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

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.