Printer Friendly

Nonalcoholic fatty liver.


Nonalcoholic fatty liver disease is a common presentation that often involves a complex array of management decisions. The American Association for the Advancement of Liver Diseases and two gastrointestinal professional associations recently published a guideline that provides a framework for the diagnosis and management of these patients.


Nonalcoholic fatty liver disease (NAFLD) implies hepatic steatosis documented by biopsy or imaging without evidence of a secondary cause. NAFLD is associated with metabolic conditions such as obesity diabetes, and hyperlipidemia. Morbidly obese patients who receive bariatric surgery have rates of NAFLD approaching 90%, with 5% having undiagnosed cirrhosis. NAFLD is further subclassified as either nonalcoholic fatty liver (NAFL) or the less common, but more serious, nonalcoholic steatohepatitis (NASH).

NAFL requires hepatic steatosis without evidence of hepatocellular injury. NASH implies steatosis and inflammatory hepatic injury often seen as ballooning of hepatocytes. Fibrosis is not a requirement for diagnosing NASH.

NAFL generally takes a benign long-term course while NASH can lead to cirrhosis and its attendant complications. Estimates of the prevalence of NAFLD vary dramatically, but the disorder appears to be quite common in the general population (6%-33%; 20%, median). NASH appears to be far less prevalent (3%-5%) while the extent of NASH cirrhosis is not known. NASH does not appear to increase the risk of hepatocellular carcinoma as is seen in other inflammatory hepatitic conditions. NAFLD appears to be more common in men and in patients of Hispanic background. Other medical conditions that may be associated with NAFLD include hypothyroidism, sleep apnea, polycystic ovary disease, and hypogonadism.


* Diagnosis of NAFLD requires the exclusion of secondary causes of steatosis such as excessive alcohol intake, genotype 3 hepatitis C, tamoxifen, corticosteroids, methotrexate, amiodarone, Wilson's disease, parenteral nutrition, and starvation. Microvesicular steatosis can occur with valproate, antiretrovirals, pregnancy-related hepatic conditions, and inborn errors of metabolism. Defining "excessive" alcohol intake can be controversial. The guidelines consider more than 21 drinks a week for men or more than 14 drinks a week for women to be reasonable thresholds for excessive drinking.

* Asymptomatic patients who appear to have NAFLD on an imaging study should be assessed for metabolic and secondary causes of steatosis. If they are asymptomatic and have normal liver chemistries, they should not undergo liver biopsy.

* Screening for NAFLD is not recommended because of the uncertainty regarding the long-term benefits of diagnosing and treating the condition apart from managing the intrinsic metabolic conditions. Screening of the family members of patients with NAFLD is not recommended.

* NAFLD is associated with mildly elevated ferritin levels that do not imply abnormalities of iron stores. Persistently high ferritin and increased iron saturation levels should prompt a diagnostic work-up, however.

* Weight loss reduces hepatic steatosis. While a 3%-5% body weight reduction can reduce steatosis, greater weight loss is usually necessary to improve the inflammatory processes associated with NASH. Bariatric surgery is not contraindicated in noncir-rhotic patients with NAFLD.

* Vitamin E, 800 IU/day, improves liver histology in nondiabetic patients with NASH and is first-line therapy for this population in the absence of other comorbid liver diseases. It is not recommended at this time for diabetic NASH patients or subjects with NAFLD who do not have biopsy-proven inflammatory cellular damage.

* Metformin does not change liver histology and is not appropriate therapy for NASH. Clinical trials indicate that pioglitazone, even in the absence of diabetes, might improve the liver injury seen in NASH if there are no coexisting liver conditions. Ur-sodeoxycholic acid and omega-3 fatty acids are not recommended therapies for the liver manifestations of NAFL or NASH.

* Patients with NAFLD should avoid heavy alcohol consumption, defined as more than 14 drinks a week in men and 7 drinks a week in women.

* Few data support the increased risks of statin therapy for patients with NAFLD. Statins should continue to be used to treat dyslipidemia common in this population. They do not appear to be valuable to directly treat NASH.

* There are no data to support routine follow up biopsies in patients with NAFL or NASH after diagnosis.


Chalasani, N. et al. The Diagnosis and Management of Nonalcoholic Fatty Liver Disease (Hepatology 2012;55:2005-18).

William E. Golden, M.D., and Robert H. Hopkins, M.D. Dr. Golden (left) is medical director of Arkansas Medicaid and professor of medicine and public health at the University of Arkansas, Little Rock. Dr. Hopkins is director of the division of general internal medicine at the University of Arkansas. E-mail them at They reported having no relevant financial conflicts.
COPYRIGHT 2012 International Medical News Group
No portion of this article can be reproduced without the express written permission from the copyright holder.
Copyright 2012 Gale, Cengage Learning. All rights reserved.

Article Details
Printer friendly Cite/link Email Feedback
Author:Golden, William E.; Hopkins, Robert H.
Publication:Internal Medicine News
Date:Oct 1, 2012
Previous Article:Antiplatelet plus aspirin promising for secondary prevention.
Next Article:Metformin may reduce the risk of some liver cancers.

Terms of use | Copyright © 2017 Farlex, Inc. | Feedback | For webmasters