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* = Presenting author

P734 Gene expression of SELENBP1 is upregulated in the colonic mucosa and is associated with a long-term remission in patients with ulcerative colitis

J. Yamamoto-Furusho*1, L. Salazar-Salas1, G. Fonseca-Camarillo1, R. Barreto2

1IBD Clinic, Instituto Nacional de Ciencias Medicas y Nutricion, Gastroenterology, Mexico, Mexico, 2Instituto Nacional de Ciencias Medicas y Nutricion, Endoscopy, Mexico, Mexico


Studies have looked at connections between diet, aetiology, and signs and symptoms associated with inflammatory bowel disease (IBD). Inadequate dietary intake of the essential trace element selenium (Se) is thought to be a risk factor for several chronic diseases associated with oxidative stress and inflammation. Biological actions of Se occur through low-molecular weight metabolites and through selenium-binding protein 1 (SELENBP1) has been detected in the intestine. The gene expression of SELENBP1 as molecule responsible for the absorption of selenium has not been studied in patients with ulcerative colitis (UC). The aim was to determine the gene expression of SELENBP1 in patients with UC and to evaluate its association with clinical outcomes.


In total, 55 individuals were studied and divided in 35 patients with UC (20 active and 15 in remission) and 20 normal controls without inflammation. Colonic mucosa biopsies were taken by colonoscopy and preserved in RNA later. The RNA extraction was performed and cDNA was synthesised with polymerase chain reaction (PCR) technique. The SELENBP1 gene expression was measured on real-time PCR using specific primers and GAPDH (Glyceraldehyde 3-phospate dehydrogenase) as a reference gene. Statistical analysis was performed using the SSPS program v.20.


In the study, 35 patients with UC and 20 normal controls were included. The clinical characteristic of UC patients were as follows: (1) extent of UC: 62.9% had pancolitis; 11.4% left colitis; and 25.7% proctosigmoiditis. (2) Clinical course of disease was characterised: 68.6% had an intermittent pattern; 17.1% continuous activity; and 14.3% active and then long-term remission. (3) Treatment response was favourable in 91.4%; steroid resistance in 5.7%; and steroid-dependent 2.9%. (4) UC activity was severe in 11.4%; moderate activity in 20%; mild in 22.9%; and 45.7% were clinical and endoscopic remission. The SELENBP1 gene expression was significantly higher in patients with active UC compared with UC in remission (p = 0.001) and in the normal control group (p = 0.007). An up-regulation of SELENBP1 gene was associated with a more benign clinical course characterised by the presence of initial activity and then long-term remission for more than 5 years (p = 0.003 OR = 23.7). No association was found with other clinical outcomes.


The up-regulation of SELENBP1 gene was found in patients with active UC, and it was associated with a long-term remission in patients with UC. These findings suggest that SELENBP1 might play a role as a molecular marker of clinical course of UC.