Aim: We evaluated the long-term effects of olmesartan, an angiotensin type 1 receptor blocker, in patients with non-alcoholic steatohepatitis (NASH) complicated with hypertension. Methods: All patients were given a st...Aim: We evaluated the long-term effects of olmesartan, an angiotensin type 1 receptor blocker, in patients with non-alcoholic steatohepatitis (NASH) complicated with hypertension. Methods: All patients were given a standard calorie diet and exercise counseling more than 3 months before the treatment. Seven patients with NASH received olmesartan treatment for 1 year. Liver biopsy, clinical parameters and blood markers of hepatic fibrosis, including serum hyaluronic acid, type IV collagen, and procollagen III N-terminal propeptide levels, were also examined at the beginning and the end of the study. Results: The median dose of the final administration was 20 mg (range, 10 - 40 mg). Olmesartan reduced MAP by –11.3 ± 13.0% (P = 0.046) after 1 year. In the laboratory data, serum AST, ALT, and ferritin significantly decreased after a year of administration (AST, 62 ± 24 vs. 39 ± 20 IU/L, P = 0.018;ALT, 106 ± 79 vs. 55 ± 35 IU/L, P = 0.043;ferritin, 323.8 ± 252.8 vs. 202.3 ± 194.1 ng/ml, P = 0.028). Furthermore, fasting glucose significantly decreased. However, transforming growth factor-beta1, the serum concentration of the fibrosis markers, and all histological features were unchanged at the end of the study. No side effects of the treatment were noted at any time during the study. Conclusion: Olmesartan significantly reduced blood pressure, fasting glucose, aminotransferase, and serum ferritin but could not suppress the hepatic fibrosis markers or histological features after 1 year. Therefore, olmesartan is advisable only for its anti-inflammatory effect in patients with NASH-complicated hypertension.展开更多
文摘Aim: We evaluated the long-term effects of olmesartan, an angiotensin type 1 receptor blocker, in patients with non-alcoholic steatohepatitis (NASH) complicated with hypertension. Methods: All patients were given a standard calorie diet and exercise counseling more than 3 months before the treatment. Seven patients with NASH received olmesartan treatment for 1 year. Liver biopsy, clinical parameters and blood markers of hepatic fibrosis, including serum hyaluronic acid, type IV collagen, and procollagen III N-terminal propeptide levels, were also examined at the beginning and the end of the study. Results: The median dose of the final administration was 20 mg (range, 10 - 40 mg). Olmesartan reduced MAP by –11.3 ± 13.0% (P = 0.046) after 1 year. In the laboratory data, serum AST, ALT, and ferritin significantly decreased after a year of administration (AST, 62 ± 24 vs. 39 ± 20 IU/L, P = 0.018;ALT, 106 ± 79 vs. 55 ± 35 IU/L, P = 0.043;ferritin, 323.8 ± 252.8 vs. 202.3 ± 194.1 ng/ml, P = 0.028). Furthermore, fasting glucose significantly decreased. However, transforming growth factor-beta1, the serum concentration of the fibrosis markers, and all histological features were unchanged at the end of the study. No side effects of the treatment were noted at any time during the study. Conclusion: Olmesartan significantly reduced blood pressure, fasting glucose, aminotransferase, and serum ferritin but could not suppress the hepatic fibrosis markers or histological features after 1 year. Therefore, olmesartan is advisable only for its anti-inflammatory effect in patients with NASH-complicated hypertension.
