Correlation between antioxidant defense system biomarkers and infarct size in ischemic stroke

Sotomayor, Camilo; Cortes, Ignacio; Karachon, Lucas; Rodrigo, Ramon

Abstract

Background/Introduction: Stroke is the second most common cause of mortality worldwide, after heart disease. Oxidative Stress plays a key role in the pathophysiology of ischemia-reperfusion events such as Stroke. Oxidative Stress occurs when there is an imbalance between the generation of reactive oxygen species (ROS) and the antioxidant defense systems, so that the latter becomes overwhelmed. The aim of the present study is to determine the correlation between antioxidant defense system biomarkers and the Infarct Size (volume) in patients with ischemic stroke. Objectives: The general objective was to study the relationship between antioxidant defense system biomarkers and Infarct Size following Ischemic Stroke.The specific objectives are: To determine uric acid plasma levels following Ischemic Stroke at days 1, 2, 3, 4, 5, 6, 30. To determine ferric reducing ability of plasma levels following stroke at days 1, 2, 3, 4, 5, 6, 30. To determine Infarct Size volume following stroke at days 0 and 30. Methods: An observational, prospective and analytical study was carried on 20 patients with Ischemic Stroke. It was taken blood samples from every patient, following stroke at days 1, 2, 3, 4, 5, 6 and 30. From every blood sample it was measured FRAP and Uric Acid levels. The Infarct Size volume was measured using magnetic resonance imaging at days 0 and 30 following Ischemic Stroke. Results (preliminary): There is a negative correlation between uric acid levels and Final Infarct Size volume at day 30 (p<0.05). Discussion/Conclusion: This is the first study that determines antioxidant defense system biomarkers progression over time following Ischemic Stroke and its relationship with Infarct Size volume. These findings support the role of Oxidative Stress in the pathophysiology of Ischemic Stroke and suggest a possible antioxidant therapeutic approach in order to reduce the ischemia-reperfusion injury (Final Infarct Size).

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Fecha de publicación: 2016