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AT1 blockers and uric acid metabolism: are there relevant differences?

Juan Puig, Rosa J. Torres, Luis Miguel Ruilope

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Abstract

BACKGROUND: Serum urate is commonly elevated in essential hypertension (26-33%). Some studies have claimed that losartan increases urinary uric acid excretion and diminishes serum urate levels. However, a detailed, controlled study on the influence of losartan on uric acid metabolism in hypertensive patients has not been performed and the existent results are conflicting. Two small studies claimed that losartan reduced serum urate levels but only one showed a simultaneous increased uric acid excretion rate. The development of several AT1 receptor blockers raises the question whether these antihypertensive drugs influence uric acid metabolism. STUDY: In a randomized, prospective (4 weeks), double blind, parallel study we have compared the influence of losartan (50 mg/day) versus eprosartan (600 mg/day) on uric acid metabolism in 58 patients with mild to moderate essential hypertension. The mean uric acid to creatinine ratio change from baseline at 4 weeks was +0.11 for losartan and -0.04 for eprosartan (P < 0.01). The mean increase in 24-h urinary uric acid excretion with losartan was +0.7 mmol/24 h (25% increase from baseline). The change in serum urate levels versus baseline was similar after 4 weeks with losartan (-23.4 mumol/l) and eprosartan (-19.5 mumol/l). Patients with hyperuricemia in both treatment groups showed similar modifications of uric acid metabolism compared with non-hyperuricemic subjects. Blood pressure control was achieved in 22 patients (73%) with eprosartan and in 16 (53%) with losartan. CONCLUSIONS: Losartan increased uric acid excretion in hypertensive patients but eprosartan did not. Neither AT1 receptor antagonist substantially modified serum urate concentrations.

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What this paper is about

BACKGROUND: Serum urate is commonly elevated in essential hypertension (26-33%). Some studies have claimed that losartan increases urinary uric acid excretion and diminishes serum urate levels. However, a detailed, controlled study on the influence of losartan on uric acid metabolism in hypertensive patients has not been performed and the existent results are conflicting. Two small studies claimed that losartan reduced serum urate levels but only one showed a simultaneous increased uric acid excretion rate. The development of several AT1 receptor blockers raises the question whether these antihypertensive drugs influence uric acid metabolism. STUDY: In a randomized, prospective (4 weeks), double blind, parallel study we have compared the influence of losartan (50 mg/day) versus eprosartan (600 mg/day) on uric acid metabolism in 58 patients with mild to moderate essential hypertension. The mean uric acid to creatinine ratio change from baseline at 4 weeks was +0.11 for losartan and -0.04 for eprosartan (P < 0.01). The mean increase in 24-h urinary uric acid excretion with losartan was +0.7 mmol/24 h (25% increase from baseline). The change in serum urate levels versus baseline was similar after 4 weeks with losartan (-23.4 mumol/l) and eprosartan (-19.5 mumol/l). Patients with hyperuricemia in both treatment groups showed similar modifications of uric acid metabolism compared with non-hyperuricemic subjects. Blood pressure control was achieved in 22 patients (73%) with eprosartan and in 16 (53%) with losartan. CONCLUSIONS: Losartan increased uric acid excretion in hypertensive patients but eprosartan did not. Neither AT1 receptor antagonist substantially modified serum urate concentrations.

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Available abstract

BACKGROUND: Serum urate is commonly elevated in essential hypertension (26-33%). Some studies have claimed that losartan increases urinary uric acid excretion and diminishes serum urate levels. However, a detailed, controlled study on the influence of losartan on uric acid metabolism in hypertensive patients has not been performed and the existent results are conflicting. Two small studies claimed that losartan reduced serum urate levels but only one showed a simultaneous increased uric acid excretion rate. The development of several AT1 receptor blockers raises the question whether these antihypertensive drugs influence uric acid metabolism. STUDY: In a randomized, prospective (4 weeks), double blind, parallel study we have compared the influence of losartan (50 mg/day) versus eprosartan (600 mg/day) on uric acid metabolism in 58 patients with mild to moderate essential hypertension. The mean uric acid to creatinine ratio change from baseline at 4 weeks was +0.11 for losartan and -0.04 for eprosartan (P < 0.01). The mean increase in 24-h urinary uric acid excretion with losartan was +0.7 mmol/24 h (25% increase from baseline). The change in serum urate levels versus baseline was similar after 4 weeks with losartan (-23.4 mumol/l) and eprosartan (-19.5 mumol/l). Patients with hyperuricemia in both treatment groups showed similar modifications of uric acid metabolism compared with non-hyperuricemic subjects. Blood pressure control was achieved in 22 patients (73%) with eprosartan and in 16 (53%) with losartan. CONCLUSIONS: Losartan increased uric acid excretion in hypertensive patients but eprosartan did not. Neither AT1 receptor antagonist substantially modified serum urate concentrations.

Key concepts: Losartan, Uric acid, Hyperuricemia, Medicine, Internal medicine, Endocrinology, Excretion, Angiotensin II receptor antagonist

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