So followup research needs to occur on preventing these pro-inflammatory cytokines. That will never occur, your doctors and stroke hospital don't initiate contact with researchers. And we have NO STROKE LEADERSHIP TO GO TO OR ANY STROKE STRATEGY TO UPDATE.
EXPRESS: Inflammatory cytokines, high sensitivity CRP, and risk of 1-year vascular events, death and poor functional outcome after stroke and TIA
Abstract
Background
Inflammation driven by pro-inflammatory cytokines is a new therapeutic target in coronary disease. Few data exist on the association of key upstream cytokines and post-stroke recurrence. In a prospective cohort study, we investigated the association between pivotal cytokines, CRP and 1-year outcomes.
Methods
BIO-STROKETIA is a multi-centre prospective cohort study of non-severe ischemic stroke (mRSâ¤3) and TIA. Controls were patients with transient symptoms attending TIA clinics with non-ischemic final diagnosis. Exclusion criteria were severe stroke, infection and other pro-inflammatory disease. High-sensitivity serum C-reactive protein (CRP) and cytokines (interleukin [IL] 6, IL-1β, IL-8, IL-10, IL-12, interferon-γ [IFN-γ], tumor-necrosis factor-α [TNF-α]) were measured. The primary outcome was 1-year recurrent stroke/coronary events (fatal and non-fatal).
Results
680 patients (439 stroke, 241 TIA) and 68 controls were included. IL-6, IL-1β, IL-8, IFN-γ, TNF-α, and CRP were higher in stroke/TIA cases (pâ¤0.01 for all). On multivariable Cox regression, IL-6, IL-8, and CRP independently predicted 1-year recurrent vascular events (adjusted HRs [aHR] per-quartile increase IL-6 1.31,CI 1.02-1.68, p=0.03; IL-8 1.47, CI 1.15-1.89, p=0.002; CRP 1.28 CI, 1.01-1.62, p=0.04). IL-6 (aHR 1.98, CI 1.26-3.14, p=0.003) and CRP (aHR 1.81, CI 1.20-2.74, p=0.005) independently predicted 1-year fatality. IL-6 and CRP (adjusted OR per-unit increase 1.02, CI 1.01-1.04) predicted poor functional outcome, with a trend for IL-1ï¢ (p=0.054).
Conclusion
Baseline inflammatory cytokines independently predicted late recurrence, supporting a rationale for randomised trials of anti-inflammatory agents for prevention after stroke and suggesting that targeted therapy to high-risk patients with high baseline inflammation may be beneficial.
No comments:
Post a Comment