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Nonalcoholic Fatty Liver Disease: An Under Diagnosed, Growing Epidemic that Deserves Our Attention

| May 1, 2016

A Message from Dr. Christopher Still

Christopher Still, DO, FACN, FACP, Co-Clinical Editor, Bariatric Times; Medical Director for the Center for Nutrition and Weight Management, and Director for Geisinger Obesity Research Institute, Geisinger Medical Center, Danville, Pennsylvania. Dr. Still is also a board member of the Obesity Action Coalition, Tampa, Florida.


Dear Colleagues,
Welcome to another issue of Bariatric Times. This month, I’d like to discuss one of the most under diagnosed comorbid conditions of obesity—nonalcoholic fatty liver disease (NAFLD). NAFLD is a growing epidemic that deserves more attention. Behind hepatitis C virus (HCV), nonalcoholic steatohepatitis (NASH)—a disease under the NAFLD umbrella—is the second-leading cause of liver transplants in adults in the United States,[1] and it is projected to claim the number one spot by 2020.

NAFLD encompasses a wide spectrum of fatty liver disorders all caused by the build up of extra fat in liver cells. While it is normal for the liver to contain some fat, if fat content rises to more than 5 to 10 percent of the liver’s weight, then it is considered a fatty liver or steatosis. Steatosis can progress to fibrosis and NASH, which causes inflammation and accumulation of fat and scar tissue in the liver. NASH can then progress even further to cirrhosis. These conditions can cause enough liver damage to require liver transplantation.
As many as 80 percent of patients with obesity have NAFLD.[2] The problem is that, although prevalent, the condition often goes undiagnosed because 1) patients do not present with definitive physical symptoms and 2) in-depth examination of NAFLD severity requires further testing. Ultrasounds do not show histological changes that occur along the NAFLD spectrum and liver function studies show only a minimal picture. The gold standard for detection is liver biopsy, but very few people who meet the criteria want to go through with one, as it is invasive.

From a clinical standpoint, you cannot really blame people for choosing to forgo biopsy because, although other therapies are being developed, as of now the only treatment we have is weight loss. The good news is that even modest weight loss of 5 to 10 percent, has been shown to improve NAFLD.[3] Weight loss between 10 and 12 percent, as might be achieved via bariatric surgery, has been shown to improve the NASH activity score measured on biopsy.[4]
Another problem with NAFLD is that its progression varies among individuals. Some stay in the earlier stage of steotosis and others move on to develop fibrosis, NASH, and cirrhosis. Research is being focused on predicting those who are at risk of disease progression so more targeted interventions can be developed for this patient population. We are interested in learning more about the impact of proteomics, genetics, and other markers in order to increase the sensitivity and specificity of noninvasive testing.

At Geisinger, we perform liver biopsies on all bariatric surgery patients. Through data analysis of these patients, we have found that non-invasive clinical assessments demonstrate low sensitivity, specificity, and accuracy for detecting the presence of steatosis, steatohepatitis, or fibrosis.[5] Even livers that appear normal in appearance and on liver function tests might deceive clinicians as biopsy may still reveal histological changes pointing to disease progression.

I think that both clinicians and patients need to be aware of NAFLD, the importance and accuracy of testing methods, and the role of weight loss in disease improvement. We can start by clarifying a common misconception that one can only get liver damage through alcohol consumption. When I tell patients that we’d like to perform a liver biopsy at the time of their bariatric surgery, I’m often met with the following response, “I don’t have to worry about liver damage because I don’t drink.” A lot of people have no idea that they can get the same type of cirrhosis without consuming alcohol. In addition, patients who do consume alcohol are doubly at risk for liver damage with alcohol and fat taxing the liver simultaneously.

The main message is that NAFLD is a prevalent comorbidity and it deserves the attention of clinicians and patients alike. Perhaps through increased awareness, diagnosis, and treatment through the multiple weight loss methods now available we can help slow NAFLD’s prevalence in the coming years.

Sincerely,

Christopher Still, DO, FACN, FACP

References
1.    Wong RJ, Aguilar M, Cheung R, et al. Nonalcoholic steatohepatitis is the second leading etiology of liver disease among adults awaiting liver transplantation in the United States. Gastroenterology. 2015;148(3):547–555.
2.    Milic S, et al. Non-alcoholic fatty liver disease and obesity: Biochemical, metabolic and clinical presentations. World J Gastroenterol. 2014;20(29):9330–9337.
3.    Lazo M, Solga SF, Horska A, et al. Effect of a 12-month intensive lifestyle intervention on hepatic steatosis in adults with type 2 diabetes. Diabetes Care. 2010;33(10):2156–2163.
4.    Promrat K, Kleiner DE, Niemeier HM, et al. Randomized controlled trial testing the effects of weight loss on nonalcoholic steatohepatitis. Hepatology. 2010;51(1):121–129.
5.    Petrick A, Benotti P, Wood GC, et al. Utility of ultrasound, transaminases, and visual inspection to assess nonalcoholic fatty liver disease in bariatric surgery patients. Obes Surg. 2015;25(12):2368–2375.

Category: Editorial Message, Past Articles

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