title: Triflusal and aspirin have different effects on inflammatory biomarkers measured in patients with acute ischemic stroke.
abstract: OBJECTIVE
  Triflusal is a 4-fluoromethyl derivative of salicylic acid used for secondary prevention of ischemic stroke. Recent experimental data (permanent middle cerebral artery occlusion in rats) have shown a possible role of triflusal in neuroprotection through inhibition of inflammatory pathways.
  
  
  METHODS
  To explore whether triflusal may modulate those pathways in human stroke, evolution of several inflammation markers (pro-inflammatory, adhesion molecules, chemokines, metalloproteinases, apoptosis and angiogenesis-related biomarkers) and neurological outcome were evaluated at baseline, and at days 1, 3, 7 and 90 in a pilot study in which 30 patients with acute ischemic stroke were randomly allocated to receive triflusal or aspirin.
  
  
  RESULTS
  An increase in IL-6 level was found in the aspirin group when compared to the triflusal group at the third and seventh day (p < 0.05). FGF-basic level was significantly increased at days 1 and 90 in the triflusal group (p = 0.040). The triflusal group also had higher levels of MIP-1alpha and MIP-1beta (p < 0.05) at day 1. Also among triflusal-treated patients, MCP-1 and TARC levels were increased as compared with the aspirin group at day 90 (p < 0.05). Interestingly, some of those markers modified by triflusal (MCP-1 and IL-6) were associated with neurological outcome: higher MCP-1 measured at day 3 among patients who improve at day 7 [462.3 (419.2-735.2) vs. 285 (242.1-428.2), p < 0.05], and lower levels of IL-6 at day 3 among patients who improve at day 90 [24.8 (5.6-77.3) vs. 5.4 (2.0-13.8), p < 0.05].
  
  
  CONCLUSIONS
  Triflusal modulates additional mechanisms to those of aspirin [pro-inflammatory (IL-6) and chemokine (MIP-1 and MCP-1) pathways] that could participate in the ischemic damage process following human acute stroke.
authors.affiliation: Neurovascular Research Laboratory, Vall d'Hebron University Hospital, Barcelona, Spain.
authors.forename: José
authors.initials: J
authors.lastname: Alvarez-Sabín
authors.forename: Anna
authors.initials: A
authors.lastname: Penalba
authors.forename: Manolo
authors.initials: M
authors.lastname: Quintana
authors.forename: Jerzy
authors.initials: J
authors.lastname: Krupinski
authors.forename: Lidia
authors.initials: L
authors.lastname: García-Bonilla
authors.forename: Joan
authors.initials: J
authors.lastname: Montaner
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use*; D001241:Aspirin / Q000627:therapeutic use*; D015415:Biomarkers / Q000097:blood; D002545:Brain Ischemia / Q000097:blood / Q000150:complications / Q000188:drug therapy*; D005260:Female; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood*; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D018696:Neuroprotective Agents / Q000627:therapeutic use*; D010865:Pilot Projects; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use*; D011446:Prospective Studies; D012459:Salicylates / Q000627:therapeutic use*; D020521:Stroke / Q000097:blood / Q000188:drug therapy* / Q000209:etiology; D013997:Time Factors; D016896:Treatment Outcome
chemical_list: D000893:Anti-Inflammatory Agents; D015415:Biomarkers; D018836:Inflammation Mediators; D018696:Neuroprotective Agents; D010975:Platelet Aggregation Inhibitors; D012459:Salicylates; C016167:triflusal; D001241:Aspirin