Abstract
Elevated serum uric acid (SUA) levels have been associated with an increased risk of cardiovascular (CV) disease and acute ischemic stroke (AIS) as well as many other medical conditions. AIS is a CV complication that is the second most common cause of mortality worldwide. It results from reduced blood flow to the brain by means of thrombosis, embolism, or systemic hypoperfusion. Studies have demonstrated an association between SUA levels and CV events, with a significant dose-response relationship between elevated SUA levels and stroke risk. Since the relationship between SUA levels and AIS risk has been established, studies are also being conducted in order to evaluate whether antihyperuricemic drugs can lower this risk. Allopurinol use in hyperuricemic patients has been shown to decrease the risk of major CV events, which include AIS. This narrative review aims to investigate the role of SUA as an independent risk factor for AIS along with the proposed biological mechanisms by thoroughly appraising research findings from relevant full-text articles and abstracts indexed in PubMed and the Cochrane Library. In this literature, we will be discussing hyperuricemia, AIS, the association between the two, and the use of antihyperuricemic medications on stroke prognosis. This review will also shed new light on studies that have begun to provide insight into the predictive role of hyperuricemia in AIS.
Highlights
BackgroundStroke is the second most common cause of mortality in the world
This review aims to study the association between hyperuricemia and stroke and the role of anti-hyperuricemic medication on stroke prognosis
It is evident that hyperuricemia shares a relationship with ischemic stroke
Summary
Stroke is the second most common cause of mortality in the world. It is responsible for 11% of deaths and is a major cause of disability worldwide [1]. A study conducted by Chamorro et al concluded good clinical outcomes in patients with acute ischemic stroke (AIS) and increasing uric acid levels [10]. There are many more studies that indicated worsening outcomes in AIS patients with the rise in serum uric acid (SUA) levels [11,12]. Solute carrier family 22 - member 12 (URAT1/SLC22A12), solute carrier family 2 - facilitated glucose transporter member 9 (GLUT9/SLC2A9), and ATP-binding cassette superfamily G member 2/breast cancer resistance protein (ABCG2/BCRP) are urate transporters which play a vital role in the regulation of uric acid levels Among these transporters, ABCG2 exporter dysfunction is known to be a major and common cause of hyperuricemia since it acts on both the kidney and GI systems [13,21].
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