(Stroke. 2001;32:1234-a.)
© 2001 American Heart Association, Inc.
Letters to the Editor |
ICMSN, IDIBAPS, Hospital Clinic, Barcelona, Spain
Neurology Service, Hospital Clinico Universitario, Santiago de Compostela, Spain
Neurology Service, Hospital Universitario Doctor Josep Trueta, Girona, Spain
To the Editor:
We appreciate Dr Christensens interest in our work, recently published in Stroke.1 As we stated in the Subjects and Methods section of that article, the 231 patients analyzed in our study were selected form a larger cohort of 249 patients admitted consecutively between October 1992 and December 1996. Shrewdly, Christensen correctly guesses that this larger cohort includes the 128 patients that supported our report on glutamate excitotoxicity in acute ischemic stroke.2 Therefore, this larger series gives additional ground and further credit to the role of glutamate and IL-6 on neurological deterioration in patients with ischemic stroke.
The concentrations of glutamate in plasma
(309.6±64.8 versus 106.3±49.3 µmol/L;
P<0.0001) and CSF (13.3±3.8
versus 6.4±4.2 µmol/L;
P<0.0001) were significantly
higher in patients with clinical deterioration than in patients who
remained stable or improved during the first 48 hours. Glutamate and
IL-6 levels were positively correlated in samples of both plasma
(Spearman coefficient 0.66,
P<0.001) and cerebrospinal
fluid (CSF) (Spearman coefficient 0.49,
P<0.001). As shown in the
Table
, variables that remained independently
associated with early clinical deterioration on
multivariate analysis included IL-6 >21.5
pg/mL in plasma or >6.3 pg/mL in CSF, glutamate >200 µmol/L in
plasma or >8.2 µmol/L in CSF, admission Canadian Stroke Scale score,
and serum glucose.
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As pointed out by Dr Christensen, IL-6 has complex
mechanisms of action that at present are not clearly understood.
While we and others3 suggest
proinflammatory properties in acute stroke, a
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