Does active smoking really influence the course of Crohn's disease? A retrospective observational study
ABSTRACT BACKGROUND: Active smoking has been associated with a higher risk of developing Crohn's disease (CD). However, its impact on clinical outcomes has been controversial among studies. AIMS: To evaluate the influence of active smoking on initial manifestations of CD, the development of disease-related complications, and therapeutic requirements. METHODS: Patients diagnosed with CD within a ten-year period (1994-2003) were identified. Clinical and therapeutic features until October 2008 or loss of follow-up were recorded. Smoking status was assessed at each major disease-related event (e.g. penetrating and stricturing complications, perianal disease, intestinal resection, introduction of immunomodulators or biological agents). RESULTS: A total of 259 patients were included in the study with a median follow-up period of 91months. At diagnosis, 50.5% were active smokers and only 12% of them quit smoking during follow-up, mostly after a major disease-related event occurred. Smoking at diagnosis was not associated with a particular CD presentation. Active smoking did not influence the development of strictures, intraabdominal and perianal penetrating complications, or increased resectional surgery, biological therapy or immunomodulators requirements. CONCLUSIONS: Patients who develop CD while smoking seem to have a similar disease course to those who never smoked.
SourceAvailable from: Anita Annahazi[Show abstract] [Hide abstract]
ABSTRACT: The pathogenesis of inflammatory bowel diseases (IBD), such as ulcerative colitis (UC) and Crohn’s disease (CD) is complex, and our knowledge on the topic is constantly growing. The two disorders are distinct, yet overlap in their clinical manifestations and underlying causes. This review aims to provide a broad overview of the numerous pathogenetic factors that can lead to the development of IBD, focusing on novel findings and on the differences between UC and CD. Recent advances in genetics have identified new components in the pathogenesis, as an example, the importance of Th17 lymphocytes and the IL-17/IL-23 pathway have been highlighted in both diseases, apart from the previously known Th1-Th2 driven processes. Genetic background of increased permeability has been explored in UC, and the role of defective autophagy was recently described in CD. Genetic alterations can lead to an exaggerated immune response to the resident microbial flora. This microflora is altered in IBD patients, probably due to their reduced ability to stabilize its bacterial components and due to different environmental factors. An exhaustive exploration of environmental factors is particularly important, as they can be influential in many cases. The impact of smoking is the most established environmental factor, having deleterious effects in CD and protective in UC. Recent opinions on other factors, such as early appendectomy, diet, reduced vitamin D levels, the use of specific medications, breastfeeding, personal hygiene and psychological factors are also discussed. Epigenetics, a new field of research, links environmental factors to genetics. Understanding these factors is of great significance as changing lifestyles and improving life circumstances have started to increase the prevalence of IBD also in developing countries.
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ABSTRACT: The chronic intestinal inflammation that characterises Crohn's disease and ulcerative colitis arises from a complex interplay between host genotype, the immune system, and the intestinal microbiota. In addition, environmental factors such as smoking impact on disease onset and progression. Individuals who smoke are more likely to develop Crohn's disease, and smoking is associated with recurrence after surgery and a poor response to medical therapy. Conversely, smoking appears protective against ulcerative colitis and smokers are less likely to require colectomy. The mechanism by which smoking exerts its impact on disease and the rational for the dichotomous effect in patients with Crohn's disease and ulcerative colitis is not clear. Recent evidence suggests that smoking induces alterations to both the innate and acquired immune system. In addition, smoking is associated with a distinct alteration in the intestinal microbiota both in patients with active Crohn's disease and healthy subjects.Journal of Crohn s and Colitis 08/2014; 8(8). DOI:10.1016/j.crohns.2014.02.002 · 3.56 Impact Factor
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ABSTRACT: Recently, the notion that smoking may adversely affect Crohn's disease (CD) outcomes has been challenged by the suggestion that the widespread use of immunosuppressants and anti-TNF drugs might offset the adverse effects of tobacco. To reassess the influence of tobacco smoking on disease phenotype and complications on a time-dependent analysis, taking into account the different therapeutic interventions. We designed a retrospective cohort study of 3224 patients with Crohn's disease. The data were collected from the Spanish national inflammatory bowel disease registry (ENEIDA), including information regarding demographics, clinical characteristics, disease complications, therapeutic interventions and smoking status. Patients were classified as nonsmokers, smokers and former smokers, according to their present and past smoking habits. In the univariate analysis, smokers had more strictures (22.6% vs. 19.3%, P < 0.05) and less colonic involvement (7.2% vs. 10.9%, P < 0.05), and were more frequently under treatment with steroids (91.6% vs. 85.8%, P < 0.05), immunosuppressants (73.5% vs. 63.6% P < 0.05) or anti-TNF drugs (31.4% vs. 25.1%, P < 0.05) than nonsmokers. In the time-dependent multivariate analysis, smokers were found to have a significantly decreased survival free of stricturing disease (HR: 1.5, CI 95% 1.18-1.90) or perianal complications (HR: 1.50, CI 95% 1.01-1.46), and had a higher risk for requiring thiopurine therapy (HR: 1.20, CI 95% 1.05-1.30). These results suggest that, despite the widespread use of immunosuppressants and anti-TNF drugs, smokers with Crohn's disease still have a more severe disease course, with increased therapeutic requirements when compared with nonsmokers.Alimentary Pharmacology & Therapeutics 08/2013; DOI:10.1111/apt.12440 · 4.55 Impact Factor