The effects of the addition of losartan on uric acid metabolism in patients receiving indapamide

Nikas, Spyros N.; Rizos, Evagelos; Milionis, Haralampos; Bairaktari, Eleni; Kalaitzidis, Rigas; Siamopoulos, Kostas C.; Elisaf, Moses

doi:10.3317/jraas.2000.045

Cited by 11 publications

(4 citation statements)

References 14 publications

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“…However, the combination treatment significantly decreased SUA levels (from 5.9 ± 1.2 to 5.0 ± 1.1 mg/dl; 0.35 ± 0.07 to 0.30 ± 0.07 mmol/l, p < 0.01). This was mainly due to a significant increase in the fractional excretion of urate (from 7.0% ± 5.5% to 8.7% ± 6.0%, p < 0.05) [47,48]. Thus, losartan can blunt the hyperuricaemia induced by diuretics.…”

Section: Losartan and Other Angiotensin II Receptor Blockersmentioning

confidence: 91%

“…HCTZ), thus alleviating the diuretic-induced elevation in SUA levels [6,45,46]. We studied [47] the effect of indapamide (2.5 mg once daily) alone and in combination with losartan (50 mg once daily) in 20 hypertensive patients. Metabolic parameters, including SUA levels were studied before and after 8 weeks of indapamide administration, as well as after the addition of losartan.…”

Section: Losartan and Other Angiotensin II Receptor Blockersmentioning

confidence: 99%

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Effect on Serum Uric Acid Levels of Drugs Prescribed for Indications other than Treating Hyperuricaemia

Daskalopoulou

Tzovaras²,

Mikhailidis³

et al. 2005

CPD

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Beyond allopurinol and the well-established uricosuric drugs, several other agents can decrease serum uric acid (SUA) levels, such as losartan, fenofibrate and some non-steroidal anti-inflammatory drugs (NSAIDs). Some of these drugs increase renal urate excretion. Hyperuricaemia and gout are common problems (at least 1% of Western men are affected by gout). Raised SUA levels increase the incidence of acute gout and renal calculi. Hyperuricaemia may also predict an increased risk of vascular events. Therefore, lowering SUA levels is of clinical relevance. In this review we consider the effect on SUA levels of drugs that are prescribed for indications other than treating hyperuricaemia. These drugs may obviate the need for specific treatment (e.g. allopurinol) aimed at lowering SUA levels. Furthermore, because hyperuricaemic patients may already be on several drugs (e.g. due to associated dyslipidaemia, hypertension and/or arthritis) compliance may be improved by avoiding additional medication. The potential for adverse effects associated with polypharmacy would also be decreased.

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Section: Losartan and Other Angiotensin II Receptor Blockersmentioning

confidence: 91%

Section: Losartan and Other Angiotensin II Receptor Blockersmentioning

confidence: 99%

Effect on Serum Uric Acid Levels of Drugs Prescribed for Indications other than Treating Hyperuricaemia

Daskalopoulou

Tzovaras²,

Mikhailidis³

et al. 2005

CPD

View full text Add to dashboard Cite

show abstract

“…Furthermore, drugs, such as losartan and fenofibrate, can increase urinary urate excretion, resulting in a fall in SUA levels. [97][98][99][100] There is also evidence [101][102][103][104][105][106][107] that statins (atorvastatin, simvastatin) can reduce SUA levels.…”

Section: Management Of Other Metabolic Abnormalities Associated With the Metabolic Syndromementioning

confidence: 99%

Prevention and Treatment of the Metabolic Syndrome

2004

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The prevalence of the metabolic syndrome is increasing owing to lifestyle changes leading to obesity. This syndrome is a complex association of several interrelated abnormalities that increase the risk for cardiovascular disease and progression to diabetes mellitus (DM). Insulin resistance is the key factor for the clustering of risk factors characterizing the metabolic syndrome. The National Cholesterol Education Program (NCEP) Adult Treatment Panel (ATP) III defined the criteria for the diagnosis of the metabolic syndrome and established the basic principles for its management. According to these guidelines, treatment involves the improvement of the underlying insulin resistance through lifestyle modification (eg, weight reduction and increased physical activity) and possibly by drugs. The coexistent risk factors (mainly dyslipidemia and hypertension) should also be addressed. Since the main goal of lipid-lowering treatment is to achieve the NCEP low-density lipoprotein cholesterol (LDL-C) target, statins are a good option. However, fibrates (as monotherapy or in combination with statins) are useful for the treatment of the metabolic syndrome that is commonly associated with hypertriglyceridemia and decreased high-density lipoprotein cholesterol (HDL-C) levels. The blood pressure target is < 140/90 mm Hg. The effect on carbohydrate homeostasis should possibly be taken into account in selecting an antihypertensive drug. Patients with the metabolic syndrome commonly have other less well-defined metabolic abnormalities (eg, hyperuricemia and raised C-reactive protein levels) that may also be associated with an increased cardiovascular risk. It seems appropriate to manage these abnormalities. Drugs that beneficially affect carbohydrate metabolism and delay or even prevent the onset of DM (eg, thiazolidinediones or acarbose) could be useful in patients with the metabolic syndrome. Furthermore, among the more speculative benefits of treatment are improved liver function in nonalcoholic fatty liver disease and a reduction in the risk of acute gout.

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“…80 Losartan can attenuate the increases in serum uric acid levels occurring with hydrochlorothiazide or indapamide. [81][82][83] The mechanism by which losartan increased uric acid secretion appears to involve a reduction in the postsecretory reabsorption of uric acid in the proximal tubule of the kidney. 60 Studies using human proximal brush border membrane vesicles indicate that tubular secretion and reabsorption of urate are mediated via a urate/anion exchanger and a urate voltage-sensitive transporter.…”

Section: Effects Of Arbs On Uric Acidmentioning

confidence: 99%

Review: Molecular-specific effects of angiotensin II antagonists: clinical relevance to treating hypertension?

Reid

2005

J Renin Angiotensin Aldosterone Syst

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Angiotensin II receptor blockers (ARBs) may produce a number of molecule-specific effects that appear to be independent of interaction with the angiotensin II type 1 (AT 1) -receptor. These include antagonism of the thromboxane A 2 receptor, inhibition of platelet aggregation, induction of peroxisome proliferatoractivated receptor gamma (PPARγ) activity, and reduction of serum uric acid levels. However, definitive evidence is lacking that these moleculespecific effects give rise to a therapeutic advantage of one ARB over another. Currently, the possibility of a link between a molecule-specific effect of an ARB and an improvement in clinical outcomes is best illustrated by a reduction in serum uric acid levels with losartan. Data from Losartan Intervention For Endpoint reduction in hypertension (LIFE) study suggest a treatment-induced decrease in serum uric acid may contribute to the treatment benefit of a losartan-based versus atenolol-based therapy on the composite endpoint (death, myocardial infarction, or stroke). This finding should prompt further studies to investigate the long-term cardioprotective benefits issue of reducing hyperuricaemia in hypertensive patients. IntroductionAngiotensin II receptor blockers (ARBs) are widely used to treat patients with hypertension, heart failure, and diabetic nephropathy.1-4 While most beneficial cardiovascular (CV) effects of ARBs are attributed to blockade of the angiotensin II type 1 (AT 1 )-receptor, it is becoming increasingly apparent that members of the ARB class also possess molecule-specific-effects that are potentially beneficial or harmful but appear unrelated to the blockade of the AT 1 -receptor.A variety of AT 1 -receptor-independent effects of ARBs have been described, including antagonism of the thromboxane A 2 receptor, inhibition of platelet aggregation, induction of peroxisome proliferator-activated receptor gamma (PPARγ) activity, and reduction of serum uric acid levels, as well as inhibition of prostaglandin production, stimulation of nitric oxide (NO) synthesis, blockade of the tachykinin receptor, and antagonism of the imidazoline/guanidinium receptor.

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The effects of the addition of losartan on uric acid metabolism in patients receiving indapamide

Abstract: The addition of losartan could offset the hyperuricaemic effect of indapamide administration.

Cited by 11 publications

References 14 publications

Effect on Serum Uric Acid Levels of Drugs Prescribed for Indications other than Treating Hyperuricaemia

Effect on Serum Uric Acid Levels of Drugs Prescribed for Indications other than Treating Hyperuricaemia

Prevention and Treatment of the Metabolic Syndrome

Review: Molecular-specific effects of angiotensin II antagonists: clinical relevance to treating hypertension?

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