Serum unconjugated (indirect) bilirubin can be increased in hemolysis or Gilbert syndrome, which is diagnosed when unconjugated hyperbilirubinemia is the only abnormal liver function test and conjugated bilirubin and complete blood count are normal. OR Discussion of Procedures by Variant Variant 1: Abnormal liver function tests. Hepatocellular predominance with mild aminotransferase increase. Initial imaging. Hepatocellular predominant liver chemistry is seen when aminotransferases are elevated much higher than ALP (cholestatic-pattern). Hepatocellular injury causes the release of ALT and AST in serum. Increase in ALT (mild or moderate to severe) is directly linked to hepatocyte injury. In addition to fatty liver disease, other causes of rising ALT include acute or chronic viral hepatitis, acute Budd-Chiari syndrome, ischemic hepatitis, autoimmune, hemochromatosis, medications/toxins, autoimmune, alpha1-antitrypsin deficiency, and Wilson disease. AST levels are also increased in fatty liver disease and cirrhosis. However, if the aminotransferase rise is predominantly AST, nonhepatic causes (hemolysis, myopathy, thyroid disease, exercise) should also be considered. Common causes of mild increases in aminotransferases are nonalcoholic fatty liver disease (NAFLD) and alcohol- induced liver disease; uncommon causes include drug-induced liver injury, hepatitis B, hepatitis C, and hereditary hemochromatosis. Rare causes are alpha1-antitrypsin deficiency, autoimmune hepatitis, and Wilson disease. The 2 most common causes of fatty liver disease are NAFLD and alcohol-induced steatosis/steatohepatitis. Excessive intake of alcohol results in alcohol-induced fatty liver disease. The AST:ALT ratio is generally >2 in alcohol-induced fatty liver disease and <1 in metabolic disease-related fatty liver. Alcohol-induced liver disease is caused by excess alcohol consumption, whereas the nonalcoholic variant is related to insulin resistance and the metabolic syndrome.
Abnormal Liver Function Tests. Serum unconjugated (indirect) bilirubin can be increased in hemolysis or Gilbert syndrome, which is diagnosed when unconjugated hyperbilirubinemia is the only abnormal liver function test and conjugated bilirubin and complete blood count are normal. OR Discussion of Procedures by Variant Variant 1: Abnormal liver function tests. Hepatocellular predominance with mild aminotransferase increase. Initial imaging. Hepatocellular predominant liver chemistry is seen when aminotransferases are elevated much higher than ALP (cholestatic-pattern). Hepatocellular injury causes the release of ALT and AST in serum. Increase in ALT (mild or moderate to severe) is directly linked to hepatocyte injury. In addition to fatty liver disease, other causes of rising ALT include acute or chronic viral hepatitis, acute Budd-Chiari syndrome, ischemic hepatitis, autoimmune, hemochromatosis, medications/toxins, autoimmune, alpha1-antitrypsin deficiency, and Wilson disease. AST levels are also increased in fatty liver disease and cirrhosis. However, if the aminotransferase rise is predominantly AST, nonhepatic causes (hemolysis, myopathy, thyroid disease, exercise) should also be considered. Common causes of mild increases in aminotransferases are nonalcoholic fatty liver disease (NAFLD) and alcohol- induced liver disease; uncommon causes include drug-induced liver injury, hepatitis B, hepatitis C, and hereditary hemochromatosis. Rare causes are alpha1-antitrypsin deficiency, autoimmune hepatitis, and Wilson disease. The 2 most common causes of fatty liver disease are NAFLD and alcohol-induced steatosis/steatohepatitis. Excessive intake of alcohol results in alcohol-induced fatty liver disease. The AST:ALT ratio is generally >2 in alcohol-induced fatty liver disease and <1 in metabolic disease-related fatty liver. Alcohol-induced liver disease is caused by excess alcohol consumption, whereas the nonalcoholic variant is related to insulin resistance and the metabolic syndrome.