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Conjugated bilirubin, being water-soluble, is excreted through urine. Hence, dark urine tested bilirubin positive signifies conjugated hyperbilirubinemia. [3] A peripheral blood smear showing signs of haemolysis. Red blood cells are normally in a biconcave shape (round cells in this picture).
Bilirubin (BR) (from the Latin for "red bile") is a red-orange compound that occurs in the normal catabolic pathway that breaks down heme in vertebrates.This catabolism is a necessary process in the body's clearance of waste products that arise from the destruction of aged or abnormal red blood cells. [3]
Pathological jaundice in newborns should be suspected when the serum bilirubin level rises by more than 5 mg/dL per day, serum bilirubin more than the physiological range, clinical jaundice more than 2 weeks, and conjugated bilirubin (dark urine staining clothes). Haemolytic jaundice is the commonest cause of pathological jaundice.
Van den Bergh reaction is a chemical reaction used to measure bilirubin levels in blood. [1] [2] More specifically, it determines the amount of conjugated bilirubin in the blood. The reaction produces azobilirubin. Principle: bilirubin reacts with diazotised sulphanilic acid to produce purple coloured azobilirubin. [3]
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]
Around 80 to 99% of people with Dubin–Johnson syndrome have jaundice, [3] [4] abnormal urinary color, biliary tract abnormality, and conjugated bilirubinemia. [4] Around 30 to 79% of people with the disorder have abnormality of the gastric mucosa. [4] Other rare symptoms include fever and fatigue. [3]
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
Rotor type hyperbilirubinemia is a distinct yet similar disorder to Dubin–Johnson syndrome [1] – both diseases cause an increase in conjugated bilirubin, but Rotor syndrome differs in that it is a result of impaired hepatocellular storage of conjugated bilirubin that leaks into plasma causing hyperbilirubinemia.