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P-440: Losartan but not irbesartan reduces serum uric acid in hypertensive patients with hyperuricemia and/or gout

Wuerzner, Grégoire ; Chioléro, Arnaud ; Maillard, Marc P. ; Gerster, Charles A. ; Burnier, Michel

In: American Journal of Hypertension, 2001, vol. 14, no. S1, p. 179A-179A

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    Titre
    • P-440: Losartan but not irbesartan reduces serum uric acid in hypertensive patients with hyperuricemia and/or gout
    Auteur
    • Wuerzner, Grégoire. Division of Hypertension and Vascular Medicine and Division of Rheumatology, Lausanne University Hospital, Lausanne, Switzerland
    • Chioléro, Arnaud. Division of Hypertension and Vascular Medicine and Division of Rheumatology, Lausanne University Hospital, Lausanne, Switzerland
    • Maillard, Marc P.. Division of Hypertension and Vascular Medicine and Division of Rheumatology, Lausanne University Hospital, Lausanne, Switzerland
    • Gerster, Charles A.. Division of Hypertension and Vascular Medicine and Division of Rheumatology, Lausanne University Hospital, Lausanne, Switzerland
    • Burnier, Michel. Division of Hypertension and Vascular Medicine and Division of Rheumatology, Lausanne University Hospital, Lausanne, Switzerland
    Type de document
    • Postprint
    Langue
    • Anglais
    Publié dans
    • American Journal of Hypertension, 2001, vol. 14, no. S1, p. 179A-179A. Oxford University Press
    Autre version électronique
    Identifiant OAI-PMH
    • oai:doc.rero.ch:289751
    Summary
    Losartan has unique uricosuric properties and has been shown to decrease serum uric acid (SUA) levels in normal subjects as well as in hypertensive patients. The purpose of the present study was to compare the effects of losartan and irbesartan on serum uric acid in hypertensive hyperuricemic patients with or without gout. Twelve hyperuricemic (SUA>420mmol/L), hypertensive patients (mean age: 58 yr) participated in this randomized, double-blind, crossover study. After a 3-week run-in period during which patients received enalapril 20 mg o.d, patients were randomized to receive either losartan 50 mg o.d for 4 weeks followed by losartan 50 mg bid for another 4 week period or irbesartan 150 mg o.d followed by irbesartan 150 mg bid for 4 weeks. The losartan and irbesartan phases were separated by 3 weeks of the ACE inhibitor. All drugs were provided in an electronic pill container allowing to monitor compliance (MEMS system). Losartan decreased SUA significantly from 539±28 mmol/L to 490±22 mmol/L (p<0.01) at 50 mg od and to 482±28 mmol/L at 50 mg bid, in contrast to irbesartan which had no effect on SUA. The first dose of losartan increased the urinary uric acid/creatinine ratio during the first 4h after drug intake, when compared with irbesartan (0.545±0.074 vs 0.361±0.049, p=0.016). This increase was still present at week 4 (0.494±0.092 vs 0.332±0.062, p<0.01) but was not found at week 8 when patients received a bid regimen (0.284±0.031 vs 0.329±0.032,p=ns). The monitoring of compliance showed that the adherence to the morning dose was good (90.4±1.7%) and significantly greater than that to the evening dose (81.30±2.2%, p<0.001). The changes in blood pressure induced by losartan and irbesartan were comparable. These results demonstrate the potential benefits of using losartan in hypertensive patients with hyperuricemia and gout. They also suggest that losartan-treated patients reach a new uric acid steady-state during a sustained administration (>1 month). Hence, the uricosuric effect tends to decrease with time as SUA is reduced. Increasing the dose of losartan to 50 mg bid does not appear to induce a further decrease in serum uric acid