Bustamante A, Dominguez C, Rodriguez-Sureda V, Vilches A, Penalba A, Giralt D, García-Berrocoso T, Llombart V, Flores A, Rubiera M, Molina C, Alvarez-Sabín J, Montaner J.

Int J Stroke. 2014 Oct;9(7):910-6. doi: 10.1111/ijs.12160. Epub 2013 Oct 22.




Chitotriosidase, a component of innate immunity, constitutes a sensitive parameter of macrophage activation and its elevated plasma activity reflects an inflammatory response. Given the deleterious effects of inflammation in brain ischemia, we aimed to assess the prognostic value of chitotriosidase activity in acute stroke patients.


The study comprised 159 acute stroke patients and 51 age-matched controls. Plasma chitotriosidase activity was serially determined by fluorometric assay. Short-term neurological outcome was determined at 48 h and functional outcome at three-months. Predictors of neurological and functional outcome were determined via multivariate analysis, and the additional predictive value of chitotriosidase was tested with the Integrated Discrimination Index and the Net Reclassification Improvement.


Stroke patients showed increased levels of baseline chitotriosidase activity compared to controls [114·2 (74·65-182·95) nmol/ml/h vs. 54·4 (32·7-76·4); P < 0·0001]. Chitotriosidase activity (<118·75) was found to be an independent predictor of neurological improvement at 48 h (odds ratio: 3·25; 95% confidence interval: 1·54-6·85; P=0·002), and the addition of plasma chitotriosidase activity showed a better prediction of improvement at 48 h (Integrated Discrimination Index=5·7%, Net Reclassification Improvement=11·6%, P<0·05) over the predictive model constituted only with clinical information. Although patients disabled at three-months showed higher baseline chitotriosidase levels, it was not an independent predictor of long-term disability.


Baseline chitotriosidase activity in acute stroke patients treated with tissue plasminogen activator (tPA) may constitute a prognostic predictor of short-term outcome, adding a moderate additional predictive value. Our results underline the deleterious role of inflammation in acute stroke patients.