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 C-reactive 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.
| Original language | English |
|---|---|
| Pages (from-to) | 390-396 |
| Number of pages | 7 |
| Journal | Neurological Sciences |
| Volume | 24 |
| Issue number | 6 |
| DOIs | |
| Publication status | Published - Feb 2004 |
Fingerprint
Keywords
- Computed tomography
- Cytokine
- Inflammation response
- Ischemic stroke
- Tumor necrosis factor
ASJC Scopus subject areas
- Neuroscience(all)
- Clinical Neurology
Cite this
Tumor necrosis factor alpha serum levels and inflammatory response in acute ischemic stroke patients. / Intiso, Do; Zarrelli, M. M.; Lagioia, G.; Di Rienzo, F.; Checchia De Ambrosio, C.; Simone, P.; Tonali, P.; Cioffi, R. P.
In: Neurological Sciences, Vol. 24, No. 6, 02.2004, p. 390-396.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Tumor necrosis factor alpha serum levels and inflammatory response in acute ischemic stroke patients
AU - Intiso, Do
AU - Zarrelli, M. M.
AU - Lagioia, G.
AU - Di Rienzo, F.
AU - Checchia De Ambrosio, C.
AU - Simone, P.
AU - Tonali, P.
AU - Cioffi, R. P.
PY - 2004/2
Y1 - 2004/2
N2 - 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 C-reactive 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.
AB - 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 C-reactive 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.
KW - Computed tomography
KW - Cytokine
KW - Inflammation response
KW - Ischemic stroke
KW - Tumor necrosis factor
UR - http://www.scopus.com/inward/record.url?scp=1342291175&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=1342291175&partnerID=8YFLogxK
U2 - 10.1007/s10072-003-0194-z
DO - 10.1007/s10072-003-0194-z
M3 - Article
C2 - 14767684
AN - SCOPUS:1342291175
VL - 24
SP - 390
EP - 396
JO - Neurological Sciences
JF - Neurological Sciences
SN - 1590-1874
IS - 6
ER -