INTERLEUKIN-6 AND INTERLEUKIN-1 RECEPTOR ANTAGONIST IN ACUTE STROKE

Citation
Nb. Beamer et al., INTERLEUKIN-6 AND INTERLEUKIN-1 RECEPTOR ANTAGONIST IN ACUTE STROKE, Annals of neurology, 37(6), 1995, pp. 800-805
Citations number
29
Categorie Soggetti
Clinical Neurology",Neurosciences
Journal title
ISSN journal
03645134
Volume
37
Issue
6
Year of publication
1995
Pages
800 - 805
Database
ISI
SICI code
0364-5134(1995)37:6<800:IAIRAI>2.0.ZU;2-C
Abstract
Elevated plasma levels of interleukin-6 (IL-6), a key regulator of the acute phase response that includes increased fibrinogen synthesis, ha ve recently been detected in patients with acute stroke. Nevertheless, the role of the acute phase response in stroke has been controversial , with some studies suggesting that preexisting infection accounts for most of the acute phase response. Increased IL-6 could signal the inv olvement of antiinflammatory activity, since IL-6 stimulates the produ ction of endogenous antiinflammatory mediators such as interleukin-L r eceptor antagonist (IL-1RA). To better understand the interaction of p ro- and antiinflammatory acute phase processes in brain infarction, pl asma levels of IL-1RA, IL-6, and acute phase proteins including fibrin ogen and c-reactive protein (CRP) were measured within 4 +/- 2 days of onset in 50 patients with acute ischemic stroke and in 20 age-matched healthy controls. After excluding patients with evidence of infection , both IL-IRA and IL-6 were significantly elevated in stoke patients c ompared with controls (p < 0.0001). IL-1RA and IL-6 were both signific antly correlated with levels of CRP, p < 0.05 and p < 0.001, respectiv ely, but not with each other. Levels of IL-6 and IL-IRA, together with fibrinogen and CRP were higher in patients with infarcts of greater t han 3 cm and lowest in patients with lacunar syndromes. Detection of i ncreased peripheral levels of IL-1RA, IL-6, and additional acute phase reactants, including CRP, in acute stroke uncomplicated by infection suggests that an acute phase response to brain infarction occurs and t hat the magnitude of this response may be related to the volume of inf arcted brain.