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

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.