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=== Laboratory tests === {| class="wikitable" ! !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<ref>{{cite book| vauthors =Llewelyn H, Ang HA, Lewis K, Al-Abdullah A |url=https://books.google.com/books?id=rNFLBAAAQBAJ&pg=PA18|title=Oxford Handbook of Clinical Diagnosis |date=2014|publisher=Oxford University Press|isbn=978-0-19-967986-7|page=18|language=en |archive-url=https://web.archive.org/web/20170908204555/https://books.google.com/books?id=rNFLBAAAQBAJ&pg=PA18|archive-date=2017-09-08|url-status=live}}</ref> |Dark (urobilinogen, conjugated bilirubin) |Dark (conjugated bilirubin) |- !Stool color |Brown |Slightly pale |Pale, white |- !Alkaline phosphatase levels | rowspan="2" |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 (10β45 IU/L) and GGT (18β85 IU/L) levels rise proportionately as high as the AST (12β38 IU/L) and ALT (10β45 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.{{citation needed|date=July 2015}} 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 5β10 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 20β30 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 than normal.{{citation needed|date=July 2015}} Laboratory findings depend on the cause of jaundice: * Urine: conjugated bilirubin present, urobilinogen > 2 units but variable (except in children) * [[Plasma protein]]s show characteristic changes. * Plasma albumin level is low, but plasma [[globulin]]s are raised due to an increased formation of [[Antibody|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.<ref>{{cite web| vauthors = Cadogen M |date=2019-04-21|title=Bilirubin and Jaundice|url=https://litfl.com/bilirubin-and-jaundice/|access-date=2019-11-19|website=Life in the Fast Lane|language=en-US}}</ref> Urobilinogen will be greater than 2 units, as hemolytic anemia causes increased heme metabolism; one exception being the case of infants, where the [[gut flora]] has not developed). Conversely, conjugated bilirubin is hydrophilic and thus can be detected as present in the urineβ[[bilirubinuria]]βin contrast to unconjugated bilirubin, which is absent in the urine.<ref name="AFP2004">{{cite journal|vauthors=Roche SP, Kobos R|date=January 2004|title=Jaundice in the adult patient|journal=American Family Physician|volume=69|issue=2|pages=299β304|pmid=14765767}}</ref>
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