title: [Peripheral blood indicators of inflammatory response during the first twenty-four hours of ischemic stroke].
abstract: BACKGROUND
  Reports point to the significant role of inflammatory mechanisms in stroke. These mechanisms are activated in peripheral blood in response to acute ischemic injury of cerebral tissues. The aim of this study was to determine whether peripheral inflammatory response to acute ischemia of the nervous tissue develops during the first twenty-four hours of ischemic stroke.
  
  
  METHODS
  We studied 53 persons divided into three groups: 25 patients with ischemic stroke, arterial hypertension, and/or type 2 diabetes mellitus, and/or dyslipidemia (group I); 17 patients with arterial hypertension, and/or type 2 diabetes mellitus, and/or dyslipidemia but without stroke (group II); 11 young, healthy individuals (group III). TNF-alpha concentrations in peripheral blood were measured in each group using a sandwich enzyme-linked immunosorbent assay (ELISA). Other markers of inflammation in peripheral blood--C-reactive protein, fibrinogen, and leukocyte count--were assayed as well. The results were analyzed in relation to age, gender, co-morbidities, and blood-brain barrier injury.
  
  
  RESULTS
  TNF-alpha concentrations in peripheral blood of stroke patients were similar as in the other two groups. No associations between TNF-alpha and other inflammatory parameters were found. Injury of the blood-brain barrier was not accompanied by a significant change in the concentration of TNF-alpha.
  
  
  CONCLUSIONS
  No significant peripheral inflammatory response to brain ischemia develops during the first twenty-four hours of ischemic stroke. This finding suggests that early anti-inflammatory prevention protocols can be devised to limit further injury of ischemic nervous tissue caused by activation of inflammatory processes.
authors.affiliation: Katedra i Klinika Neurologii Pomorskiej Akademii Medycznej w Szczecinie, ul. Unii Lubelskiej 1, 71-252 Szczecin.
authors.forename: Marta
authors.initials: M
authors.lastname: Masztalewicz
authors.forename: Przemysław
authors.initials: P
authors.lastname: Nowacki
authors.forename: Jolanta
authors.initials: J
authors.lastname: Turowska-Kowalska
authors.forename: Krzysztof
authors.initials: K
authors.lastname: Safranow
mesh_terms: D000368:Aged; D015415:Biomarkers / Q000097:blood; D002545:Brain Ischemia / Q000150:complications*; D002097:C-Reactive Protein / Q000378:metabolism; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000150:complications; D050171:Dyslipidemias / Q000097:blood / Q000150:complications; D005260:Female; D005340:Fibrinogen / Q000378:metabolism; D006801:Humans; D006973:Hypertension / Q000097:blood / Q000150:complications; D018836:Inflammation Mediators / Q000097:blood*; D007958:Leukocyte Count; D008297:Male; D020521:Stroke / Q000097:blood* / Q000175:diagnosis* / Q000209:etiology; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D015415:Biomarkers; D018836:Inflammation Mediators; D014409:Tumor Necrosis Factor-alpha; D005340:Fibrinogen; D002097:C-Reactive Protein