Urobilinogen (urobilinogenuria): small amounts are normal, excessive amounts could indicate urinary system dysfunctioning or possibly liver dysfunction, congestive heart failure, cirrhosis of the liver or infectious mononucleosis
Bilirubinuria (Urinary Bilirubin)
Bile (mainly conjugated bilirubin) is converted to urobilinogen by intestinal bacteria. Most of the urobilinogen is excreted in faeces or reabsorbed and transported back to the liver to be converted back into bile. The remaining urobilinogen (about 1% of total) is excreted in the urine.
The amount of conjugated bilirubin present in serum in healthy subjects is small (less than 10% of total bilirubin). An elevated level of conjugated serum bilirubin implies liver disease. Therefore, because only conjugated bilirubin appears in urine, bilirubinuria also implies liver disease.
Unconjugated hyperbilirubin is tightly bound to albumin, not filtered by the glomerulus and absent from urine even with raised serum levels of unconjugated bilirubin. A positive test for urine bilirubin confirms that any raised plasma levels are from conjugated hyperbilirubinemia.
In the assessment of a patient with raised total bilirubin, urinanalysis for bilirubin and urobilinogen, together with liver function tests may be helpful in identifying the underlying pathology.
Bilirubin Fractions Present in Blood and Urine
In Serum As: Measured As: Present in Urine
Unconjugated Albumin-bound Indirect-reacting bilirubin Never
Conjugated Unbound Direct-reacting bilirubin Yes
Method of testing
The bilirubin pad on the multireagent dipstick detects bilirubin using a specific diazo reagent. It allows a very approximate quantification of bilirubinuria.
The colour change indicating a positive reaction may be a subtle transition among shades of beige and is sometimes is obscured by colour of the urine itself (e.g. in marked hemoglobinuria).
Common Causes of Raised Bilirubin and Urobilinogen:
Raised conjugated bilirubin (bilirubinuria):
Heptocellular disease and post-hepatic or cholestatic disease (intrahepatic and extrahepatic), including drug toxicity as well as pancreatic causes of obstructive jaundice. An early feature of hepatobiliary disease can be bilirubinuria, which develops in acute viral hepatitis even before clinical jaundice appears. It may be absent, however, under other circumstances despite increased serum bilirubin.
Inherited defects in excretion, e.g. Dubin-Johnson and Rotor's syndromes.
Raised unconjugated bilirubin (no bilirubinuria):
Gilbert's syndrome (4% of the population).
Haemolysis.
Post viral hepatitis.
Mild chronic hepatitis.
Crigler-Najjar syndrome.
Urinary urobilinogen:
Normally excreted in small amounts into the urine.
Very sensitive but non-specific test to determine liver damage, haemolytic disease and severe infections.
Increases in early hepatitis, mild liver cell damage and mild toxic injury, even without an increase in serum bilirubin.
Decreased or absent in obstructive jaundice.
False negative and false positive reactions
False negative:
Aged urine samples: Conjugated bilirubin hydrolyzes to unconjugated bilirubin if left at room temperature.
Exposure to UV light: UV light converts bilirubin to biliverdin, resulting in false negative reactions.
Patient taking rifampicin
Ascorbic acid: High concentrations of vitamin C inhibit the reaction.
False positive:
Patient taking phenothiazines
2006-09-18 15:45:25
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answer #1
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answered by Mysterious 3
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