<unk>  is a colorless by-product of bilirubin reduction. It is formed in the intestines by bacterial action on bilirubin. About half of the<unk>  formed is reabsorbed and taken up via the portal vein to the liver, enters circulation and is excreted by the kidney. Increased amounts of bilirubin are formed in hemolysis, which generates increased<unk>  in the gut. In liver disease (such as hepatitis), the intrahepatic<unk>  cycle is inhibited also increasing<unk>  levels.<unk>  is converted to the yellow pigmented<unk> ilin apparent in urine. The<unk>  in the intestine is directly reduced to brown stercobilin, which gives the feces their characteristic color. It can also be reduced to stercobilinogen, which can then be further oxidized to stercobilin. In biliary obstruction, below-normal amounts of conjugated bilirubin reach the intestine for conversion to<unk> . With limited<unk>  available for reabsorption and excretion, the amount of<unk> ilin found in the urine is low. High amounts of the soluble conjugated bilirubin enter the circulation where they are excreted via the kidneys. These mechanisms are responsible for the dark urine and pale stools observed in biliary obstruction. Low urine<unk>  may result from complete obstructive jaundice or treatment with broad-spectrum antibiotics, which destroy the intestinal bacterial flora. (Obstruction of bilirubin passage into the gut or failure of<unk>  production in the gut.) Low urine<unk>  levels may result from congenital enzymatic jaundice (hyperbilirubinemia syndromes) or from treatment with drugs that acidify urine, such as ammonium chloride or ascorbic acid. Elevated levels may indicate hemolytic anaemia (excessive breakdown of red blood cells RBC), overburdening of the liver, increased<unk>  production, re-absorption – a large hematoma, restricted liver function, hepatic infection, poisoning or liver cirrhosis.
Urobilinogen
Niquitin
Cellulite
Orthosilicic acid
Ferric maltol
Glucomannan
Mirificin
Wobenzym