Giant cell arteritis and inflammatory bowel disease - Is there a connection? Results from a population-based study.

BACKGROUND: Giant cell arteritis (GCA) is an autoimmune disorder which primarily affects large vessels, whilst inflammatory bowel diseases (IBD) mainly target the gut. Co-existence of the two maladies has been reported sporadically in the literature; therefore the purpose of this study was to assess the authenticity of such an association in a large, cross-sectional study. METHODS: Utilizing data derived from the Clalit Health Services' registry, the largest health maintenance organization in Israel, we compared the proportion of CD and UC in GCA patients with age- and gender-matched controls. Univariate analysis was performed using Chi-square and student t-test and a multivariate analysis was performed using a logistic regression model. RESULTS: The study included 3938 GCA patients and 21,623 age- and gender-matched controls. GCA patients had a significantly increased proportion of both CD and UC in comparison with controls (0.79% vs. 0.12% and 0.84% vs. 0.21%, P-value < .001, respectively). The strength of the association between GCA and IBD was negatively correlated with the patients' age; thus the association was more robust amongst middle-aged patients (ages 50-69, OR = 8.13) than in elderly patients (ages 70-85, OR = 3.81). The association between GCA and IBD remained significant when evaluated independently of confounding factors (OR = 2.63, P-value < .001). CONCLUSIONS: The probability that GCA patients also suffer from IBD is increased in comparison with age- and gender-matched controls. Our findings indicate that this association is more prominent in middle-aged patients (50-69 years of age). Screening for IBD amongst GCA patients in this age group may be warranted.

Smoke and autoimmunity: The fire behind the disease.

The association between smoke habit and autoimmunity has been hypothesized a long time ago. Smoke has been found to play a pathogenic role in certain autoimmune disease as it may trigger the development of autoantibodies and act on pathogenic mechanism possibly related with an imbalance of the immune system. Indeed, both epidemiological studies and animal models have showed the potential deleterious effect caused by smoke. For instance, smoke, by provoking oxidative stress, may contribute to lupus disease by dysregulating DNA demethylation, upregulating immune genes, thereby leading to autoreactivity. Moreover, it can alter the lung microenvironment, facilitating infections, which, in turn, may trigger the development of an autoimmune condition. This, in turn, may result in a dysregulation of immune system leading to autoimmune phenomena. Not only cigarette smoke but also air pollution has been reported as being responsible for the development of autoimmunity. Large epidemiological studies are needed to further explore the accountability of smoking effect in the pathogenesis of autoimmune diseases.