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Bezafibrate for primary biliary cirrhosis

Primary biliary cirrhosis is a chronic disease of the liver that is characterised by progressive inflammation and destruction of the liver tissue, eventually progressing to liver cirrhosis and the need for liver transplantation. Primary biliary cirrhosis primarily affects middle‐aged women. Bezafibrate is a hypolipidaemic agent used in treatment of hypertriglyceridaemia. There are studies suggesting that bezafibrate, alone or in combination with ursodeoxycholic acid, is effective in treatment of primary biliary cirrhosis. Mechanisms through which bezafibrate improves lipid serum concentration balance and prevents biliary cell damage still need to be fully understood. This review evaluates all data on the benefits and harms of bezafibrate for patients with primary biliary cirrhosis in randomised clinical trials. The findings of this review are based on six randomised clinical trials with 151 Japanese patients. Bezafibrate was compared with no intervention in four trials (with co‐intervention of ursodeoxycholic acid in both the bezafibrate and control groups) and with ursodeoxycholic acid in two trials. The primary findings of the review are that bezafibrate has no statistically significant effects on mortality, liver‐related morbidity, adverse events, and quality of life of patients with primary biliary cirrhosis. A possible positive intervention effect of bezafibrate versus no intervention on liver biochemistry measures can be real but could also be due to systematic errors or random errors. The benefits and harms of bezafibrate for patients with primary biliary cirrhosis need further assessment in randomised clinical trials comparing bezafibrate with placebo. Such trials ought to be conducted with impeccable methodology to reduce the risks of random errors and sufficiently large patient groups to reduce the risks of random errors.

Cochrane Database of Systematic Reviews: Plain Language Summaries [Internet] - John Wiley & Sons, Ltd.

Version: 2012

No evidence to support or refute antioxidant supplements for patients with non‐alcoholic fatty liver disease and/or steatohepatitis

Non‐alcoholic fatty liver disease is characterised by fatty deposition in the hepatocytes in the absence of excessive alcohol intake and of other known causes of fatty liver. Hepatic injury might be improved by antioxidant supplements. This systematic review identified six randomised clinical trials. No liver‐related or unrelated deaths occurred in any of the included trials. Adverse events were minor and non‐specific. Treatment with antioxidant supplements showed a significant, though not clinically relevant, amelioration of aspartate aminotransferase, but not of alanine aminotransferase, as compared to placebo or other interventions. Data on the radiological and/or histological response were too limited to draw any conclusions. Further placebo‐controlled trials are necessary.

Cochrane Database of Systematic Reviews: Plain Language Summaries [Internet] - John Wiley & Sons, Ltd.

Version: 2008

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, gammaglutamyl 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.

Cochrane Database of Systematic Reviews: Plain Language Summaries [Internet] - John Wiley & Sons, Ltd.

Version: 2014

Antioxidant supplements for liver disease

Beta‐carotene, vitamin A, vitamin C, and vitamin E cannot be recommended for treatment of liver diseases.

Cochrane Database of Systematic Reviews: Plain Language Summaries [Internet] - John Wiley & Sons, Ltd.

Version: 2011

Interleukin‐1 inhibitors for acute gout

Gout results from the deposition of crystals of uric acid in and around joints. The main treatments for gout are drugs that lower uric acid blood levels and resolve the crystal deposits. Acute gout flares result in significant pain and disability and treatment aims at reducing the pain and resolving the arthritis quickly.

Cochrane Database of Systematic Reviews: Plain Language Summaries [Internet] - John Wiley & Sons, Ltd.

Version: 2014

Naltrexone and nalmefene for alcohol dependent patients

Alcohol dependence is a chronic disease, which can develop when alcohol is heavily used over longer periods of time. Alcohol affects various brain regions, including the opioid receptor system, which mediates euphoric and pleasurable effects of alcohol. By blocking alcohol effects at these receptors, the opioid antagonists naltrexone and nalmefene can reduce alcohol "liking" and "craving" and thus support alcohol dependent patients in cutting down their drinking. 50 studies with 7793 participants were included in the review, in most studies treatment was provided over a period of three months. The review shows that more patients who took naltrexone were able to reduce the amount and frequency of drinking than those who took an identical appearing, but inert substance (placebo). On average, one out of nine patients was helped by naltrexone. Naltrexone does not have serious side effects, but gastrointestinal symptoms like nausea, stomach pain and loss of appetite are common. Some patients also get tired from naltrexone. For injectable formulations of naltrexone, which can be advantageous for patients who have problems with taking their medication on schedule, and the second opioid antagonist nalmefene, the database is still too sparse to allow final conclusions. Nevertheless, the available studies indicate that these drugs might have comparable effects on drinking than oral naltrexone has. Naltrexone does not cause dependency and unlike disulfiram, another medicine that is sometimes used to treat alcohol dependence, it does not make patients feel sick if they drink alcohol while taking it.

Cochrane Database of Systematic Reviews: Plain Language Summaries [Internet] - John Wiley & Sons, Ltd.

Version: 2010

Acamprosate for alcohol dependent patients

Alcohol dependence is an important health risk factor that can lead to disability and death for people in developed and developing countries. Alcohol consumption is potentially avoidable, which emphasizes the need for effective strategies to help people who are dependent on alcohol to reduce excessive drinking and maintain abstinence following detoxification. Psychosocial programs have limited success in preventing relapse after detoxification programs. The addition of a pharmacological agent could provide support in achieving or maintaining abstinence or to cut down alcohol consumption. The synthetic glutamate antagonist acamprosate and naltrexone, which is an opioid antagonist, are used for this purpose.

Cochrane Database of Systematic Reviews: Plain Language Summaries [Internet] - John Wiley & Sons, Ltd.

Version: 2011

Ursodeoxycholic acid for primary biliary cirrhosis

Primary biliary cirrhosis is an uncommon and slowly progressive autoimmune disease of the liver that primarily affects middle‐aged women. The cause of the disease is unknown. Over the last 30 years, the prevalence of primary biliary cirrhosis has increased substantially. Primary biliary cirrhosis is now a frequent cause of liver morbidity, and the patients are significant users of health resources, including liver transplantation.

Cochrane Database of Systematic Reviews: Plain Language Summaries [Internet] - John Wiley & Sons, Ltd.

Version: 2012

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