Among a group of almost 4,000 patients with GCA, the odds ratio for Crohn’s disease was 6.58 (95% CI 3.9-11.2, P<0.001) compared with age- and sex-matched controls, according to Howard Amital, MD, of Sheba Medical Center in Tel-Hashomer, Israel, and colleagues.
GCA patients also were at risk for ulcerative colitis, with an odds ratio of 4.06 (95% CI 2.56-6.35, P<0.001), the researchers reported in Autoimmunity Reviews.
Giant cell arteritis (also known as temporal arteritis) is a T-cell-mediated vasculitis that predominantly affects the external branches of the aorta and carotid artery. It usually develops in individuals older than 50.
The two types of IBD, Crohn’s disease and ulcerative colitis, differ in the location and extent of inflammation in the gut, but are both commonly associated with extra-intestinal manifestations such as fatigue, weight loss, and fever. Histopathologic analyses have detected vasculitis in bowel specimens of affected individuals, and there have been reports of vasculitis developing in patients with IBD.
However, it’s unclear whether this is a true association or simply incidental, so Amital and colleagues analyzed data from a national healthcare registry that includes more than four million individuals.
The team identified 3,938 patients with GCA who were older than 50 in the database; these were matched with 21,623 controls. Covariates included body mass index, socioeconomic status, and outcomes such as ischemic heart disease and stroke.
Patients’ mean age was 71, and more than two-thirds were women.
A total of 0.79% of patients with GCA also had Crohn’s disease compared with 0.12% of controls, while the percentages for ulcerative colitis were 0.84% versus 0.21%.
The association between GCA and IBD were similar for men (OR 4.84, 95% CI 2.42-9.59) and women (OR 5.08, 95% CI 3.42-7.54), and was higher among patients ages 50 to 69 (OR 8.13, 95% CI 4.53-14.8) than among those ages 70 to 85 (OR 3.81, 95% CI 2.48-5.80).
On a multivariate analysis that adjusted for potential confounders, a strong independent association was seen between GCA and IBD (OR 2.63, 95% CI 1.82-3.82, P<0.001), while independent associations were not found for age, sex, or socioeconomic status.
The authors offered several potential explanations for the association between GCA and IBD, noting that GCA and Crohn’s disease are mediated through the Th1 pathway and are characterized by granulomatous inflammation.
“A more recently recognized T-cell-mediated inflammatory pathway, which appears to be involved in the pathogenesis of Crohn’s disease and possibly ulcerative colitis, involves the Th17 cell lineage. Increased levels of Th17 cells and IL-17 have also been found in the inflamed arteries of untreated GCA patients.”
There also may be shared genetic factors such as HLA-DRB1 alleles, and environmental influences such as smoking, the researchers said. In addition, markers of fibrinolysis and coagulation such as the thrombin-antithrombin complex and plasminogen-activator inhibitor-1 have been reported to be dysregulated in both GCA and IBD.
The study provides “ample evidence” for a significant association between GCA and IBD, particularly in middle-age individuals, the authors stated.
“Physicians treating GCA patients should consider evaluation for IBD in patients with gastrointestinal symptoms. Further research focused on assessing the sequential aspect of the association, as well as discovering shared etiologic immunologic mechanisms, is needed.”
A limitation of the study, Amital and colleagues said, was the lack of validation of diagnoses in the healthcare registry.
The authors had no financial disclosures.
Dori F. Zaleznik, MD Associate Clinical Professor of Medicine (Retired), Harvard Medical School, Boston and Dorothy Caputo, MA, BSN, RN, Nurse Planner