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34 LIVER ENZYME INTERPRETATION PEER REVIEWED • Severe hypoalbuminemia (<2.0 g/dL) in dogs • Unexplained ammonium urate urolithiasis • Hyperbilirubinemia when hemolysis cannot be definitely diagnosed/excluded (uncommon) In a healthy patient, SBA are synthesized from cholesterol. In dogs, bile acids are conjugated to glycine or taurine and then stored in the gallbladder, whereas in cats they are conjugated almost exclusively with taurine. 10 After a meal, the gallbladder contracts because of secretion of cholecystokinin, emptying bile into the duodenum. Bile acids are absorbed in the ileum. They are transported via the portal circulation to the liver, where they are subsequently reabsorbed. Normally this process is about 95% to 98% efficient. The enterohepatic recirculation of bile acids is impeded in dogs without gallbladders and patients with ileal disease or that have had ileal resection, causing a decrease in SBA concentration. Other conditions that can cause decreased SBA concentrations include GI malabsorption and decreased gastric motility. 2 Causes of increased total SBA concentrations are listed in Box 2 . Diseases that cause intrahepatic cholestasis (lipidosis, diabetes mellitus, lymphoma, histoplasmosis, cirrhosis) or extrahepatic cholestasis (cholangitis, bile duct carcinoma, liver flukes, cholelithiasis, pancreatitis) can cause decreased bile acid excretion, despite no decrease in functional hepatic mass. In patients with hyperbilirubinemia, once hemolysis has been ruled out, measuring SBA is not indicated because their concentration will be predictably increased. Compared with plasma ammonia, SBA are easy to measure and do not not require special sample handling. Paired preprandial and 2-hour postprandial SBA measurements are usually performed to increase the sensitivity of this test ( Box 3 ). While SBA measurement is arguably the best test of liver function and portosystemic shunting in dogs and cats, increased concentrations are not specific for any single hepatobiliary disease. Therefore, this test can be helpful for evaluating the likelihood of hepatobiliary disease; however, it cannot definitively determine the underlying liver disease. Additionally, this test does not provide a truly quantitative assessment of hepatic function. Because of the hepatic reserve capacity, it is possible for dogs with normal SBA concentrations to have hepatobiliary disease; therefore, this test BOX 2 Biochemical Test Results That Can Indicate Hepatic Disease and Important Differential Diagnoses Severe hypoalbuminemia (<2.0 g/dL) • Decreased hepatic synthesis (portosystemic shunting, hepatic parenchymal disease) • Differential diagnoses: protein-losing nephropathy and protein-losing enteropathy Hypocholesterolemia • Decreased hepatic synthesis (portosystemic shunting, hepatic parenchymal disease) • Hypoadrenocorticism • Malassimilation • Starvation Hypercholesterolemia • Cholestasis (intrahepatic, extrahepatic) • Differential diagnoses: endocrine disease (diabetes mellitus, hyperadrenocorticism, hypothyroidism), nephrotic syndrome, postprandial Hypoglycemia • Severely decreased functional hepatic mass (<75% of normal 5 ) • Differential diagnoses: sepsis, hypoadrenocorticism, toy breeds/puppies, insulinoma/other neoplasia, starvation, polycythemia, leukemia Hyperbilirubinemia • Cholestasis (intrahepatic, extrahepatic) • Differential diagnosis: hemolysis (in vivo, ex vivo) Decreased BUN • Decreased hepatic synthesis (portosystemic shunting, hepatic parenchymal disease) • Differential diagnosis: p olyuria (eg, fluid therapy, polydipsia) Increased SBA • Portosystemic shunting • Microvascular dysplasia (portal vein hypoplasia without portal hypertension) • Hepatic parenchymal disease • Extrahepatic bile duct obstruction • Differential diagnosis: small intestinal dysbiosis (possibly)