OBJECTIVES: The inhibition of the renin-angiotensin system and of the 3-hydroxy-3-methylglutaryl-coenzyme A reductase could improve hepatic steatosis. The aim of this study was to evaluate the effects of losartan or amlodipine alone or combined with simvastatin on hepatic steatosis degree, and on insulin sensitivity in normocholesterolemic, hypertensive patients with nonalcoholic hepatic steatosis. METHODS: Patients were treated with losartan, 100 mg/day, or amlodipine, 10 mg/day, for 6 months; subsequently simvastatin, 20 mg/day was added to both treatments for a further 6 months. The patients performed an ultrasound examination [steatosis degree, subcutaneous adipose tissue (SAT) and visceral adipose tissue (VAT) diameter], an euglycemic hyperinsulinemic clamp [glucose infusion rate (GIR)], and a blood sample (fasting plasma glucose, fasting plasma insulin, triglycerides, and inflammatory parameters) at baseline, and after 6 and 12 months, respectively. RESULTS: Both losartan and amlodipine induced a significant and similar systolic blood pressure/diastolic blood pressure reduction (P<0.001 vs. baseline). Losartan significantly increased GIR (P<0.05 vs. baseline) compared with amlodipine therapy, and the addition of simvastatin to losartan further increased GIR compared with the simvastatin added to amlodipine therapy (P<0.01 and P<0.05 vs. baseline, respectively). Losartan significantly decreased the steatosis degree, SAT, and VAT diameter compared with amlodipine therapy (P<0.05 vs. baseline with losartan for all). The addition of simvastatin to losartan therapy further decreased the steatosis degree, SAT, and VAT diameter. CONCLUSION:Losartan and simvastatin combination significantly improved the hepatic steatosis indices compared with amlodipine and simvastatin combination.
RCT Entities:
OBJECTIVES: The inhibition of the renin-angiotensin system and of the 3-hydroxy-3-methylglutaryl-coenzyme A reductase could improve hepatic steatosis. The aim of this study was to evaluate the effects of losartan or amlodipine alone or combined with simvastatin on hepatic steatosis degree, and on insulin sensitivity in normocholesterolemic, hypertensivepatients with nonalcoholic hepatic steatosis. METHODS:Patients were treated with losartan, 100 mg/day, or amlodipine, 10 mg/day, for 6 months; subsequently simvastatin, 20 mg/day was added to both treatments for a further 6 months. The patients performed an ultrasound examination [steatosis degree, subcutaneous adipose tissue (SAT) and visceral adipose tissue (VAT) diameter], an euglycemic hyperinsulinemic clamp [glucose infusion rate (GIR)], and a blood sample (fasting plasma glucose, fasting plasma insulin, triglycerides, and inflammatory parameters) at baseline, and after 6 and 12 months, respectively. RESULTS: Both losartan and amlodipine induced a significant and similar systolic blood pressure/diastolic blood pressure reduction (P<0.001 vs. baseline). Losartan significantly increased GIR (P<0.05 vs. baseline) compared with amlodipine therapy, and the addition of simvastatin to losartan further increased GIR compared with the simvastatin added to amlodipine therapy (P<0.01 and P<0.05 vs. baseline, respectively). Losartan significantly decreased the steatosis degree, SAT, and VAT diameter compared with amlodipine therapy (P<0.05 vs. baseline with losartan for all). The addition of simvastatin to losartan therapy further decreased the steatosis degree, SAT, and VAT diameter. CONCLUSION:Losartan and simvastatin combination significantly improved the hepatic steatosis indices compared with amlodipine and simvastatin combination.
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