Apoptosis plays a role in epithelial and mucosal injury, which is 1 of the mechanisms in the pathogenesis of ulcerative colitis. Apoptotic cells increase as a result of injured mucosa in ulcerative colitis and serum M 30 levels increase in epithelial cell apoptosis. In this study, we aimed to evaluate the relation between M 30 serum levels and ulcerative colitis activity.
Eighty patients with ulcerative colitis and 40 healthy controls were enrolled into the study. The patient group consisted of 31 extensive colitis, 30 left-sided colitis, and 19 proctitis. The activity of ulcerative colitis was determined with clinical and endoscopic findings. Serum M 30 levels, acute phase reactants, and biochemical tests were analyzed in all subjects.
Serum M 30 levels in patients with active ulcerative colitis were significantly higher when compared with the healthy controls (165.6 ± 60.6 and 129.6 ± 37.4; P = 0.003). Serum M 30 levels in active left-sided colitis patients was significantly higher when compared with patients in remission phase (180.6 ± 58.5, 141.5 ± 35.4; P = 0.044). When we exclude patients with ulcerative proctitis, M 30 levels in active ulcerative colitis patients were significantly higher than that the patients in remission phase (174.0 ± 63.5, 135.0 ± 29.9; P = 0.017).
We found that M 30 levels increase in patients with active ulcerative colitis. Our findings support the role of apoptosis demonstrated by serum M 30 levels in the pathogenesis of active ulcerative colitis.
Article first published online 13 August 2013
*Department of Gastroenterology, Dişkapi Yildirim Beyazit Education and Research Hospital, Ankara, Turkey;
†Department of Gastroenterology, Akdeniz University School of Medicine, Antalya, Turkey; and
‡Department of Biochemistry, Dişkapi Yildirim Beyazit Education and Research Hospital, Ankara, Turkey.
Reprints: Bora Aktaş, MD, Department of Gastroenterology, Dişkapi Yildirim Beyazit Education and Research Hospital, Aşik Veysel Mahallesi, 315 Sokak, 23/16 Abidinpaşa, Ankara 06620, Turkey (e-mail: email@example.com).
The authors have no conflicts of interest to disclose.
Received June 04, 2013
Accepted June 17, 2013