Hyperuricemia and cardiovascular risk
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REVIEW ARTICLE
Hyperuricemia and cardiovascular risk Davide Grassi • Giovambattista Desideri • Anna Vittoria Di Giacomantonio • Paolo Di Giosia Claudio Ferri
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Received: 10 December 2013 / Accepted: 7 February 2014 Ó Springer International Publishing Switzerland 2014
Abstract There is an increasing prevalence of gout and hyperuricemia worldwide. Gout confers a significant individual and social burden and is increasingly recognized as a prevalent chronic disease state requiring appropriate long-term management. Gout and hyperuricemia appear to be independent risk factors for incident hypertension, renal disease and cardiovascular disease. Multiple epidemiologic studies confirm an association between hyperuricemia and ‘‘cardiometabolic disease’’. We review the evidence stating the relationship between hyperuricemia and the development of comorbid conditions contributing to cardiovascular risk and disease. Keywords Uric acid Hypertension Cardiovascular risk Metabolic risk
1 Introduction Uric acid is the end product of purine metabolism in humans. Sources of purines are either endogenous, from de novo synthesis or nucleic acid breakdown (approximately 600 mg/day), or exogenous, from dietary purine intake (approximately 100 mg/day) [1–3]. De novo synthesis of purines depends on the compound 5-phosphoribosyl-l-pyrophosphate, which is enzymatically converted to inosinic acid. In turn, it can additionally be converted into bases for formation of nucleic acids or be
D. Grassi (&) G. Desideri A. V. Di Giacomantonio P. Di Giosia C. Ferri Department of Life, Health and Environmental Sciences, University of L’Aquila, Viale S Salvatore, Delta 6 Medicina, 67100 Coppito L’Aquila, Italy e-mail: [email protected]
broken down into xanthine to form uric acid [1–4]. Uric acid is the final product of purine nucleotides metabolism, in mammalians uricase in the liver converts urate into allantoin, substantially reducing uric acid plasma levels. Finally, uric acid is eliminated by the kidney [1–4]. Hyperuricaemia can be due to increased urate production, decreased excretion, or both. Hyperuricemia is common in the general population and is often caused by a combination of a high purine diet, alcohol use, diuretic therapy, and reduced renal clearance. In particular, alcohol is able to increase the production of uric acid and to impair its renal excretion [4–6]. When the blood level of urate goes beyond the physiologic limit of solubility, it may crystallize into monosodium urate in the tissues and cause gout. Gout is a debilitating form of chronic inflammatory arthritis, caused by deposition of monosodium urate crystals in synovial fluid and other tissues. It affects at least 1–2 % of the population in Western countries and is the most common inflammatory joint disease in men older than 40 years of age [1, 6, 7]. It may lead to a significant reduction of health-related quality of life and people suffering from recurrent attacks frequently report pain and disability, reduced productivity and increased morbidity
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