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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.
Hyperbilirubinemia is classified into unconjugated and conjugated hyperbilirubinemia. The former, referring to elevated unconjugated bilirubin, is often caused by haemolytic diseases resulting in increased bilirubin production and impaired bilirubin conjugation.
Rotor syndrome (also known as Rotor type hyperbilirubinemia) [2] is a rare cause of mixed direct (conjugated) and indirect (unconjugated) hyperbilirubinemia, relatively benign, autosomal recessive [3] bilirubin disorder characterized by non-hemolytic jaundice due to the chronic elevation of predominantly conjugated bilirubin.
Hyperbilirubinemia may refer to increased levels of conjugated, unconjugated or both conjugated and unconjugated bilirubin. The causes of hyperbilirubinemia can also be classified into prehepatic, intrahepatic, and posthepatic. [21] Prehepatic causes are associated mostly with an increase of unconjugated (indirect) bilirubin. [21] They include:
These conditions are conventionally split into conjugated or unconjugated hyperbilirubinemias based on where the enzyme mutation occurs in bilirubin metabolism. [1] Unconjugated bilirubin is byproduct of red blood cell breakdown from the spleen which is not water soluble and is transported via albumin to the liver.
The bilirubin present in the plasma is largely unconjugated in this setting as they haven't been taken up and conjugated by the liver. [3] In this case, total serum bilirubin increases while the ratio of direct bilirubin to indirect bilirubin remains 96 to 4 as up to 96%-99% of bilirubin in the bile are conjugated mentioned above. [9] [1]
Bilirubin is conjugated with glucuronic acid in the liver by the enzyme glucuronyltransferase, making it soluble in water. Much of it goes into the bile and thus out into the small intestine. Although 20% of the secreted bilirubinoid bile is reabsorbed by the small intestine, [2] conjugated
Crigler–Najjar syndrome is a rare inherited disorder affecting the metabolism of bilirubin, a chemical formed from the breakdown of the heme in red blood cells. The disorder results in a form of nonhemolytic jaundice, which results in high levels of unconjugated bilirubin and often leads to brain damage in infants.