selected from construction workers in Sweden.
The primary outcome measured was the development of symptomatic diverticular disease and complicated diverticular disease (abscess and perforation) as identified in the Swedish Hospital Discharge Register. Adjusted relative risks of symptomatic diverticular disease according to smoking status were estimated by using negative binomial regression analysis.
In total, the study included 232,685 men and 14,592 women. During follow-up, 3891 men and 318 women had a diagnosis of later symptomatic diverticular disease. In men, heavy smokers (≥15 cigarettes a day) had a 1.6-fold increased risk of developing symptomatic diverticular disease compared with nonsmokers (adjusted relative risk, 1.56; 95% CI, 1.42–1.72). There was evidence of a dose-response relationship, because moderate and ex-smokers had a 1.4- and 1.2-fold increased risk compared with nonsmokers (adjusted relative risk, 1.39; 95% CI, 1.27–1.52 and adjusted relative risk, 1.14; 95% CI, 1.04–1.27). These relationships were similar in women, but the risk estimates were less precise owing to smaller numbers. Male ever-smokers had a 2.7-fold increased risk of developing complicated diverticular disease (perforation/abscess) compared with nonsmokers (adjusted relative risks, 2.73; 95% CI, 1.69–4.41).
We were unable to account for other confounding variables such as comorbidity, prescription medication, or lifestyle factors.
Smoking is associated with symptomatic diverticular disease in both men and women and with an increased risk of developing complicated diverticular disease.
1 Division of Epidemiology and Public Health, School of Medicine, University of Nottingham, City Hospital, Nottingham, United Kingdom
2 Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden
3 Department of Paediatrics, Örebro University Hospital, Örebro, Sweden
4 Department of Public Health and Clinical Medicine, Umea University, Umea, Sweden
5 Nottingham Digestive Diseases Biomedical Research Unit, University of Nottingham, Nottingham, United Kingdom
Funding/Support: Dr Humes is funded by an NIHR Post-Doctoral Fellowship award. Dr Ludvigsson is funded by the Swedish Research Council. Dr Järvholm is funded by the Swedish Research Council for Health, Working Life and Welfare (contract 2011–426). None of the funders had a role in the design and conduct of the study; collection, management, analysis, and interpretation of the data; and preparation, review, or approval of the manuscript.
Financial Disclosures: None reported.
Correspondence: David J. Humes, B.Sc., M.B.B.S., Ph.D., F.R.C.S., Division of Epidemiology and Public Health, School of Community Health Sciences, University of Nottingham, Clinical Sciences Building 2, City Hospital, Nottingham, UK, NG5 1PB. E-mail: email@example.com