Chitotriosidase in patients with acute ischemic stroke

Background: Following an acute brain ischemia, local endothelia allow monocyte chemoattraction into the lesion site which contributes to brain damage through a group of neurotoxic factors. A relationship exists between the extent of brain damage and the plasma level of monocyte products, including chitotriosidase, though usually strictly related to preexisting infectious-inflammatory diseases. Purpose: Since chitotriosidase activity is also elevated in pathogen-free conditions, we tested whether chitotriosidase upregulation might be specifically related to stroke and unrelated to clinically relevant infectious diseases. Methods: We studied the plasma level of chitotriosidase activity, TNF-alpha and IL-6 in 44 consecutive patients with acute brain ischemia without concomitant symptoms or signs of inflammatory-infectious diseases. Results were compared with stroke severity and outcome as detected by brain CT and NIH scale. Blood samples were collected, on average, 11 h after stroke onset. Results: Chitotriosidase activity positively correlates with stroke severity, as measured by NIH scale ( r = 0.69, p < 0.01), to the extent of brain damage as documented by CT ( r = 0.75, p <= 0.001) and the TNF-alpha level ( r = 0.76, p < 0.001); it also inversely correlates with the IL-6 level ( r = - 0.43, p <= 0.05). Conclusion: Our results indicate that chitotriosidase is a specific marker of macrophage activation occurring in stroke which directly correlates with stroke severity independently of preexisting inflammatory or infectious conditions. Copyright (C) 2005 S. Karger AG, Basel.

Background: Following an acute brain ischemia, local endothelia allow monocyte chemoattraction into the lesion site which contributes to brain damage through a group of neurotoxic factors. A relationship exists between the extent of brain damage and the plasma level of monocyte products, including chitotriosidase, though usually strictly related to preexisting infectious-inflammatory diseases. Purpose: Since chitotriosidase activity is also elevated in pathogen-free conditions, we tested whether chitotriosidase upregulation might be specifically related to stroke and unrelated to clinically relevant infectious diseases. Methods: We studied the plasma level of chitotriosidase activity, TNF-alpha and IL-6 in 44 consecutive patients with acute brain ischemia without concomitant symptoms or signs of inflammatory-infectious diseases. Results were compared with stroke severity and outcome as detected by brain CT and NIH scale. Blood samples were collected, on average, 11 h after stroke onset. Results: Chitotriosidase activity positively correlates with stroke severity, as measured by NIH scale ( r = 0.69, p < 0.01), to the extent of brain damage as documented by CT ( r = 0.75, p <= 0.001) and the TNF-alpha level ( r = 0.76, p < 0.001); it also inversely correlates with the IL-6 level ( r = - 0.43, p <= 0.05). Conclusion: Our results indicate that chitotriosidase is a specific marker of macrophage activation occurring in stroke which directly correlates with stroke severity independently of preexisting inflammatory or infectious conditions.