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Fenofibrate (By mouth)

Lowers high cholesterol and triglyceride levels.

What works?

Learn more about the effects of these drugs. The most reliable research is summed up for you in our featured article.

Fenofibrate is used together with a proper diet to treat high cholesterol and triglyceride (fat-like substances) levels in the blood. This may help prevent the development of pancreatitis (inflammation or swelling of the pancreas) caused by high levels of triglycerides in the blood. This medicine is available only with your doctor's prescription… Read more
Brand names include
Antara, Fenoglide, Lipofen, Lofibra, Tricor, Triglide
Drug classes About this
Antihyperlipidemic

What works? Research summarized

Evidence reviews

Effects of fenofibrate on kidney function: a meta-analysis

Bibliographic details: Xu C, Yuan ZJ, Zhu J.  Effects of fenofibrate on kidney function: a meta-analysis. Chinese Journal of Evidence-Based Medicine 2013; 13(11): 1361-1366 Available from: http://www.cjebm.org.cn/oa/DArticle.aspx?type=view&id=20131116

[A meta-analysis on the safety of combination therapy with fenofibrate and statins]

OBJECTIVE: The aim of this study was to assess the safety of fenofibrate-statin combination therapy.

Statins for non‐alcoholic steatohepatitis

Non‐alcoholic fatty liver disease (NAFLD) and non‐alcoholic steatohepatitis (NASH) in patients with no or very little alcohol consumption is characterised by hepatic histological changes similar to those associated with alcohol‐induced liver injury. A range of histological changes can be seen. Some patients have fat accumulation in hepatocytes without significant inflammation or fibrosis (simple hepatic steatosis or NAFLD), but others have hepatic steatosis with prominent necro‐inflammatory changes with or without associated fibrosis (this is NASH). Although NAFLD and NASH are common conditions, no effective medical treatment is available to correct the abnormal liver enzymes and adverse outcomes associated with them. This systematic review identified two randomised clinical trials with very small numbers of participants. One of the trials was a pilot trial and compared simvastatin with placebo, and the other trial assessed atorvastatin versus fenofibrate versus a combination of the two. The small pilot trial (n = 16 patients) assessing simvastatin versus placebo in NASH patients did not show significant effects on liver enzyme activities or liver histology. No adverse events were reported. The other trial compared atorvastatin versus fenofibrate versus a group receiving both interventions in 186 patients with NAFLD. There were no statistically significant differences between any of the three intervention groups regarding the 54 week mean activities of aspartate aminotransferase, alanine aminotransferase, gamma‐glutamyl transpeptidase, or alkaline phosphatases (liver enzymes) in the blood. The triglyceride levels seemed higher in the fenofibrate group compared with the atorvastatin group. Liver histology was not assessed in this trial. The presence of biochemical and ultrasonographic evidence of NAFLD seemed higher in the fenofibrate group compared with the other two intervention groups. Three patients discontinued treatment due to myalgia and elevated serum creatine kinase activity, one from the atorvastatin group and two from the combination group. Another patient from the atorvastatin group discontinued treatment due to raised alanine aminotransferase activity, over three times the upper normal limit. Both trials were at high risk of bias (that is, overestimation of benefits and underestimation of harms). Furthermore, the groups were small raising the risks of random errors (that is, play of chance). Accordingly, we did not find evidence to support or refute the use of statins for patients with NAFLD or NASH. Further unbiased trials with larger numbers of patients looking explicitly at patient‐related outcomes of interest (for example, quality of life, development of cirrhosis, and mortality) are needed to assess the effects of statins on NAFLD or NASH.

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Summaries for consumers

Statins for non‐alcoholic steatohepatitis

Non‐alcoholic fatty liver disease (NAFLD) and non‐alcoholic steatohepatitis (NASH) in patients with no or very little alcohol consumption is characterised by hepatic histological changes similar to those associated with alcohol‐induced liver injury. A range of histological changes can be seen. Some patients have fat accumulation in hepatocytes without significant inflammation or fibrosis (simple hepatic steatosis or NAFLD), but others have hepatic steatosis with prominent necro‐inflammatory changes with or without associated fibrosis (this is NASH). Although NAFLD and NASH are common conditions, no effective medical treatment is available to correct the abnormal liver enzymes and adverse outcomes associated with them. This systematic review identified two randomised clinical trials with very small numbers of participants. One of the trials was a pilot trial and compared simvastatin with placebo, and the other trial assessed atorvastatin versus fenofibrate versus a combination of the two. The small pilot trial (n = 16 patients) assessing simvastatin versus placebo in NASH patients did not show significant effects on liver enzyme activities or liver histology. No adverse events were reported. The other trial compared atorvastatin versus fenofibrate versus a group receiving both interventions in 186 patients with NAFLD. There were no statistically significant differences between any of the three intervention groups regarding the 54 week mean activities of aspartate aminotransferase, alanine aminotransferase, gamma‐glutamyl transpeptidase, or alkaline phosphatases (liver enzymes) in the blood. The triglyceride levels seemed higher in the fenofibrate group compared with the atorvastatin group. Liver histology was not assessed in this trial. The presence of biochemical and ultrasonographic evidence of NAFLD seemed higher in the fenofibrate group compared with the other two intervention groups. Three patients discontinued treatment due to myalgia and elevated serum creatine kinase activity, one from the atorvastatin group and two from the combination group. Another patient from the atorvastatin group discontinued treatment due to raised alanine aminotransferase activity, over three times the upper normal limit. Both trials were at high risk of bias (that is, overestimation of benefits and underestimation of harms). Furthermore, the groups were small raising the risks of random errors (that is, play of chance). Accordingly, we did not find evidence to support or refute the use of statins for patients with NAFLD or NASH. Further unbiased trials with larger numbers of patients looking explicitly at patient‐related outcomes of interest (for example, quality of life, development of cirrhosis, and mortality) are needed to assess the effects of statins on NAFLD or NASH.

Fibrates for patients without established cardiovascular disease

Cardiovascular disease is the most common cause of death, illness, disability, and reduced quality of life in industrialised countries. One of the major risk factors for cardiovascular disease is elevated low‐density lipoprotein cholesterol (LDL‐C, 'bad' cholesterol). In addition, persons with elevated serum triglycerides and low levels of high‐density lipoprotein cholesterol (HDL‐C, 'good' cholesterol) are also at increased risk for cardiovascular disease events such as heart attacks or strokes. Fibrates lower serum triglycerides, modestly raise HDL‐C, and modestly lower LDL‐C. Therefore, long‐term therapy with fibrates may help prevent cardiovascular disease events, in particular in combination with statins, for which it has been shown that they substantially lower LDL‐C and reduce the risk of heart attack, stroke, and overall mortality.

Fibrates for secondary prevention of cardiovascular disease and stroke

The aim of this study was to assess the effect of fibrates for the prevention of major events including heart attacks, strokes, and circulatory disease death in people with existing circulatory disease.

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