INFLAMMATORY MECHANISMS AND STROKE: THE ROLE OF C-REACTIVE PROTEIN, AS A BIOMARKER

Abstract

Inflammation is involved in stroke pathogenesis. Proinflammmatory factors cause damage of brain parenchyma, during the acute phase of stroke, while anti-inflammatory factors are responsible for the containment of tissue damage and augmenting of neuroplasticity, during subacute phase of stroke. For that reason acute phase proteins fluctuations during inflammatory procedures could be utilized as useful biomarkers in every day clinical practice. Compared to other systemic inflammation markers, C-reactive protein (CRP) and high sensitivity CRP (hsCRP) are more widely available, as they can be easily and accurately measured. CRP also seems to be involved in atheromatosis progression and clot formation. This may be attributed to the binding of CRP with low density lipoprotein of atheromatic plaques, which in turn may cause further activation of the coagulation cascade. Therefore, prospective studies concentrate on the existence of a possible association between stroke and CRP levels. These reports underscore a positive correlation between CRP and the risk of first-ever or recurrent ischemic stroke. Other studies indicate further correlation between the incidence of different, ischemic stroke subtypes and CRP concentrations, finding higher levels of CRP among patients with cardioembolic or atherothrombotic stroke compared to patients with lacunar infarcts.
Moreover, the prognostic value of CRP is being evaluated in acute ischemic stroke patients undergoing intravenous thrombolysis or in early detection of post-stroke infections. Once more, higher levels of CRP are related to unfavorable outcome. Nevertheless further research is required to draw firm conclusions, regarding the diagnostic utility of CRP in the differential diagnosis and prognosis of ischemic stroke. Finally, more studies are needed to further elucidate the interaction between CRP and hemorrhagic stroke, since the available data are scarce and contradictory.