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Chitotriosidase in Patients with Acute Ischemic Stroke
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<i>Background:</i> 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. <i>Purpose:</i> 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. <i>Methods:</i> We studied the plasma level of chitotriosidase activity, TNF-α 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. <i>Results:</i> 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-α level (r = 0.76, p<0.001); it also inversely correlates with the IL-6 level (r = –0.43, p ≤ 0.05). <i>Conclusion:</i> 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.
Title: Chitotriosidase in Patients with Acute Ischemic Stroke
Description:
<i>Background:</i> 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.
<i>Purpose:</i> 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.
<i>Methods:</i> We studied the plasma level of chitotriosidase activity, TNF-α 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.
<i>Results:</i> 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-α level (r = 0.
76, p<0.
001); it also inversely correlates with the IL-6 level (r = –0.
43, p ≤ 0.
05).
<i>Conclusion:</i> 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.
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