BackgroundPrevious studies have suggested that adipokines play a role in inflammatory bowel disease by inducing proinflammatory cytokines, but it is uncertain whether visfatin is causally involved in ulcerative colitis (UC). We evaluated visfatin levels in patients who presented with UC flares before and after treatment.MethodsIn this cohort study, we assessed 31 patients with UC in the activation period and remission in the same patients after treatment, and a healthy control group, consisting of 29 persons, at a single academic medical centre between 2010 and 2013. Disease severity was evaluated clinically using Trulove and Witt's criteria.ResultsSerum visfatin levels did not vary according to the extent of disease and were significantly higher in patients in the activation period (7.77 ± 2.41 ng/ml) than in remission (6.18 ± 2.04 ng/ml) and the healthy controls (6.54 ± 2.20 ng/ml; P < 0.01 and < 0.05, respectively). In a comparison of patients in the inactive period with the control group, there was no statistically significant difference (P > 0.05). To assess activation of the disease, a visfatin cut‐off point for active UC was determined as 6.40, with sensitivity, specificity, positive predictive value (PPV) and negative predictive values (NPV) of 72%, 52%, 66.7% (43.0–85.4) and 50.0% (29.1–70.9), respectively.ConclusionsThe visfatin level was higher in the active group than in post‐treatment remission and the healthy control group. Sensitivity and specificity were similar to other inflammatory markers for assessing clinical activity, which did not improve clinical outcomes in patients with acute respiratory distress syndrome (ARDS). These findings did not provide a rationale for assessment of UC activation.