Premium
Decreased anti‐S accharomyces cerevisiae antibody titer by mesalazine in patients with Crohn’s disease
Author(s) -
Oshitani Nobuhibe,
Hato Fumihiko,
Matsumoto Takayuki,
Jinno Yoshio,
Sawa Yoshinori,
Hara Junichi,
Nakamura Shiro,
Seki Shuichi,
Arakawa Tetsuo,
Kitano Atsuo,
Kitagawa Seiichi,
Kuroki Tetsuo
Publication year - 2000
Publication title -
journal of gastroenterology and hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.214
H-Index - 130
eISSN - 1440-1746
pISSN - 0815-9319
DOI - 10.1046/j.1440-1746.2000.02357.x
Subject(s) - mesalazine , medicine , ulcerative colitis , inflammatory bowel disease , crohn's disease , gastroenterology , immunology , disease , antibody , pathophysiology , titer
Background Saccharomyces cerevisiae may contribute to the pathophysiology of Crohn’s disease. We determined serum anti‐ Saccharomyces cerevisiae antibody (ASCA) levels in patients with inflammatory bowel disease. Methods and Results Immunoglobulin G (IgG) ASCA was measured by using an ELISA in serum samples from 19 patients with ulcerative colitis, 18 patients with Crohn’s disease and 7 healthy controls. The ASCA level was significantly higher in patients with ulcerative colitis and patients with Crohn’s disease than in controls, and was significantly higher in patients with Crohn’s disease compared with patients with ulcerative colitis. Age, gender, disease activity, extent of disease and small bowel involvement each did not affect ASCA levels. The use of elemental or polymeric diet therapy for Crohn’s disease and administration of corticosteroids to patients with inflammatory bowel disease also did not affect ASCA levels. The ASCA titer was significantly lower in patients with Crohn’s disease taking mesalazine than in those not taking it, although, serum IgG levels did not differ between these two groups, which might imply a suppression of IgG production by mesalazine at the intestinal level. Conclusions The finding of increased serum ASCA titers in patients with inflammatory bowel disease suggests that Saccharomyces cerevisiae may play a role in the pathophysiology of this condition.