Sibel Bakirci Ureyen1, Cengiz Karacaer2, Bilal Toka3, Zeynep Erturk2, Ahmet Tarik Eminler3, Muhammed Kaya2, Koray Tascilar4, Ali Tamer2, Ihsan Uslan3, Esra Kurum5, Dennis McGonagle6,7, Sibel Zehra Aydin8. 1. Department of Internal Medicine, Division of Rheumatology, University of Ottawa Faculty of Medicine, Ottawa, Canada. 2. Department of Internal Medicine, Sakarya Education and Research Hospital, Sakarya, Turkey. 3. Department of Internal Medicine, Division of Gastroenterology, Sakarya Education and Research Hospital, Sakarya, Turkey. 4. Department of Internal Medicine, Division of Rheumatology, Istanbul Okmeydani Education and Research Hospital, Istanbul, Turkey. 5. Department of Statistics, University of California, Riverside, Riverside, CA, USA. 6. Depertment of Internal Medicine, Division of Rheumatology, Leeds Institute of the Rheumatic and Musculoskeletal Disease, Leeds, UK. 7. University of Leeds, Faculty of Medicine, Rheumatology, Leeds, UK. 8. Department of Internal Medicine, Division of Rheumatology, University of Ottawa Faculty of Medicine, Ottawa Hospital Research Institute, Ottawa, Canada.
Abstract
Objective: Higher subclinical enthesitis on US has been reported in IBD and celiac disease, separately. The objective of this study was to compare IBD and celiac disease for enthesitis on US. Higher enthesitis scores in IBD compared with celiac disease would support a shared pathogenic mechanism between IBD and spondyloarthritis, whereas similar scores may suggest a general impact of gut inflammation on the enthesis. Methods: Patients with IBD, celiac disease and healthy controls (HCs) were recruited and 12 entheses were scanned by US, blind to the diagnosis and clinical assessment. Elementary lesions for enthesitis were scored on a scale between 0 and 3, for inflammation, damage and total US scores. Results: A total of 1260 entheses were scanned in 44 patients with celiac disease, 43 patients with IBD and 18 HCs. The three groups were matched for age and BMI. Patients with celiac disease and IBD had higher inflammation scores than HCs [10.4 (6.5), 9.6 (5.4) and 5.6 (5.2), respectively, P = 0.007) whereas damage scores were similar. Both age and BMI had significant effects on the entheseal scores, mostly for inflammation scores but when controlling for these the US enthesopathy scores were still higher in celiac disease and IBD. Conclusion: The magnitude of subclinical enthesopathy scores is similar between celiac disease and IBD in comparison with HCs. These findings suggest that the common factor between both diseases and enthesopathy is abnormal gut permeability, which may be modified by the genetic architecture of IBD leading to clinical arthropathy.
Objective: Higher subclinical enthesitis on US has been reported in IBD and celiac disease, separately. The objective of this study was to compare IBD and celiac disease for enthesitis on US. Higher enthesitis scores in IBD compared with celiac disease would support a shared pathogenic mechanism between IBD and spondyloarthritis, whereas similar scores may suggest a general impact of gut inflammation on the enthesis. Methods:Patients with IBD, celiac disease and healthy controls (HCs) were recruited and 12 entheses were scanned by US, blind to the diagnosis and clinical assessment. Elementary lesions for enthesitis were scored on a scale between 0 and 3, for inflammation, damage and total US scores. Results: A total of 1260 entheses were scanned in 44 patients with celiac disease, 43 patients with IBD and 18 HCs. The three groups were matched for age and BMI. Patients with celiac disease and IBD had higher inflammation scores than HCs [10.4 (6.5), 9.6 (5.4) and 5.6 (5.2), respectively, P = 0.007) whereas damage scores were similar. Both age and BMI had significant effects on the entheseal scores, mostly for inflammation scores but when controlling for these the US enthesopathy scores were still higher in celiac disease and IBD. Conclusion: The magnitude of subclinical enthesopathy scores is similar between celiac disease and IBD in comparison with HCs. These findings suggest that the common factor between both diseases and enthesopathy is abnormal gut permeability, which may be modified by the genetic architecture of IBD leading to clinical arthropathy.