Approach to the Patient With Evidence of Fatty Liver on Ultrasound
Approach to the Patient With Evidence of Fatty Liver on Ultrasound
Question
A patient underwent an ultrasound exam that showed evidence of fatty liver; what is the recommended approach to managing this patient?
As always, the first step is to make an accurate diagnosis. Does the patient have nonalcoholic fatty liver disease (NAFLD) as a hepatic consequence of underlying obesity? Or is the fatty liver due to ethanol ingestion or some other metabolic liver disease? NAFLD refers to a spectrum of disorders characterized by macrovesicular steatosis which occurs in the absence of consumption of harmful amounts of alcohol; it is the hepatic component of the metabolic syndrome (central obesity, type 2 diabetes mellitus, insulin resistance, dyslipidemia, and hypertension). NAFLD encompasses a range of liver lesions, from simple steatosis alone to nonalcoholic steatohepatitis (NASH), an inflammatory and fibrosing disease that may lead to progressive fibrosis and cirrhosis. Thus, it would be important to know whether this patient has features of the metabolic syndrome. Waist circumference is a crude measure of central obesity, which correlates with NAFLD.
Assuming that this patient indeed has NAFLD (unfortunately, NAFLD is very common compared with all of the other lesions that could present in this fashion), it would be important to document its extent and severity. Although liver biopsy remains the gold standard for grading and staging (ie, recognition of inflammation and fibrosis) in this setting, the presence of fat in the liver can be suggested by imaging modalities. However, no current noninvasive method can distinguish NASH from NAFLD because no radiologic modality can detect the presence of hepatocyte ballooning and inflammatory changes. However, the severity of steatosis and fibrosis can be detected radiologically. Hepatic ultrasonography, the most commonly used imaging technique to evaluate for the presence of hepatic steatosis, is cost-effective in screening. However, ultrasonography suffers from some flaws: It cannot quantify liver steatosis and there is interobserver variation that results in poor comparability. The sonographic features of fatty liver (increased hepatic parenchymal echotexture and vascular blurring) are also seen in patients with other forms of chronic liver disease with fibrosis, and therefore are nonspecific. In addition, detection of fat is optimal only with steatosis of more than 15%. Therefore, ultrasonography is not diagnostic of NAFLD/NASH given the rate of both false-positive and false-negative results. Computed tomography (CT) is more specific than ultrasonography for the detection of fatty liver, and liver attenuation values decrease with hepatic fat accumulation. However, CT is rarely used as a screening test for fatty liver because of the inherent radiation exposure.
So, assuming that the lesions seen on this patient's ultrasound exam do indeed represent NAFLD, are there targeted effective strategies to halt progression? Treatment of risk factors, specifically weight reduction, is the only proven effective therapy for NAFLD. A decrease in body mass index (via diet and exercise) is associated with an improvement in serum aminotransferase levels as well as inflammatory grade and fibrosis stage on liver biopsy. There is also an improvement in steatosis seen after 1 year of weight loss following bariatric surgery. A spate of pharmacologic approaches has been attempted, including the use of drugs that block fat absorption, drugs that improve insulin sensitivity, drugs that prevent fat accumulation in the liver, and drugs that act as antioxidants. Unfortunately, to date, none of these strategies has been shown to have a consistent effect on liver test results or histology.
Question
A patient underwent an ultrasound exam that showed evidence of fatty liver; what is the recommended approach to managing this patient?
Response from the Expert
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Response from William F. Balistreri, MD Dorothy M. M. Kersten Professor of Pediatrics, University of Cincinnati College of Medicine, Cincinnati, Ohio; Medical Director, Liver Transplantation Program, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio |
As always, the first step is to make an accurate diagnosis. Does the patient have nonalcoholic fatty liver disease (NAFLD) as a hepatic consequence of underlying obesity? Or is the fatty liver due to ethanol ingestion or some other metabolic liver disease? NAFLD refers to a spectrum of disorders characterized by macrovesicular steatosis which occurs in the absence of consumption of harmful amounts of alcohol; it is the hepatic component of the metabolic syndrome (central obesity, type 2 diabetes mellitus, insulin resistance, dyslipidemia, and hypertension). NAFLD encompasses a range of liver lesions, from simple steatosis alone to nonalcoholic steatohepatitis (NASH), an inflammatory and fibrosing disease that may lead to progressive fibrosis and cirrhosis. Thus, it would be important to know whether this patient has features of the metabolic syndrome. Waist circumference is a crude measure of central obesity, which correlates with NAFLD.
Assuming that this patient indeed has NAFLD (unfortunately, NAFLD is very common compared with all of the other lesions that could present in this fashion), it would be important to document its extent and severity. Although liver biopsy remains the gold standard for grading and staging (ie, recognition of inflammation and fibrosis) in this setting, the presence of fat in the liver can be suggested by imaging modalities. However, no current noninvasive method can distinguish NASH from NAFLD because no radiologic modality can detect the presence of hepatocyte ballooning and inflammatory changes. However, the severity of steatosis and fibrosis can be detected radiologically. Hepatic ultrasonography, the most commonly used imaging technique to evaluate for the presence of hepatic steatosis, is cost-effective in screening. However, ultrasonography suffers from some flaws: It cannot quantify liver steatosis and there is interobserver variation that results in poor comparability. The sonographic features of fatty liver (increased hepatic parenchymal echotexture and vascular blurring) are also seen in patients with other forms of chronic liver disease with fibrosis, and therefore are nonspecific. In addition, detection of fat is optimal only with steatosis of more than 15%. Therefore, ultrasonography is not diagnostic of NAFLD/NASH given the rate of both false-positive and false-negative results. Computed tomography (CT) is more specific than ultrasonography for the detection of fatty liver, and liver attenuation values decrease with hepatic fat accumulation. However, CT is rarely used as a screening test for fatty liver because of the inherent radiation exposure.
So, assuming that the lesions seen on this patient's ultrasound exam do indeed represent NAFLD, are there targeted effective strategies to halt progression? Treatment of risk factors, specifically weight reduction, is the only proven effective therapy for NAFLD. A decrease in body mass index (via diet and exercise) is associated with an improvement in serum aminotransferase levels as well as inflammatory grade and fibrosis stage on liver biopsy. There is also an improvement in steatosis seen after 1 year of weight loss following bariatric surgery. A spate of pharmacologic approaches has been attempted, including the use of drugs that block fat absorption, drugs that improve insulin sensitivity, drugs that prevent fat accumulation in the liver, and drugs that act as antioxidants. Unfortunately, to date, none of these strategies has been shown to have a consistent effect on liver test results or histology.
