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Neonatal cholestasis refers to elevated levels of conjugated bilirubin identified in newborn infants within the first few months of life. [1] Conjugated hyperbilirubinemia is clinically defined as >20% of total serum bilirubin or conjugated bilirubin concentration greater than 1.0 mg/dL regardless of total serum bilirubin concentration. [2]
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.
Prolonged hyperbilirubinemia (severe jaundice) can result in chronic bilirubin encephalopathy (kernicterus). [5] [6] Quick and accurate treatment of neonatal jaundice helps to reduce the risk of neonates developing kernicterus. [7] Infants with kernicterus may have a fever [8] or seizures. [9] High pitched crying is an effect of kernicterus.
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.
The syndrome cannot cause severe indirect hyperbilirubinemia in neonates by itself, but it may have a summative effect on rising bilirubin when combined with other factors, [10] for example in the presence of increased red blood cell destruction due to diseases such as G6PD deficiency.
The conjugated hyperbilirubinemia is a result of defective endogenous and exogenous transfer of anionic conjugates from hepatocytes into bile. [5] Impaired biliary excretion of bilirubin glucuronides is due to a mutation in the canalicular multiple drug-resistance protein 2 (MRP2). A darkly pigmented liver is due to polymerized epinephrine ...
Moreover, the unconjugated hyperbilirubinemia arises in case the components of liver transfer the indirect bilirubin into bilirubin glucuronide in the rate slower than they should be. [3] This condition is associated with either decreased uptake of bilirubin into hepatocytes ( Rotor syndrome [ 34 ] ) or defective intracellular protein binding.
In some cases, the direct coombs will be negative but severe, even fatal HDN can occur. [35] An indirect coombs needs to be run in cases of anti-C, [36] anti-c, [36] and anti-M. Anti-M also recommends antigen testing to rule out the presence of HDN. [26] Hgb - the infant's hemoglobin should be tested from cord blood. [2]