Pilot Study of Atorvastatin Treatment in NAFLD
Pilot Study of Atorvastatin Treatment in NAFLD
Background: Non-alcoholic fatty liver disease (NAFLD) encompasses a wide spectrum of liver injury. Currently, there are no proven effective therapies available. Atorvastatin is a new 3-hydroxy-3-metylglutaryl coenzyme A reductase inhibitor that reduces lipid serum levels.
Aim: To evaluate the effectiveness and safety of atorvastatin in dyslipemid, non-alcoholic fatty liver patients.
Patients and methods: We prospectively enrolled 25 patients with NAFLD; 22 of them completed the study. Body mass index, serum lipids, liver function tests and liver density assessed by echography were measured at baseline and after 1, 3, 6, 9 and 12 months of treatment. Normalization of transaminases and/or improvement in liver density were treatment end points. Patients received atorvastatin (1080 mg/daily) according to basal serum cholesterol levels; additionally, they were given standard weight-loss counselling and encouraged to follow a low fat diet.
Results: All 22 patients (14 men, mean age 47 ± 10 years) had high cholesterol levels at baseline and 11 (44%) also presented high trygliceride levels. After 6 months of treatment, eight patients (36.3%) presented normal transaminase levels. The remaining patients continued treatment for 12 months when 20% of patients presented with normal transaminase levels, while the other patients showed a 10% reduction in basal levels. Mean cholesterol levels were 268.5 ± 44.2 and 186.8 ± 14.4 mg/dL before and after treatment, respectively (P < 0.05). The mean body mass index was 27.4 ± 3.1 at baseline and 26.3 ± 2.8 kg/cm at the end of treatment (P > 0.05). No side effects were reported.
Conclusions: Serum aminotransferase and lipid levels were reduced significantly in all patients with atorvastatin treatment. Therapy with atorvastatin in NAFLD patients with hyperlipidemia was found to be both effective and safe.
Non-alcoholic fatty liver disease (NAFLD) encompasses a range of progressive conditions. Its natural history is not yet well understood, but it is currently believed that patients with steatosis alone rarely deteriorate over time, and has been demonstrated with the increasing incidence of obesity and diabetes in Western countries, NAFLD has become a growing problem. Although its true prevalence is unknown, some estimates suggest that it might affect one-third of American adults a figure also suggested for Europe and Japan.
Non-alcoholic fatty liver disease, is the hepatic manifestation of the metabolic syndrome that encompasses central obesity, hypertension, hypertriglyceridaemia, low levels of high-density lipoprotein cholesterol and hyperglycaemia. The pathogenesis of NAFLD includes two steps: first, the healthy liver becomes steatotic; then, the second step is elicited by oxidative stress and cytokine synthesis. This leads to exacerbation of insulin resistance, followed by oxidative stress and organelle dysfunction within liver cells, resulting in an inflammatory process, hepatocellular degeneration and fibrosis.
Currently, there are no proven effective therapies available for the treatment of NAFLD and strategies have mainly led to treat or control underlying risk factors. Promising pharmacological treatments have been observed with the use of antioxidants, insulin sensitizers, hepatoprotectants or lipid-lowering agents. Therapeutic results have been demonstrated with multiple agents and currently larger randomized trials are underway; these will hopefully clarify the role of specific pharmacological treatments. Control of hyperlipaemia with hypolipaemic drugs is controversial in these patients. Approximately 80% have elevated cholesterol and triglyceride serum levels. Controlling elevated levels of cholesterol and triglycerides with diet, exercise and cholesterol-lowering medications may help to stabilize or reverse NAFLD. Atorvastatin, an inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase, catalyses the conversion of HMG-CoA to mevalonate, an early and rate-limiting step in cholesterol biosynthesis. The aim of our pilot study was to evaluate the effectiveness and safety of atorvastatin in the treatment of patients with NAFLD.
Background: Non-alcoholic fatty liver disease (NAFLD) encompasses a wide spectrum of liver injury. Currently, there are no proven effective therapies available. Atorvastatin is a new 3-hydroxy-3-metylglutaryl coenzyme A reductase inhibitor that reduces lipid serum levels.
Aim: To evaluate the effectiveness and safety of atorvastatin in dyslipemid, non-alcoholic fatty liver patients.
Patients and methods: We prospectively enrolled 25 patients with NAFLD; 22 of them completed the study. Body mass index, serum lipids, liver function tests and liver density assessed by echography were measured at baseline and after 1, 3, 6, 9 and 12 months of treatment. Normalization of transaminases and/or improvement in liver density were treatment end points. Patients received atorvastatin (1080 mg/daily) according to basal serum cholesterol levels; additionally, they were given standard weight-loss counselling and encouraged to follow a low fat diet.
Results: All 22 patients (14 men, mean age 47 ± 10 years) had high cholesterol levels at baseline and 11 (44%) also presented high trygliceride levels. After 6 months of treatment, eight patients (36.3%) presented normal transaminase levels. The remaining patients continued treatment for 12 months when 20% of patients presented with normal transaminase levels, while the other patients showed a 10% reduction in basal levels. Mean cholesterol levels were 268.5 ± 44.2 and 186.8 ± 14.4 mg/dL before and after treatment, respectively (P < 0.05). The mean body mass index was 27.4 ± 3.1 at baseline and 26.3 ± 2.8 kg/cm at the end of treatment (P > 0.05). No side effects were reported.
Conclusions: Serum aminotransferase and lipid levels were reduced significantly in all patients with atorvastatin treatment. Therapy with atorvastatin in NAFLD patients with hyperlipidemia was found to be both effective and safe.
Non-alcoholic fatty liver disease (NAFLD) encompasses a range of progressive conditions. Its natural history is not yet well understood, but it is currently believed that patients with steatosis alone rarely deteriorate over time, and has been demonstrated with the increasing incidence of obesity and diabetes in Western countries, NAFLD has become a growing problem. Although its true prevalence is unknown, some estimates suggest that it might affect one-third of American adults a figure also suggested for Europe and Japan.
Non-alcoholic fatty liver disease, is the hepatic manifestation of the metabolic syndrome that encompasses central obesity, hypertension, hypertriglyceridaemia, low levels of high-density lipoprotein cholesterol and hyperglycaemia. The pathogenesis of NAFLD includes two steps: first, the healthy liver becomes steatotic; then, the second step is elicited by oxidative stress and cytokine synthesis. This leads to exacerbation of insulin resistance, followed by oxidative stress and organelle dysfunction within liver cells, resulting in an inflammatory process, hepatocellular degeneration and fibrosis.
Currently, there are no proven effective therapies available for the treatment of NAFLD and strategies have mainly led to treat or control underlying risk factors. Promising pharmacological treatments have been observed with the use of antioxidants, insulin sensitizers, hepatoprotectants or lipid-lowering agents. Therapeutic results have been demonstrated with multiple agents and currently larger randomized trials are underway; these will hopefully clarify the role of specific pharmacological treatments. Control of hyperlipaemia with hypolipaemic drugs is controversial in these patients. Approximately 80% have elevated cholesterol and triglyceride serum levels. Controlling elevated levels of cholesterol and triglycerides with diet, exercise and cholesterol-lowering medications may help to stabilize or reverse NAFLD. Atorvastatin, an inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase, catalyses the conversion of HMG-CoA to mevalonate, an early and rate-limiting step in cholesterol biosynthesis. The aim of our pilot study was to evaluate the effectiveness and safety of atorvastatin in the treatment of patients with NAFLD.
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