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Analysis and Interpretation of Classic Liver Enzymes

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Analysis and Interpretation of Classic Liver Enzymes LIVER DISORDERS, SERIES #9 LIVER DISORDERS, SERIES #9 Rad Agrawal, MD, FACP, FACG, AGAF, FASGE Analysis and Interpretation of Classic Liver Enzymes Archana Kulkarni Mrinal Garg Rad M. Agrawal Michael Babich INTRODUCTION ccessibility, ease of collection, and relatively as many of these tests do not naturally reflect low cost give serum chemistries an integral hepatobiliary function and are rather used as a Ainitial role in medical diagnosis. With the determinant of liver injury. Furthermore, the liver being a critical organ in the metabolism of origin of these tests may not be specific to the carbohydrates, lipids and proteins as well as in liver and, as such, abnormal results may be related first pass metabolism of exogenous medications, to alternative organ injury. It is vital to use these a great deal can be learned about hepatobiliary test results in the context of patient history and processes by having an appropriate grasp of physical examination in order to form an accurate specific liver chemistry tests. Liver enzymes are diagnosis. For the purposes of this article, the also commonly ordered for evaluation of other non- liver chemistries that will be focused on will be hepatic diagnoses and as part of health screening, bilirubin, alkaline phosphatase, aminotransferases which makes it imperative for all primary care and gamma-glutamyl transferase. In addition, physicians and specialists to have an accurate albumin and prothrombin time will be discussed understanding of their normal values and an ability briefly. It will also provide a reference of normal to interpret abnormal levels. Symptoms and signs laboratory values for an average adult male of of liver disease are often seen late in the disease. individual tests based on information provided by As a result laboratory testing helps in identifying the Mayo Clinic. Furthermore, as clinicians will and characterizing liver disease. be ordering these tests on a routine basis, the cost The term “liver function tests” is a misnomer, is relevant and Medicare pricing guidelines will be provided for each laboratory test. Following Archana Kulkarni, MD1 Mrinal Garg, MD2 discussion of these tests individually, this article Rad M. Agrawal, MD3 Michael Babich, MD4 will focus on different patterns of abnormalities 1Department of Internal Medicine 2Division that relate to different disease processes. of Gastroenterology, Department of Internal Medicine 3Professor Emeritus, Division of Bilirubin Gastroenterology, Department of Internal Medicine 4 Bilirubin is a product of the digestion of hemoglobin. Associate Professor of Medicine, Division of During the catabolism of erythrocytes, an initial Gastroenterology, Department of Internal Medicine, Allegheny General Hospital, Pittsburgh, PA unconjugated or “indirect” form of bilirubin is 76 PRACTICAL GASTROENTEROLOGY • NOVEMBER 2018 Analysis and Interpretation of Classic Liver Enzymes LIVER DISORDERS, SERIES #9 LIVER DISORDERS, SERIES #9 released into the reticuloendothelial system. the direct bilirubin level from the total bilirubin. As unconjugated bilirubin is water insoluble, Identifying the subtype of bilirubin, which it binds with albumin and is transported to the is elevated, allows for accurate diagnosis when liver. Unconjugated bilirubin exists in majority analyzing bilirubin levels. Isolated elevation of as a component of total bilirubin when compared unconjugated bilirubin occurs mainly secondary to to direct bilirubin. In the liver, the unconjugated increased bilirubin production, decreased hepatic bilirubin enters the hepatocyte and is conjugated uptake and decreased bilirubin conjugation. with glucuronic acid by the enzyme UDP- Elevated levels of unsuccessful erythrocyte glucuronyltransferase (UGT), rendering it water production, hemolysis, or reabsorption of large soluble.1 This conversion process, from the hematomas may lead to increased unconjugated unconjugated form to “direct”, or conjugated, bilirubin levels. Fulminant Wilson’s disease can form allows bilirubin to be transported through the cause isolated elevation in unconjugated bilirubin canalicular membrane, mix with other components secondary to the release of copper in the blood of bile within the biliary tree, and flow into the resulting in cellular lysis 8 Unsuccessful erythrocyte duodenum.2,3,4 In the duodenum, part of the direct production exists in the setting of rapid heme and bilirubin is reabsorbed while the rest is converted hemoglobin turnover in the bone marrow due to to urobilinogen by intestinal flora and excreted premature destruction of red blood cells. There in the urine and stool. In addition, there is also exists evidence that in these conditions there is a delta bilirubin, which can also be referred to also presence of erythroid hyperplasia of bone as biliprotein, which is produced by reaction of marrow, reticulocytosis, increased iron turnover conjugated bilirubin with albumin.5 It is important with diminished red blood cell incorporation, and to note that the half-life of this product is about hemosiderosis of hepatic parenchymal cells and 17-20 days (the same as albumin) accounting for Kupffer cells. However, why this occurs in the prolonged jaundice in patients recovering from bone marrow is not known.8 hepatitis or obstruction.6 The total bilirubin, which Isolated elevation of unconjugated bilirubin is a measure of both direct and indirect forms, has also may be due to genetically inadequate UGT a normal reference range of 0.1-1.0 mg/dL. production preventing conjugation in disease Historically, in order to determine the serum processes such as Gilbert’s syndrome and Crigler- levels of the two types of bilirubin, laboratories Najjar disease.9 Gilbert’s syndrome is a commonly utilized the technique developed through the van seen disorder, which is relatively benign. The den Bergh diazo reaction,7 which was able to hyperbilirubinemia in Gilbert’s syndrome is separate water soluble conjugated bilirubin from exacerbated with fasting.10 Elevated conjugated unconjugated bilirubin for individual measurement. bilirubin can be caused secondary to inherited or The accuracy of the direct bilirubin levels increased acquired conditions. Genetic disease processes as the total bilirubin rose. The direct, or conjugated, such as Dubin-Johnson and Rotor syndrome bilirubin reference range is 0.0-0.3 mg/dL in a cause an impaired hepatocellular secretion normal individual and should be no more than of bilirubin into the bile canaliculus causing 20% of the total bilirubin when the total bilirubin elevated conjugated bilirubin.11,12 As the anatomy is elevated due to non-hepatic causes, such as suggests, elevations in conjugated bilirubin can hemolysis or congestive heart failure. The indirect occur secondary to hepatocellular dysfunction or unconjugated bilirubin is obtained by subtracting and cholestatic processes, which impair bile, flow. Table 1. Definitions to describe the magnitude of elevations of AST and ALT Borderline elevation in AST and ALT <2X the upper limit of normal Mild elevation in AST and ALT 2-5 X the upper limit of normal Moderate elevation in AST and ALT 5-15 X the upper limit of normal Severe elevation in AST and ALT >15 X the upper limit of normal Massive AST and ALT elevation >10,000 IU/l PRACTICAL GASTROENTEROLOGY • NOVEMBER 2018 77 Analysis and Interpretation of Classic Liver Enzymes LIVER DISORDERS, SERIES #9 It has been found that despite the loss of liver order to distinguish whether an isolated elevation function in hepatocellular disease processes, such of ALP is of hepatic origin, one could order ALP as cirrhosis, UGT is produced at an increased rate isozymes, which fractionate the total ALP into its in the remaining functioning hepatocytes forming tissues of origin. Alternatively, confirmation via conjugated bilirubin, such that increase in total a gamma-glutamyltransferase (GGT) level can bilirubin may not occur until late in the course of be performed since GGT is more concentrated disease.13,14 Cholestasis can occur either because in hepatic tissue1 and is not present in bone. A of impaired secretion into a bile canaliculus concurrent elevation of ALP and GGT excludes or impaired transit through the biliary tree and a boney origin of the enzyme. It is important to into the duodenum. Some of the causes of intra note that initially the only notable abnormality that hepatic cholestasis are drug toxicity, primary may be seen in infiltrative diseases such as primary biliary cirrhosis, primary sclerosing cholangitis, biliary cirrhosis, sarcoidosis, primary sclerosing viral hepatitis, cholestasis of pregnancy, benign cholangitis, etc. is isolated elevations in ALP.1 postoperative cholestasis, infiltrative liver diseases, Elevation in ALP is typically seen for duration of sepsis and total parenteral nutrition. Certain causes more than six months in these conditions. These of extra hepatic cholestasis are choledolithiasis, cases normally require follow up with imaging or malignant obstruction secondary to a mass in liver biopsy. ALP can also interestingly be raised the pancreas, bile duct, gall bladder or ampulla, in various neoplasms, which do not involve the primary sclerosing cholangitis with an extra hepatic bone or liver directly. This occurs secondary to an bile duct stricture, chronic pancreatitis and AIDS isozyme of ALP called the ‘Regan isoenzyme’.17 cholangiopathy. GGT is an enzyme primarily located in hepatocytes, epithelial lining of biliary ducts, Alkaline Phosphatase and pancreas, renal tubules and the intestine.
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