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The pathophysiology of hyperuricaemia and its possible relationship to cardiovascular disease, morbidity and mortality.

Gustafsson D, Unwin R - BMC Nephrol (2013)

Bottom Line: High levels are causative in gout and urolithiasis.Hyperuricaemia has also been implicated in the pathophysiology of hypertension, chronic kidney disease (CKD), congestive heart failure (CHF), the metabolic syndrome, type 2 diabetes mellitus (T2DM), and atherosclerosis, with or without cardiovascular events.This article briefly reviews uric acid metabolism and summarizes the current literature on hyperuricaemia in cardiovascular disease and related co-morbidities, and emerging treatment options.

View Article: PubMed Central - HTML - PubMed

Affiliation: Bioscience, CVMD iMED, AstraZeneca R&D Mölndal, Mölndal, Sweden. david.gustafsson@astrazeneca.com

ABSTRACT
Uric acid is the end product of purine metabolism in humans. High levels are causative in gout and urolithiasis. Hyperuricaemia has also been implicated in the pathophysiology of hypertension, chronic kidney disease (CKD), congestive heart failure (CHF), the metabolic syndrome, type 2 diabetes mellitus (T2DM), and atherosclerosis, with or without cardiovascular events. This article briefly reviews uric acid metabolism and summarizes the current literature on hyperuricaemia in cardiovascular disease and related co-morbidities, and emerging treatment options.

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Schematic representation of uric acid formation and elimination showing the drugs that can affect both.
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Figure 1: Schematic representation of uric acid formation and elimination showing the drugs that can affect both.

Mentions: Increased cell turnover (e.g., haemolysis, tumour growth and large tumour necrosis) leads to increased production of adenosine, inosine and guanosine. These are degraded to hypoxantine and xanthine, which are the substrates for the widely distributed xanthine oxidase (XO) in the formation of uric acid (Figure 1). Allopurinol and febuxostat are inhibitors of XO and reduce uric acid formation. In man and some higher primates, uric acid is the end-product of purine metabolism. However, most mammals can degrade uric acid further to water-soluble allantoin by the enzyme uricase and as a result serum urate levels are about 1/10 of human values [1]. Pegloticase is a pegylated uricase that reduces urate levels by increasing its metabolism and it can be used therapeutically in man [4].


The pathophysiology of hyperuricaemia and its possible relationship to cardiovascular disease, morbidity and mortality.

Gustafsson D, Unwin R - BMC Nephrol (2013)

Schematic representation of uric acid formation and elimination showing the drugs that can affect both.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3750299&req=5

Figure 1: Schematic representation of uric acid formation and elimination showing the drugs that can affect both.
Mentions: Increased cell turnover (e.g., haemolysis, tumour growth and large tumour necrosis) leads to increased production of adenosine, inosine and guanosine. These are degraded to hypoxantine and xanthine, which are the substrates for the widely distributed xanthine oxidase (XO) in the formation of uric acid (Figure 1). Allopurinol and febuxostat are inhibitors of XO and reduce uric acid formation. In man and some higher primates, uric acid is the end-product of purine metabolism. However, most mammals can degrade uric acid further to water-soluble allantoin by the enzyme uricase and as a result serum urate levels are about 1/10 of human values [1]. Pegloticase is a pegylated uricase that reduces urate levels by increasing its metabolism and it can be used therapeutically in man [4].

Bottom Line: High levels are causative in gout and urolithiasis.Hyperuricaemia has also been implicated in the pathophysiology of hypertension, chronic kidney disease (CKD), congestive heart failure (CHF), the metabolic syndrome, type 2 diabetes mellitus (T2DM), and atherosclerosis, with or without cardiovascular events.This article briefly reviews uric acid metabolism and summarizes the current literature on hyperuricaemia in cardiovascular disease and related co-morbidities, and emerging treatment options.

View Article: PubMed Central - HTML - PubMed

Affiliation: Bioscience, CVMD iMED, AstraZeneca R&D Mölndal, Mölndal, Sweden. david.gustafsson@astrazeneca.com

ABSTRACT
Uric acid is the end product of purine metabolism in humans. High levels are causative in gout and urolithiasis. Hyperuricaemia has also been implicated in the pathophysiology of hypertension, chronic kidney disease (CKD), congestive heart failure (CHF), the metabolic syndrome, type 2 diabetes mellitus (T2DM), and atherosclerosis, with or without cardiovascular events. This article briefly reviews uric acid metabolism and summarizes the current literature on hyperuricaemia in cardiovascular disease and related co-morbidities, and emerging treatment options.

Show MeSH
Related in: MedlinePlus