The Global Nonalcoholic Fatty Liver Disease Epidemic: What a Radiologist Needs to Know

Keith Pereira, Jason Salsamendi, Javier Casillas, Keith Pereira, Jason Salsamendi, Javier Casillas

Abstract

Nonalcoholic fatty liver disease (NAFLD) represents a spectrum of disorders from a benign steatosis to hepatocellular carcinoma (HCC). Metabolic syndrome, mainly obesity, plays an important role, both as an independent risk factor and in the pathogenesis of NAFLD. With the progressive epidemics of obesity and diabetes mellitus, the prevalence of NAFLD and its associated complications is expected to increase dramatically. Therapeutic strategies for treating NAFLD and metabolic syndrome, particularly obesity, are continuously being refined. Their goal is the prevention of NAFLD by the management of risk factors, prevention of progression of the disease, as well as management of complications, ultimately preventing morbidity and mortality. Optimal management of NAFLD and metabolic syndrome requires a multidisciplinary collaboration between the government as well as the health system including the nutritionist, primary care physician, radiologist, hepatologist, oncologist, and transplant surgeon. An awareness of the clinical presentation, risk factors, pathogenesis, diagnosis, and management is of paramount importance to a radiologist, both from the clinical perspective as well as from the imaging standpoint. With expertise in imaging modalities as well as minimally invasive percutaneous endovascular therapies, radiologists play an essential role in the comprehensive management, which is highlighted in this article, with cases from our practice. We also briefly discuss transarterial embolization of the left gastric artery (LGA), a novel method that promises to have an enormous potential in the minimally invasive management of obesity, with details of a case from our practice.

Keywords: Hepatocellular carcinoma; left gastric artery embolization; metabolic syndrome; nonalcoholic fatty liver disease.

Conflict of interest statement

Conflict of Interest: None declared.

Figures

Figure 1
Figure 1
Defining the NAFLD spectrum.
Figure 2
Figure 2
The natural history of NAFLD.
Figure 3
Figure 3
Metabolic syndrome as a risk factor in the NAFLD spectrum.
Figure 4
Figure 4
Summary of pathogenesis of NAFLD.
Figure 5
Figure 5
NIH criteria in the diagnosis of metabolic syndrome.
Figure 6
Figure 6
Management algorithm in the detection of NAFLD.
Figure 7
Figure 7
46-year-old asymptomatic man presented with elevated liver enzymes. Serological markers for other causes of elevated liver enzymes did not reveal any pathology. US-guided liver biopsy in the left lobe of the liver was performed. Gray-scale US longitudinal view shows the left lobe of liver with the needle in the parenchyma (seen as white echogenic line).
Figure 8
Figure 8
NASH activity grade and fibrosis stage based on Brunt classification.
Figure 9
Figure 9
Role of imaging (invasive and noninvasive) in the grading and staging of NAFLD.
Figure 10
Figure 10
(a) 56-year-old man with metabolic syndrome and mildly elevated liver enzymes. Gray-scale US transverse view through the right lobe of liver shows the following: 1. Hyperechogenic liver tissue with fine, tightly packed echoes on US examination (the so-called “bright liver”), characteristic of liver steatosis; 2. Decreased sonographic visualization of portal and hepatic veins giving rise to a “featureless or bland appearance;” and 3. Decreased ability of the US beam to penetrate the liver tissue causing posterior darkness and loss of definition of the diaphragm (posterior beam attenuation) (red arrow). (b) 68-year-old woman with metabolic syndrome. Gray-scale US longitudinal view of right lobe of liver shows the following: 1. Coarse echo pattern (within the red circle), different from fine, packed echoes of steatosis; 2. Lack of posterior beam attenuation with definite visualization of diaphragm (white arrow); 3. Fibrosis with steatosis seen as coarse echoes (“pin-head echoes”) within the fine echo pattern of steatosis (differentiation is difficult as fibrosis and steatosis have similar sonographic appearance, “fatty-fibrotic pattern”); and 4. Later there was volume loss, nodular contour, and ascites. (c) 48-year-old asymptomatic man with mildly elevated liver enzymes. Unenhanced CT scan, axial section of the liver shows HUliver 8 (white circle) and HUspleen 40 (black circle), CTL-S of −32, and hepatic attenuation index (HAI) of 0.2. Fatty infiltration is diagnosed when the criteria of HUliver

Figure 11

Comprehensive management of NAFLD.

Figure 11

Comprehensive management of NAFLD.

Figure 11
Comprehensive management of NAFLD.

Figure 12

Chart showing treatment modalities available…

Figure 12

Chart showing treatment modalities available based on BMI.

Figure 12
Chart showing treatment modalities available based on BMI.

Figure 13

Algorithm in the management of…

Figure 13

Algorithm in the management of NAFLD based on histological staging and grading.

Figure 13
Algorithm in the management of NAFLD based on histological staging and grading.

Figure 14

Bariatic surgery in the management…

Figure 14

Bariatic surgery in the management of obesity and NAFLD.

Figure 14
Bariatic surgery in the management of obesity and NAFLD.

Figure 15

68-year-old female with a past…

Figure 15

68-year-old female with a past medical history of morbid obesity, Type 2 diabetes,…

Figure 15
68-year-old female with a past medical history of morbid obesity, Type 2 diabetes, hypertension, and ultrasound features of cirrhosis was referred from an outside facility for evaluation. (a) Gray-scale US of the liver, longitudinal view through the right lobe of the liver shows a coarse echo pattern (within red circle) with a nodular surface suggestive of cirrhosis. (b) Also seen is a well-encapsulated echogenic lesion in the left lobe of the liver (between yellow marks). (c) This was confirmed (white arrow) on triple-phase contrast-enhanced axial MRI. A left gastric artery embolization was performed using using 500–700 μm embolic particles. (d) Pre-embolization angiogram shows a normal-appearing left gastric artery (black arrow) and fundal branches (white arrow). (e) Post-embolization angiogram shows absence of flow into the left gastric artery (white star) with normal flow into common hepatic and splenic arteries (white arrows). A transarterial chemoembolization (TACE) was performed via segment 2 and 3 hepatic branches. (f) Pre-TACE angiogram of the left hepatic artery reveals a small rounded hypervascular blush (black arrow). (g) Post-chemoembolization left hepatic angiogram reveals stasis (white arrow) in the segment 2/3 hepatic branch with no hypervascular blush.

Figure 16

Overview of the management algorithm…

Figure 16

Overview of the management algorithm for treatment of HCC based on the Barcelona…

Figure 16
Overview of the management algorithm for treatment of HCC based on the Barcelona Clinic Liver Cancer (BCLC) Staging System.

Figure 17

Recap of key points in…

Figure 17

Recap of key points in the clinical presentation, risk factors, pathogenesis, diagnosis, and…

Figure 17
Recap of key points in the clinical presentation, risk factors, pathogenesis, diagnosis, and management of NAFLD.
All figures (17)
Figure 11
Figure 11
Comprehensive management of NAFLD.
Figure 12
Figure 12
Chart showing treatment modalities available based on BMI.
Figure 13
Figure 13
Algorithm in the management of NAFLD based on histological staging and grading.
Figure 14
Figure 14
Bariatic surgery in the management of obesity and NAFLD.
Figure 15
Figure 15
68-year-old female with a past medical history of morbid obesity, Type 2 diabetes, hypertension, and ultrasound features of cirrhosis was referred from an outside facility for evaluation. (a) Gray-scale US of the liver, longitudinal view through the right lobe of the liver shows a coarse echo pattern (within red circle) with a nodular surface suggestive of cirrhosis. (b) Also seen is a well-encapsulated echogenic lesion in the left lobe of the liver (between yellow marks). (c) This was confirmed (white arrow) on triple-phase contrast-enhanced axial MRI. A left gastric artery embolization was performed using using 500–700 μm embolic particles. (d) Pre-embolization angiogram shows a normal-appearing left gastric artery (black arrow) and fundal branches (white arrow). (e) Post-embolization angiogram shows absence of flow into the left gastric artery (white star) with normal flow into common hepatic and splenic arteries (white arrows). A transarterial chemoembolization (TACE) was performed via segment 2 and 3 hepatic branches. (f) Pre-TACE angiogram of the left hepatic artery reveals a small rounded hypervascular blush (black arrow). (g) Post-chemoembolization left hepatic angiogram reveals stasis (white arrow) in the segment 2/3 hepatic branch with no hypervascular blush.
Figure 16
Figure 16
Overview of the management algorithm for treatment of HCC based on the Barcelona Clinic Liver Cancer (BCLC) Staging System.
Figure 17
Figure 17
Recap of key points in the clinical presentation, risk factors, pathogenesis, diagnosis, and management of NAFLD.

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