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Nonalcoholic Fatty Liver Disease (NAFLD): a Comprehensive Review William B

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Nonalcoholic Fatty Liver Disease (NAFLD): a Comprehensive Review William B JOURNAL OF INSURANCE MEDICINE Copyright Q 2004 Journal of Insurance Medicine J Insur Med 2004;36:27±41 REVIEW Nonalcoholic Fatty Liver Disease (NAFLD): A Comprehensive Review William B. Salt II, MD Nonalcoholic fatty liver disease (NAFLD) is de®ned as fatty in®ltra- Address: The Ohio State University, tion of the liver exceeding 5% to 10% by weight. It is a spectrum of Columbus, Ohio; e-mail: disorders ranging from simple fatty liver (steatosis without liver in- [email protected]. jury), nonalcoholic steatohepatitis (steatosis with in¯ammation), and Correspondent: William B. Salt II, ®brosis/cirrhosis that resembles alcohol-induced liver disease but MD; Ohio Gastroenterology Group, which develops in individuals who are not heavy drinkers. NAFLD Clinical Associate Professor in Med- is likely the most common cause of chronic liver disease in many icine. countries. NAFLD may also potentiate liver damage induced by oth- er agents, such as alcohol, industrial toxins and hepatatrophic vi- Key words: Nonalcoholic fatty liver ruses. disease (NAFLD), nonalcoholic stea- The lack of speci®c and sensitive noninvasive tests for NAFLD tohepatitis (NASH), insulin resis- limits reliable detection of the disease. It is often diagnosed on a tance syndrome, liver transaminas- presumptive basis when liver enzyme elevations are noted in over- es, liver biopsy, life insurance. weight or obese individuals without identi®able etiology for liver disease, or when imaging studies suggest hepatic steatosis. NAFLD is now considered to be a component of the insulin re- sistance syndrome (metabolic syndrome X). Controversy exists rel- ative to optimal recognition, diagnosis and management of these conditions, and treatment recommendations are evolving. atty liver disease that develops in the ab- THE SPECTRUM OF NAFLD Fsence of alcohol abuse is recognized in- creasingly as a major health burden. Esti- The diagnosis of NAFLD is based upon mates based on imaging and autopsy studies noninvasive and invasive tests, with liver bi- suggest that about 20% to 30% of adults in opsy being the most de®nitive modality. He- the United States and other Western countries patic steatosis is at the lower end of the spec- have excess fat accumulation in the liver. Ap- trum of NAFLD clinical severity. Predomi- proximately 10% of these individuals, or fully nantly large (macro-) and occasionally small 2% to 3% of adults, are estimated to meet (micro-) vesicles of fat, predominately triglyc- current diagnostic criteria for nonalcoholic erides, accumulate within hepatocytes with- steatohepatitis (NASH). Sustained liver injury out causing appreciable hepatic in¯amma- leads to progressive ®brosis and cirrhosis in tion, liver cell death, or scarring. At the mid- up to one third of those with NASH, which range of the severity spectrum is steatohep- may be a cause of cryptogenic cirrhosis. atitis (nonalcoholic steatohepatitis, or NASH), NASH is now a signi®cant health issue for which is an intermediate form of liver dam- obese children, leading to cirrhosis in some. age superimposed upon a background of he- 27 JOURNAL OF INSURANCE MEDICINE Table 1. Nomenclature of Fatty Disorders of the cleus to the edge of the cell. The original de- Liver scriptions of steatohepatitis included the presence of Mallory bodies, ballooning de- Histologic nomenclature generation, predominant lobular neutrophilic 1. Fatty liver (grade) in¯ammation, and Rappaport zone III peri- 2. Steatohepatitis sinusoidal ®brosis. Now it is realized that a. Grade: degree of necroin¯ammatory activity b. Stage: degree of ®brosis only some of these features may be present in a given patient. Mallory bodies are less fre- quently seen in NASH compared with alco- holic steatohepatitis and may even be absent. patic steatosis. Steatohepatitis is characterized Also, in many individuals, atypical features by the appearance of focal hepatic in¯am- (eg, predominantly lymphocytic in¯amma- mation and hepatocyte necrosis and death. At tion or portal ®brosis) are present. It is not the highest end of the severity spectrum is known whether these histologic patterns rep- cirrhosis. By the time this degree of architec- resent different stages of steatohepatitis or tural distortion develops, hepatic steatosis separate clinicopathologic conditions with has often disappeared. Because all of these overlapping histologic expression. Despite an histologic features also occur in alcohol- or attempt to standardize the histologic diag- drug-induced fatty liver diseases, liver biopsy nostic criteria for steatohepatitis during a cannot reliably distinguish among the vari- workshop at the National Institutes of Health, ous causes of this entity. no consensus exists on this subject. The best de®nition of NASH remains un- NOMENCLATURE OF FATTY settled, since there is signi®cant diversity of DISORDERS OF THE LIVER opinion among experts regarding the neces- A complete diagnosis of fatty liver disease sity and character of speci®c ®ndings. A pro- (ideally) should de®ne the histology, includ- posed NAFLD classi®cation system correlates ing the grade (severity) and stage (degree of certain histologic features with the long-term ®brosis) of the disease as well as its clinical prognosis. In 1999, researchers introduced association (Tables 1 and 2). the 4-tiered Matteoni system (Table 3) to de- 1 Traditionally, fatty disorders of the liver scribe the stages of NASH. have been classi®ed as alcoholic or nonalco- Classes 3 and 4 NAFLD in Matteoni's sys- holic. NAFLD includes both nonalcoholic fat- tem are similar and might be considered as a ty liver and NASH. NAFLD is associated single group constituting NASH. These clas- with numerous etiologies (Table 2). The term ses describe NAFLD that has progressed to ``nonalcoholic fatty liver disease'' renders the the far more serious NASH, in which varying condition heterogeneous in terms of etiology, degrees of ®brosis and/or cirrhosis develop natural history, as well as response to thera- and balloon cells or Mallory's bodies appear. py. This makes the condition harder to study Class 2 NAFLD is more controversial; it may and is therefore unsatisfactory. There is cur- be benign and includes relatively more men rently no consensus on the best way to clas- often with a normal body mass index. sify fatty disorders of the liver. In another study, Brunt et al scored a total of 10 ®ndings to develop a grading and stag- ing system for NASH.2 These included he- HISTOLOGIC CRITERIA FOR THE patic macrovesicular steatosis, hepatocellular DIAGNOSIS OF FATTY LIVER AND ballooning, intra-acinar in¯ammation, portal STEATOHEPATITIS tract in¯ammation, Mallory's hyaline, acido- The principal histologic feature of NAFLD phil bodies, glycogen nuclei, lipogranulomas, is the presence of macrovesicular fatty change and hepatocellular iron. Each of these was in hepatocytes with displacement of the nu- scored separately. Three parameters of he- 28 SALTÐNONALCOHOLIC FATTY LIVER DISEASE Table 2. Conditions Associated With Steatohepatitis19 All conditions except alcoholism are usually referred to as nonalcoholic steatohepatitis (NASH). 1. Alcoholism 2. Insulin resistance a. Syndrome X i. Obesity ii. Diabetes iii. Hypertriglyceridemia iv. Hypertension b. Lipoatrophy c. Mauriac syndrome 3. Disorders of lipid metabolism a. Abetalipoproteinemia b. Hypobetalipoproteinemia c. Andersen's disease d. Weber-Christian syndrome 4. Total parenteral nutrition 5. Severe weight loss a. Jejunoileal bypass b. Gastric bypass (much less common than after jejunoileal bypass) c. Severe starvation 6. Iatrogenic/drugs (see Secondary Causes of Steatosis, Table 5) 7. Refeeding syndrome 8. Toxic exposure a. Environmental b. Workplace Table 3. Matteoni's Classi®cation of the Stages of havior regarding lifestyle) contribute to NAFLD/NASH1 NAFLD. The pathogenesis of NAFLD has been hy- Class 1: Simple steatosis without in¯ammation or ®bro- pothesized to be a 2-stage process. In the ®rst sis stage, fatty acids accumulate in hepatocytes Class 2: Steatosis with lobular in¯ammation but without leading to steatosis. The development of ste- ®brosis Class 3: Additional presence of ballooned hepatocytes atosis is associated with obesity, particularly Class 4: Presence of either Mallory's hyaline or ®brosis central abdominal adiposity, and insulin re- sistance. Hepatic steatosis predisposes to liver injury in the second stage, which is charac- patic ®brosis were scored: perisinusoidal ®- terized by necrosis, in¯ammation and ®bro- brosis, portal ®brosis, and bridging ®brosis. sis. It has been proposed that the primary Based on these, the necroin¯ammatory activ- mediator of this second stage is oxidative ity was graded as mild, moderate or severe stress. Pro-oxidants, such as iron, would be (Table 4). expected to worsen liver injury. Conversely, antioxidants, such as certain vitamins and minerals, would be expected to protect PATHOGENESIS OF NAFLD against liver injury. The pathogenesis of NAFLD has not been clearly established. Both ``nature'' (ie, genetic Stress Response control of in¯ammatory responses) and ``nur- ture'' (ie, epigenetic causes of oxidative Insulin resistance (metabolic syndrome X) stress/in¯ammation and health-related be- and NAFLD are related to ``stress.'' Dr. Bruce 29 JOURNAL OF INSURANCE MEDICINE Table 4. Grading and Staging of NAFLD According to Brunt et al2 Grading Macrovesicular steatosis Grade 0: None Grade 1: Up to 33% Grade 2: 33%±66% Grade 3: .66% Necroin¯ammatory activity Grade 1: Mild Steatosis up to 66%, occasional ballooned hepatocyte (mainly
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