Digestive Disease Week (DDW) 2016

New Data Shine a Light on the Diagnosis and Management of Liver Disease

William F. Balistreri, MD


July 20, 2016

In This Article

Significant advances in the clinical practice of hepatology were addressed in the form of new research presented at Digestive Disease Weak (DDW) 2016. This review focuses on a few of the clinically relevant concepts that emerged from this meeting, which collectively highlight the pace of progress in diagnosing and managing common liver conditions, such as nonalcoholic fatty liver disease (NAFLD), chronic cholestatic liver diseases, and hepatotoxicity.

The Increasing Burden of NAFLD

Nonalcoholic fatty liver disease (NAFLD) is a common cause of chronic liver disease in industrialized countries, and its prevalence continues to rise in parallel with the growing obesity epidemic. With the globalization of unhealthy diet and lifestyles, the prevalence of NAFLD is increasing not just in the United States but also worldwide.

Mrad and colleagues[1] tracked the prevalence of NAFLD among young adults in the United States through cross-sectional data obtained from 14,371 persons enrolled in the National Health and Nutrition Examination Survey during three periods (1988-1994, 1999-2004, and 2005-2010). They reported a stepwise increase in the prevalence of suspected NAFLD in this cohort, rising from 9.6% in 1988-1994 to 24% in 2005-2010. The prevalence of NAFLD in the 2005-2010 period was highest among Mexican Americans (35%) and those with a body mass index (BMI) > 40 kg/m2 (57%). In stratified analyses, an increasing trend in the prevalence of suspected NAFLD was observed among all ethnic subgroups and both sexes.

Birerdinc and colleagues[2] provided an estimation of the global prevalence of NAFLD via a review of data repositories from the World Health Organization (WHO); the International Diabetes Federation; and the Global Burden of Diseases, Injuries, and Risk Factors Study, all of which collectively included findings from six WHO regions and 194 countries. The estimated global prevalence of "presumed NAFLD" in 2010 was 20% (ranging from 2% to 79%), which increased by 12% over the 4-year period up to 2014. The prevalence rates of presumed NAFLD stratified by WHO regions in 2014 were 9% for the African region, 18% for the Eastern Mediterranean region, 22% for the European region, 26% for the Americas, 22% for the Southeast Asian region, and 32% for the Western Pacific region. These rates represent a 12%-13% increase over 2010 prevalence rates for each region. The predicted prevalence of presumed NAFLD correlated positively with gross domestic product, whereas cirrhosis-attributable liver mortality correlated negatively with gross domestic product.

Consequences of Obesity-Related Liver Disease

The natural disease progression from obesity-related simple steatosis to nonalcoholic steatohepatitis (NASH), cirrhosis, and possibly hepatocellular carcinoma has been well described, as has its association with increased all-cause mortality. This relationship was further elaborated upon in studies at DDW 2016.

Ha and coworkers[3] characterized the natural history of NAFLD in an ethnically diverse cohort of 460 consecutive patients with NAFLD (128 Asian persons, 242 white persons, and 90 Hispanic persons) seen at a university medical center. Compared with white persons and Hispanic persons, affected Asian persons were significantly more likely to be male and have a lower BMI, and were less likely to be classified as extremely obese (BMI ≥ 40 kg/m2). Hypertension was more prevalent among white persons; however, all three ethnic groups had similar proportion of diabetes, hypercholesterolemia, hyperlipidemia, and coronary artery disease. White persons were significantly more likely than Asians and Hispanic persons to have fibrosis (12% vs 6% and 10%, respectively). There were no statistically significant ethnic differences in the 15-year cumulative incidence rates of disease progression to NASH.

In addition, all three groups had similar 15-year cumulative incidence rates of cirrhosis (approximately 6%), hepatic decompensation, liver cancer, and all-cause mortality. Thus, despite differences in the initial disease presentation among the three ethnic groups studied, disease progression was similar. In multivariate Cox proportional hazards models, a high probability of fibrosis was significantly associated with increased all-cause mortality (hazard ratio, 23) compared with a low or intermediate probability of fibrosis.

Kienbacher and colleagues[4] examined the prevalence of liver fibrosis among 46 morbidly obese patients undergoing metabolic surgery (gastric bypass). All patients were vitamin D deficient, 26% had diabetes mellitus, and 44% had metabolic syndrome. On biopsy, 72% demonstrated NASH, 11% had simple steatosis without NASH, and 17% had normal liver morphology. Significant fibrosis (stage ≥ F2) was present in 30%, advanced fibrosis (stage F3) in 9%, and cirrhosis (stage F4) in 4%. Notably, 88% of the patients had normal serum aspartate aminotransferase (AST) levels, including 61% of those with NASH, 24% with fibrosis ≥ stage F2, and 4% with cirrhosis.

Normal alanine aminotransferase (ALT) levels were noted in 68% (46% of those with NASH, 17% with fibrosis ≥ stage F2, and 4% with cirrhosis). Normal gamma-glutamyltransferase levels were present in 74%. Fibrosis was primarily predicted by higher homeostatic model assessment of insulin resistance values and procollagen type I propeptide levels; lower osteocalcin, calcium, parathyroid hormone, and 25-hydroxy vitamin D levels; male sex; and older age.


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