title: Tumor necrosis factor alpha serum levels and inflammatory response in acute ischemic stroke patients.
abstract: Experimental evidence indicates that tumor necrosis factor alpha (TNF-alpha) is involved in brain damage following ischemic injury. The present study was designed to monitor serum TNF-alpha levels in acute stroke patients and to correlate TNF-alpha levels with lesion size, neurological impairment and vascular risk factors. In 41 patients with ischemic stroke, serum TNF-alpha 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-alpha levels significantly increased during the study ( p=0.0001), peaking on day 7. Peak TNF-alpha 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-alpha levels. Fibrinogen, CRP, WBC and neutrophil concentrations increased, indicating an acute phase response occurred after stroke. In conclusion, serum TNF-alpha 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-alpha may be explained as part of the acute phase response occurring in stroke patients.
authors.affiliation: Department of Neurology, IRCCS Casa Sollievo della Sofferenza, Viale dei Cappuccini 1, I-71013, San Giovanni Rotondo (FG), Italy. do.intiso@tiscali.it
authors.forename: D
authors.initials: D
authors.lastname: Intiso
authors.forename: M M
authors.initials: MM
authors.lastname: Zarrelli
authors.forename: G
authors.initials: G
authors.lastname: Lagioia
authors.forename: F
authors.initials: F
authors.lastname: Di Rienzo
authors.forename: C
authors.initials: C
authors.lastname: Checchia De Ambrosio
authors.forename: P
authors.initials: P
authors.lastname: Simone
authors.forename: P
authors.initials: P
authors.lastname: Tonali
authors.forename: R P
authors.initials: RP
authors.lastname: Cioffi Dagger
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D002097:C-Reactive Protein / Q000378:metabolism; D016022:Case-Control Studies; D002490:Central Nervous System / Q000473:pathology; D004562:Electrocardiography / Q000379:methods; D004569:Electroencephalography / Q000379:methods; D004797:Enzyme-Linked Immunosorbent Assay / Q000379:methods; D005260:Female; D005340:Fibrinogen / Q000378:metabolism; D005500:Follow-Up Studies; D006801:Humans; D007249:Inflammation / Q000097:blood / Q000209:etiology; D007511:Ischemia / Q000097:blood* / Q000150:complications; D007962:Leukocytes / Q000378:metabolism; D008279:Magnetic Resonance Imaging / Q000379:methods; D008297:Male; D008875:Middle Aged; D009460:Neurologic Examination / Q000379:methods; D009504:Neutrophils / Q000378:metabolism; D020521:Stroke / Q000097:blood* / Q000209:etiology; D013997:Time Factors; D014057:Tomography, X-Ray Computed / Q000379:methods; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism*
chemical_list: D014409:Tumor Necrosis Factor-alpha; D005340:Fibrinogen; D002097:C-Reactive Protein