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Abstract Objectives: This article discusses the results of clinical and experimental studies that examine the association of hyperuricemia and gout with cardiovascular (CV) disease. Methods: Key papers for inclusion were identified by a PubMed search, and articles were selected for their relevance to the topic, according to the authors' judgment. Results and conclusions: Significant progress has been made in confirming an association, possibly causal, between hyperuricemia and CV outcomes. Xantine-oxidase (XO) inhibitors appear to be the most promising agents for prevention and treatment of CV consequences associated with hyperuricemia. Several small and medium sized studies have examined the effect of these agents on CV function in a variety of patient populations. Improvements in measures of endothelial function, oxidative stress, cardiac function, hemodynamics, and certain inflammatory indices have been demonstrated. Compounds for XO inhibition with more specific clinical effects and fewer side effects than allopurinol may be promising options to further explore the therapeutic potential in patients with CV disease. It is too early to make clinical recommendations with regard to the benefits of using XO inhibitor allopurinol or the novel febuxostat in patients with asymptomatic increased UA levels and high CV risk because only a small number of studies have shown that they may be beneficial in terms of CV outcomes. More studies are therefore needed to determine the potential of these drugs for reducing the risk of developing CV disease.
Division of Medicine and Surgery , Spedali Civili, Brescia , Italy.
This article was published in the following journal.
Name: Current medical research and opinion
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Agents that increase uric acid excretion by the kidney (URICOSURIC AGENTS), decrease uric acid production (antihyperuricemics), or alleviate the pain and inflammation of acute attacks of gout.
Excessive URIC ACID or urate in blood as defined by its solubility in plasma at 37 degrees C; greater than 0.42mmol per liter (7.0mg/dL) in men or 0.36mmol per liter (6.0mg/dL) in women. This condition is caused by overproduction of uric acid or impaired renal clearance. Hyperuricemia can be acquired, drug-induced or genetically determined (LESCH-NYHAN SYNDROME). It is associated with HYPERTENSION and GOUT.
Uricosuric that acts by increasing uric acid clearance. It is used in the treatment of gout.
Gout suppressants that act directly on the renal tubule to increase the excretion of uric acid, thus reducing its concentrations in plasma.
Hereditary metabolic disorder characterized by recurrent acute arthritis, hyperuricemia and deposition of sodium urate in and around the joints, sometimes with formation of uric acid calculi.
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