Diet and medication in the treatment of hyperuricemia in hypertensive patients

Peixoto, Maria do Rosário Gondim; Monego, Estelamaris Tronco; Jardim, Paulo César Brandão Veiga; Carvalho, Magna Maria; Sousa, Ana Luíza Lima; Oliveira, Jonivan Siqueira de; Neto, Otávio Balestra

doi:10.1590/s0066-782x2001000600004

Cited by 25 publications

(16 citation statements)

References 13 publications

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“…Values greater than 6%, 3%, 4%, and 20% were considered to be increased for FEK, FECa, FEMg, and FEP, respectively. 11 Continuous variables are expressed as the mean ± standard deviation (SD), while categorical variables are displayed as frequencies. Statistical analyses included bivariate correlation using Deming linear regression, univariate and multivariate linear regression, and Student t-test.…”

Section: Methodsmentioning

confidence: 99%

Causes of Hypouricemia Among Outpatients

Buğdaycı¹,

Balaban²,

Şahin³

2008

Laboratory Medicine

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Section: Methodsmentioning

confidence: 99%

Causes of Hypouricemia Among Outpatients

Buğdaycı¹,

Balaban²,

Şahin³

2008

Laboratory Medicine

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“…[132][133][134][135] A diet low in purines may decrease sUA levels comparably to lowdose allopurinol (150-300 mg/d); however, such a diet is not very appealing to many patients and is often unsuccessful. 136 Regular intake of low-fat dairy products decreases the risk of gout by ∼40%. 133 Vitamin C supplementation (500 mg) has also been reported to reduce sUA levels.…”

Section: Diet and Lifestyle Management-a Complementary Approachmentioning

confidence: 99%

Managing Your Patient with Gout: A Review of Treatment Options

Doghramji¹

2011

Postgraduate Medicine

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Gout is an inflammatory arthritis that typically presents as acute onset, recurrent, monoarticular pain. In most patients, management of pain, risk assessment for future flares, and disability is not optimal and diagnostic and management approaches are applied inconsistently. Obtaining an accurate patient history, including comorbidities, concomitant medications, and familial history, is important for optimal results. Recognizing the acute flare in the patient at risk and establishing a definitive diagnosis of gout should be conducted promptly. Therapeutic options appropriate for treating the acute flare include colchicine, nonsteroidal anti-inflammatory drugs, and corticosteroids. After flare remission, prophylaxis with a flare prevention medication, such as colchicine, should be administered followed by initiation of urate-lowering therapy with allopurinol or febuxostat. Patient education, especially counseling on risk factors and contributors to hyperuricemia and gout, can improve the likelihood of successful therapy for this often suboptimally managed disease.

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“…At physiological pH, almost all UA is ionized to urate and has a single negative charge [10]. Serum levels of UA are correlated with changes in the amounts of dietary purine consumed [14]. Due to urate's limited solubility in water, excess production in vivo can lead to its crystallization out of solution (e.g.…”

mentioning

confidence: 99%

Uric Acid and Oxidative Stress

Glantzounis

Tsimoyiannis²,

Kappas³

et al. 2005

CPD

793

555

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Uric acid is the final product of purine metabolism in humans. The final two reactions of its production catalyzing the conversion of hypoxanthine to xanthine and the latter to uric acid are catalysed by the enzyme xanthine oxidoreductase, which may attain two inter-convertible forms, namely xanthine dehydrogenase or xanthine oxidase. The latter uses molecular oxygen as electron acceptor and generates superoxide anion and other reactive oxygen products. The role of uric acid in conditions associated with oxidative stress is not entirely clear. Evidence mainly based on epidemiological studies suggests that increased serum levels of uric acid are a risk factor for cardiovascular disease where oxidative stress plays an important pathophysiological role. Also, allopurinol, a xanthine oxidoreductase inhibitor that lowers serum levels of uric acid exerts protective effects in situations associated with oxidative stress (e.g. ischaemia-reperfusion injury, cardiovascular disease). However, there is increasing experimental and clinical evidence showing that uric acid has an important role in vivo as an antioxidant. This review presents the current evidence regarding the antioxidant role of uric acid and suggests that it has an important role as an oxidative stress marker and a potential therapeutic role as an antioxidant. Further well designed clinical studies are needed to clarify the potential use of uric acid (or uric acid precursors) in diseases associated with oxidative stress.

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Diet and medication in the treatment of hyperuricemia in hypertensive patients

Abstract: Objective -To evaluate the effects of diet and medication, either isolated or associated, on serum levels of uric acid in patients with hyperuricemia. Methods -

Cited by 25 publications

References 13 publications

Causes of Hypouricemia Among Outpatients

Causes of Hypouricemia Among Outpatients

Managing Your Patient with Gout: A Review of Treatment Options

Uric Acid and Oxidative Stress

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