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Tumor necrosis factor alpha serum levels and inflammatory response in acute ischemic stroke patients.

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Title: Tumor necrosis factor alpha serum levels and inflammatory response in acute ischemic stroke patients.
Authors: Intiso, D., Zarretti, M. M., Lagioia, G., Di Rienzo, F., Checchia De Ambrosio, C., Simone, P., Tonali, P., Cioffi, R. P.
Source: Neurological Sciences. Feb2004, Vol. 24 Issue 6, p390-396. 7p.
Subjects: Tumor necrosis factors, Cerebrovascular disease patients, Serum, Fibrinogen, Immunoassay, Leukocytes, Neutrophils
Abstract: Experimental evidence indicates that tumor necrosis factor alpha (TNF-α) is involved in brain damage following ischemic injury. The present study was designed to monitor serum TNF-α levels in acute stroke patients and to correlate TNF-α levels with lesion size, neurological impairment and vascular risk factors. In 41 patients with ischemic stroke, serum TNF-α levels were serially measured by a solid enzyme amplified sensitivity immunoassay (EASIA) in the first 10 days after stroke onset. Serum fibrinogen and Creactive protein (CRP), white blood cell (WBC) and neutrophil counts were determined on the same days to monitor acute phase response changes. Lesion size was calculated on computed tomograms by a computer-assisted procedure. Neurological impairment was evaluated on the Canadian Neurological Scale. Forty age-matched subjects were used as controls. Compared to baseline, TNF-α levels significantly increased during the study (p=0.0001), peaking on day 7. Peak TNF-α levels did not correlate with neurological impairment or lesion size. Multivariate analysis showed that sex, age, vascular risk factors and infectious complications did not influence TNF-α levels. Fibrinogen, CRP, WBC and neutrophil concentrations increased, indicating an acute phase response occurred after stroke. In conclusion, serum TNF-α levels showed an early and prolonged increase after stroke onset, unrelated to lesion size, neurological impairment, age, sex, vascular risk factors or infectious complications. Serum increase of TNF-α may be explained as part of the acute phase response occurring in stroke patients. [ABSTRACT FROM AUTHOR]
Copyright of Neurological Sciences is the property of Springer Nature and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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  Data: <searchLink fieldCode="JN" term="%22Neurological+Sciences%22">Neurological Sciences</searchLink>. Feb2004, Vol. 24 Issue 6, p390-396. 7p.
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  Data: Experimental evidence indicates that tumor necrosis factor alpha (TNF-α) is involved in brain damage following ischemic injury. The present study was designed to monitor serum TNF-α levels in acute stroke patients and to correlate TNF-α levels with lesion size, neurological impairment and vascular risk factors. In 41 patients with ischemic stroke, serum TNF-α levels were serially measured by a solid enzyme amplified sensitivity immunoassay (EASIA) in the first 10 days after stroke onset. Serum fibrinogen and Creactive protein (CRP), white blood cell (WBC) and neutrophil counts were determined on the same days to monitor acute phase response changes. Lesion size was calculated on computed tomograms by a computer-assisted procedure. Neurological impairment was evaluated on the Canadian Neurological Scale. Forty age-matched subjects were used as controls. Compared to baseline, TNF-α levels significantly increased during the study (p=0.0001), peaking on day 7. Peak TNF-α levels did not correlate with neurological impairment or lesion size. Multivariate analysis showed that sex, age, vascular risk factors and infectious complications did not influence TNF-α levels. Fibrinogen, CRP, WBC and neutrophil concentrations increased, indicating an acute phase response occurred after stroke. In conclusion, serum TNF-α levels showed an early and prolonged increase after stroke onset, unrelated to lesion size, neurological impairment, age, sex, vascular risk factors or infectious complications. Serum increase of TNF-α may be explained as part of the acute phase response occurring in stroke patients. [ABSTRACT FROM AUTHOR]
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  Data: <i>Copyright of Neurological Sciences is the property of Springer Nature and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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