
Serum Visfatin Levels in Ulcerative Colitis
Author(s) -
Dogan Serkan,
Guven Kadri,
Celikbilek Mehmet,
Deniz Kemal,
Saraymen Berkay,
Gursoy Sebnem
Publication year - 2016
Publication title -
journal of clinical laboratory analysis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.536
H-Index - 50
eISSN - 1098-2825
pISSN - 0887-8013
DOI - 10.1002/jcla.21901
Subject(s) - ulcerative colitis , medicine , gastroenterology , adipokine , inflammatory bowel disease , proinflammatory cytokine , cohort , disease , case control study , inflammation , immunology , obesity , insulin resistance
Background Previous 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. Methods In 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. Results Serum 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. Conclusions The 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.