Serum XXXX Levels in @entity31 .

@entity1 @entity649 @entity31 @entity2286 @entity29 @entity26156
BACKGROUND: Previous studies have suggested that adipokines play a role in @entity29 by inducing proinflammatory cytokines, but it is uncertain whether @entity26156 is causally involved in @entity31 ( @entity31 ). We evaluated @entity26156 levels in @entity1 who presented with @entity31 flares before and after treatment. METHODS: In this cohort study, we assessed 31 @entity1 with @entity31 in the activation period and remission in the same @entity1 after treatment, and a healthy control group, consisting of 29 @entity1 , at a single academic medical centre between 2010 and 2013. Disease severity was evaluated clinically using Trulove and Witt's criteria. RESULTS: Serum @entity26156 levels did not vary according to the extent of disease and were significantly higher in @entity1 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 @entity1 in the inactive period with the control group, there was no statistically significant difference (P > 0.05). To assess activation of the disease, a @entity26156 cut-off point for active @entity31 was determined as 6.40, with sensitivity, specificity, positive predictive value ( @entity2286 ) and negative predictive values (NPV) of 72%, 52%, 66.7% (43.0-85.4) and 50.0% (29.1-70.9), respectively. CONCLUSIONS: The @entity26156 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 @entity1 with @entity649 ( @entity649 ). These findings did not provide a rationale for assessment of @entity31 activation.
