J Korean Rheum Assoc.
1996 Jan;3(1):57-63.
Ileocolonoscopic and Histologic Studies in Ankylosing Spondylitis
- Affiliations
-
- 1Department of Internal Medicine, College of Medicine, Korea University, Seoul, Korea.
- 2Department of Pathology, College of Medicine, Korea University, Seoul, Korea.
Abstract
OBJECTIVE
To investigate the frequency of gut inflammation in the ankylosing spondylitis and the role of gut lesion in the pathogenesis of the ankylosing spondylitis.
METHODS
Ileocolonoscopy and biopsy were performed in 24 patients with. ankylosing spondylitis.
RESULTS
1) Endoscopic lesions were observed in 7 patients(29.2%) of 24 patients and more often in the terminal ileum(6/7) than in the colon(I/7). Among 7 patients with endoscopic lesions, 5 patients were presented as juvenile chronic arthritis. 2) Histologic signs of gut inflammation were detected in 14 patients(58. 3%). Actue lesions were seen in 2 patients (8. 3%) and chronic lesions were seen in 12 patients (50%). 3) In 12 patients without the involvement of peripheral joints, acute lesion was not seen(0%), and chronic lesions were seen in 6 patients(50%). In 12 patients with the involvement of peripheral joints, acute lesions were seen in 2 patients (16.7%), and chronic lesions were seen in 6 patients(50%). Gut inflammations were more frequent in patients with the involvement of peripheral joints than in those without the involvement of peripheral joints. 4) In 12 patients without the administration of sulfasalazine, acute lesion was not seen(0%), and chronic lesions were seen in 7 patients(58.7%) In 12 patients with the administration of sulfasalazine, acute lesions were seen in 2 patients (16.7%), and chronic lesions were seen in 5 patients(41.6%). The frequency of gut lesions in patients without the administration of sulfasalazine was not different from that in patients with the administration. of sulfasalazine (p<0.05).
CONCLUSION
Gut inflammation was frequently found in patients with ankylosing spondylitis. Chronic gut inflammation could play a role in the pathogenesis of the ankylosing spondylitis.