 Introduction/Background Liver function tests are often obtained as part of standard laboratory panels in asymptomatic and symptomatic patients. Alteration in the biochemical markers of hepatocyte damage or bile flow indicate hepatobiliary insult rather than a measurement of liver function. Routine liver chemistries include alanine transaminase (ALT), aspartate transaminase (AST), alkaline phosphatase (ALP), and bilirubin. On the contrary, albumin and prothrombin time are actual markers of hepatocellular synthetic function. The severity of abnormal aminotransferase can be classified as 1) mild: <5 times the upper reference limit, 2) moderate: 5 to 10 times the upper reference limit, or 3) severe: >10 times the upper reference limit. Moderate and severe are discussed collectively as significant clinical overlap exists between these 2 categories. Pathologically increased levels of ALP may occur in cholestatic liver disease, which can show elevated ALP with or without elevated bilirubin. Cholestasis can be due to obstruction of biliary outflow or impairment in bilirubin uptake. If abnormal ALP levels are seen without impairment of other liver enzymes, the etiology is suspected to be cholestatic in origin. If ALP is elevated in isolation, a confirmation with gamma-glutamyl transpeptidase (GGT) or fractionated ALP isoenzyme helps to differentiate hepatic from nonhepatic etiologies, such as bone disease. GGT can be elevated in nonhepatic diseases such as myocardial infarction, renal failure, diabetes, pulmonary, and pancreatic disorders; therefore, it is not used in isolation to assess for liver disease when other liver function tests are normal [1]. Bilirubin is produced by the breakdown of heme. Following conjugation within the liver to increase water solubility, bilirubin is excreted into bile. Conjugated (direct) bilirubin is rapidly excreted in the alimentary tract; thus, bilirubin amounts are negligible in serum in healthy individuals.
Abnormal Liver Function Tests.  Introduction/Background Liver function tests are often obtained as part of standard laboratory panels in asymptomatic and symptomatic patients. Alteration in the biochemical markers of hepatocyte damage or bile flow indicate hepatobiliary insult rather than a measurement of liver function. Routine liver chemistries include alanine transaminase (ALT), aspartate transaminase (AST), alkaline phosphatase (ALP), and bilirubin. On the contrary, albumin and prothrombin time are actual markers of hepatocellular synthetic function. The severity of abnormal aminotransferase can be classified as 1) mild: <5 times the upper reference limit, 2) moderate: 5 to 10 times the upper reference limit, or 3) severe: >10 times the upper reference limit. Moderate and severe are discussed collectively as significant clinical overlap exists between these 2 categories. Pathologically increased levels of ALP may occur in cholestatic liver disease, which can show elevated ALP with or without elevated bilirubin. Cholestasis can be due to obstruction of biliary outflow or impairment in bilirubin uptake. If abnormal ALP levels are seen without impairment of other liver enzymes, the etiology is suspected to be cholestatic in origin. If ALP is elevated in isolation, a confirmation with gamma-glutamyl transpeptidase (GGT) or fractionated ALP isoenzyme helps to differentiate hepatic from nonhepatic etiologies, such as bone disease. GGT can be elevated in nonhepatic diseases such as myocardial infarction, renal failure, diabetes, pulmonary, and pancreatic disorders; therefore, it is not used in isolation to assess for liver disease when other liver function tests are normal [1]. Bilirubin is produced by the breakdown of heme. Following conjugation within the liver to increase water solubility, bilirubin is excreted into bile. Conjugated (direct) bilirubin is rapidly excreted in the alimentary tract; thus, bilirubin amounts are negligible in serum in healthy individuals.