Fatty Liver Treatment & Management

  • Author: Dawn Sears, MD; Chief Editor: Julian Katz, MD   more...
 
Updated: Jun 24, 2011
 

Medical Care

Abstinence from alcohol may reverse steatosis in patients with alcohol-related fatty liver. Weight loss and control of comorbidities appear to slow the disease and to possibly reverse some of the steatosis and fibrosis. In a recent randomized trial improvement of liver biopsy was seen after 7% loss of weight due to lifestyle changes of diet, exercise, and behavioral modification.[17] No established treatment is available for NASH. Several empiric treatment strategies have been suggested, as outlined below.

Treatment of underlying disease

Patients with celiac sprue who follow a gluten-free diet can have reversal of fatty liver disease.

Patients with growth hormone deficiency who receive growth hormone can have reversal of NASH.[18]

Dieting

Diets associated with improvement include those restricted in rapidly absorbed carbohydrates and those with a high protein-to-calorie ratio. Weight loss should be gradual, moderate, and controlled.[19]

Mouse models of NASH have found that a high-fat diet combined with a high-fructose diet (typical American "fast food diet" equivalent) resulted in more liver damage than a high-fat diet alone.[20] A separate group of researchers found that exercise (swimming 1 hour a day, 5 days a week) of rats on a high-fructose diet prevented development of fatty liver disease.[21]

Exercise

Multiple human studies have shown that exercise added to diet appears to improve results and increase insulin sensitivity by increasing muscle mass.

An Australian study evaluating just 4 weeks of cycling exercise found that, despite no change in body weight, liver cholesterol levels improved.[22] A California study of more than 800 adults with fatty liver found that vigorous exercise was associated with less severe scar tissue in the liver.[23]

Lipid-lowering agents and insulin sensitizers

Multiple national studies are ongoing to evaluate the role of lipid-lowering agents as well as insulin sensitizers. Specifically, thiazolidinediones (eg, pioglitazone, rosiglitazone), metformin, gemfibrozil, and atorvastatin have all shown laboratory and histologic improvement in patients in small noncontrolled trials.

Thiazolidinedione (glitazones) use includes the following:

  • This class of drugs has been shown to decrease inflammation of the liver in both humans and rats and its effects only last as long as the medication is being delivered.[24, 25]
  • This class of medication results in improved insulin sensitivity and universal weight gain, which has recently been shown to be fat gain, not water.[26]
  • A randomized placebo-controlled trial evaluating pioglitazone (Actos) with diet versus diet alone has shown improvement of transaminases and steatosis. However, the fibrosis score improved only within the pioglitazone group before versus after the 6-month treatment. The differences posttreatment between the pioglitazone group and the placebo group were not statistically significant. This study is well done, with 55 patients undergoing liver biopsy before and after a treatment specifically for NASH. Larger, longer studies are expected.[27]
  • Nearly 250 patients with NASH were described in a New England Journal of Medicine study published in 2010. These patients were placed in 3 groups: group 1 took pioglitazone 30 mg/d, group 2 took Vitamin E 800 IU/d and group 3 took a placebo. After 96 weeks, each of these patients underwent a follow-up liver biopsy. The vitamin E group had the most improvement in their liver biopsy. Both the vitamin E and pioglitazone groups had improved liver lab tests and fatty liver inflammation numbers. However, the pioglitazone group gained the most weight and did not improve their liver scar readings.[28]
  • Rosiglitazone (Avandia) has been studied for 48 weeks in 30 patients with NASH and resulted in biochemical as well as histologic improvement.[29]
  • The US Food and Drug Administration issued an alert on May 21, 2007, to patients and health care professionals of rosiglitazone potentially causing an increased risk of myocardial infarction (MI) and heart-related deaths following the online publication of a meta-analysis. Rosiglitazone is an antidiabetic agent (thiazolidinedione derivative) that improves glycemic control by improving insulin sensitivity. The drug is highly selective and a potent agonist for peroxisome proliferator-activated receptor-gamma (PPAR-gamma). Activation of PPAR-gamma receptors regulates insulin-responsive gene transcription involved in glucose production, transport, and utilization, thereby reducing both blood glucose concentrations and hyperinsulinemia. Potent PPAR-gamma agonists have been shown to increase the incidence of edema. A large scale phase III trial (RECORD) is currently underway that is specifically designed to study cardiovascular outcomes of rosiglitazone.
  • As of September 2010, the FDA is requiring a restricted access program to be developed for rosiglitazone under a risk evaluation and mitigation strategy (REMS). Patients currently taking rosiglitazone and benefiting from the drug will be able to continue if they choose to do so. Rosiglitazone will only be available to new patients if they are unable to achieve glucose control on other medications and are unable to take pioglitazone, the only other thiazolidinedione.
  • For more information, see FDA’s Safety Alert on Avandia (updated 4/30/2009). The online published meta-analysis entitled Effect of Rosiglitazone on the Risk of Myocardial Infarction and Death from Cardiovascular Causes can be viewed at The New England Journal of Medicine.
  • Additionally, responses to the controversy can be viewed at the Heartwire news (the heart.org from WebMD), including the following articles: (1) Rosiglitazone increases MI and CV death in meta-analysis, (2) The rosiglitazone aftermath: Legitimate concerns or hype?, and (3) RECORD interim analysis of rosiglitazone safety: No clear-cut answers.
  • The published studies to date on metformin do not include histologic data but do show short-term radiologic and biochemical improvement.[30, 31, 32, 33, 34]

Cholesterol-lowering studies [31, 32, 35]

  • Atorvastatin was studied for 1 year with repeat biopsies and revealed improvement in ballooning degeneration and inflammation.
  • Atorvastatin was combined with 1 g of vitamin C and 100 IU of vitamin E and compared with placebo in a 3+ year study. This study used CT scan measurements to diagnose liver disease. The results showed that the odds of developing fatty liver were 34% on treatment versus 70% on no treatment.[36]
  • Gemfibrozil has resulted in biochemical improvement, but histologic data are lacking.
  • Ezetimibe was studied in a Japanese population in conjunction with lifestyle changes and resulted in improved follow-up liver biopsy in 6 of 10 patients after only 6 months.[37]
  • Pentoxifylline has received much attention in both animal models and human trials with conflicting results.[38, 39, 40, 41]

Orlistat has shown histologic and chemical improvement in patients using the drug for several months.[42]

Vitamin E and ursodeoxycholic acid have shown improvement in specific populations.

Urso has conflicting data in both adults and children. Some studies show biochemical and histologic improvement, whereas other studies show no difference when compared to placebo.

Folic acid supplementation does not appear to improve biopsy-proven NASH.[43]

Angiotensin receptor blockers have been studied in rat models with nonuniform results.[44, 45]

Experimental therapy

Ongoing research is revealing a possible link between obstructive sleep apnea and NAFLD/NASH. Studies are ongoing to evaluate if the treatment of obstructive sleep apnea results in the improvement of fatty liver disease.[46, 47, 48]

The novel therapy of using N -acetylcysteine[49] and cannabinoid blockers is also being explored in animal studies.[50, 51]

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Surgical Care

Bariatric surgery

Several studies are emerging that indicate that bariatric surgery with appropriate weight loss results in both chemical improvement and histologic improvement of NASH.[52]

Roux-en-Y gastric bypass with repeat biopsy within 2 years has shown improvement in 100% of patients. One study showed 94% of repeat liver biopsies no longer met the pathologic criteria for NAFLD or NASH. Another study, which only rebiopsied livers of patients with NASH (not NAFLD), demonstrated that 89% no longer had NASH.[53, 54, 55, 56]

Early studies reporting possible worsening hepatic function after rapid weight loss have not been substantiated. This may be a viable option in the appropriate candidate.

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Consultations

The only way to firmly diagnosis NASH is with a liver biopsy. Often, a clinical picture of obesity, hypertriglyceridemia, and elevated transaminases is enough to conclude that a patient has NASH. However, underlying alcohol or other drug ingestion as well as smoldering autoimmune or hemochromatosis must be ruled out. Referral to a hepatologist with or without liver biopsy may help in staging and prognosis.

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Diet

  • Abstinence from alcohol may reverse steatosis in patients with alcohol-related fatty liver.
  • A low-fat, American Diabetes Association (ADA) diet is recommended.
  • More evidence is mounting that high-fructose diets (sodas and preserved foods) are factors for developing fatty liver and that their elimination may reverse fatty liver.[20, 21]
  • A weight loss goal of 1-2 pounds per week is recommended.
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Activity

Exercise that includes both cardiovascular fitness and weight training should improve NASH. Cardiovascular fitness often results in weight loss. Weight training will increase muscle mass and improve insulin sensitivity. Both of these activities together help relieve the underlying derangements of NASH. However, even regular exercise without weight loss has been shown to improve fatty liver disease.[21, 22, 23] Most experts agree that 20 minutes of walking 5-7 days a week can stabilize this liver disease.

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Contributor Information and Disclosures
Author

Dawn Sears, MD  Associate Professor of Internal Medicine, Division of Gastroenterology and Hepatology, Scott and White Memorial Hospital

Dawn Sears, MD is a member of the following medical societies: American Association for the Study of Liver Diseases and American College of Gastroenterology

Disclosure: Nothing to disclose.

Specialty Editor Board

John Gunn Lee, MD  Director of Pancreaticobiliary Service, Associate Professor, Department of Internal Medicine, Division of Gastroenterology, University of California at Irvine School of Medicine

John Gunn Lee, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, and American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Simmy Bank, MD  Chair, Professor, Department of Internal Medicine, Division of Gastroenterology, Long Island Jewish Hospital, Albert Einstein College of Medicine

Disclosure: Nothing to disclose.

Alex J Mechaber, MD, FACP  Senior Associate Dean for Undergraduate Medical Education, Associate Professor of Medicine, University of Miami Miller School of Medicine

Alex J Mechaber, MD, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, and Society of General Internal Medicine

Disclosure: Nothing to disclose.

Chief Editor

Julian Katz, MD  Clinical Professor of Medicine, Drexel University College of Medicine

Julian Katz, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Geriatrics Society, American Medical Association, American Society for Gastrointestinal Endoscopy, American Society of Law, Medicine & Ethics, American Trauma Society, Association of American Medical Colleges, and Physicians for Social Responsibility

Disclosure: Nothing to disclose.

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