Biliary-tract dilation due to obstruction as seen on CT scan (frontal plane) Biliary-tract dilation due to obstruction as seen on CT scan (axial plane) Most people presenting with jaundice have various predictable patterns of liver panel abnormalities, though significant variation does exist. The typical liver panel includes blood levels of enzymes found primarily from the liver, such as the aminotransferases (ALT, AST), and alkaline<unk> se (ALP); bilirubin (which causes the jaundice); and protein levels, specifically, total protein and albumin. Other primary lab tests for liver function include gamma glutamyl transpeptidase (GGT) and prothrombin time (PT). No single test can differentiate between various classifications of jaundice. A combination of liver function tests and other physical examination findings is essential to arrive at a diagnosis. Laboratory tests Prehepatic jaundice Hepatic jaundice Posthepatic jaundice Total serum bilirubin Normal / increased Increased Increased Conjugated bilirubin Normal Increased Increased Unconjugated bilirubin Normal / increased Increased Normal Urobilinogen Normal / increased Decreased Decreased / negative Urine color Normal Dark (urobilinogen, conjugated bilirubin) Dark (conjugated bilirubin) Stool color Brown Slightly pale Pale, white Alkaline<unk> se levels Normal Increased Highly increased Alanine transferase and aspartate transferase levels Highly increased Increased Conjugated bilirubin in urine Not present Present Present Some bone and heart disorders can lead to an increase in ALP and the aminotransferases, so the first step in differentiating these from liver problems is to compare the levels of GGT, which are only elevated in liver-specific conditions. The second step is distinguishing from biliary (cholestatic) or liver causes of jaundice and altered laboratory results. ALP and GGT levels typically rise with one pattern while aspartate aminotransferase (AST) and alanine aminotransferase (ALT) rise in a separate pattern. If the ALP (10–45 IU/l) and GGT (18–85 IU/l) levels rise proportionately as high as the AST (12–38 IU/l) and ALT (10–45 IU/l) levels, this indicates a cholestatic problem. If the AST and ALT rise is significantly higher than the ALP and GGT rise, though, this indicates a liver problem. Finally, distinguishing between liver causes of jaundice, comparing levels of AST and ALT can prove useful. AST levels typically are higher than ALT. This remains the case in most liver disorders except for hepatitis (viral or hepatotoxic). Alcoholic liver damage may have fairly normal ALT levels, with AST 10 times higher than ALT. If ALT is higher than AST, however, this is indicative of hepatitis. Levels of ALT and AST are not well correlated to the extent of liver damage, although rapid drops in these levels from very high levels can indicate severe necrosis. Low levels of albumin tend to indicate a chronic condition, while the level is normal in hepatitis and cholestasis. Laboratory results for liver panels are frequently compared by the magnitude of their differences, not the pure number, as well as by their ratios. The AST:ALT ratio can be a good indicator of whether the disorder is alcoholic liver damage (above 10), some other form of liver damage (above 1), or hepatitis (less than 1). Bilirubin levels greater than 10 times normal could indicate neoplastic or intrahepatic cholestasis. Levels lower than this tend to indicate hepatocellular causes. AST levels greater than 15 times normal tend to indicate acute hepatocellular damage. Less than this tend to indicate obstructive causes. ALP levels greater than 5 times normal tend to indicate obstruction, while levels greater than 10 times normal can indicate drug (toxin) induced cholestatic hepatitis or cytomegalovirus infection. Both of these conditions can also have ALT and AST greater than 20 times normal. GGT levels greater than 10 times normal typically indicate cholestasis. Levels 5–10 times tend to indicate viral hepatitis. Levels less than 5 times normal tend to indicate drug toxicity. Acute hepatitis typically has ALT and AST levels rising 20–30 times normal (above 1000) and may remain significantly elevated for several weeks. Acetaminophen toxicity can result in ALT and AST levels greater than 50 times normal. Laboratory findings depend on the cause of jaundice: * Urine: conjugated bilirubin present, urobilinogen > 2 units but variable (except in children) * Plasma proteins show characteristic changes. * Plasma albumin level is low, but plasma globulins are raised due to an increased formation of antibodies. Unconjugated bilirubin is hydrophobic, so cannot be excreted in urine. Thus, the finding of increased urobilinogen in the urine without the presence of bilirubin in the urine (due to its unconjugated state) suggests hemolytic jaundice as the underlying disease process. Urobilinogen will be greater than 2 units (i.e., hemolytic anemia causes increased heme metabolism; exception: infants where gut flora has not developed). Conversely, conjugated bilirubin is hydrophilic and thus can be detected as present in the urine — bilirubinuria — in contrast to unconjugated bilirubin which is absent in the urine. Imaging Medical imaging such as ultrasound, CT scan, and HIDA scan are useful for detecting bile-duct blockage. Differential diagnosis Yellow discoloration of the skin, especially on the palms and the soles, but not of the sclera or inside the mouth, is due to carotenemia—a harmless condition.
symptom of Glucose-6-phosphate dehydrogenase deficiency
symptom of Phenylketonuria
symptom of Pyruvate carboxylase deficiency
symptom of Dubin–Johnson syndrome
symptom of Glycogen storage disease type III
symptom of Arsenic poisoning
symptom of Atransferrinemia
symptom of Beta-mannosidosis