Uridine Diphosphate Glucuronosyltransfer…

It is possible that the primary title of the report Crigler Najjar Disorder is not the name you anticipated. Please inspect the words detailing to discover the alternating name(s) and problem class(s) covered by this record.


  • Genetic Unconjugated Hyperbilirubinemia
  • Domestic Nonhemolytic Unconjugated Hyperbilirubinemia

Condition Neighborhoods

  • Bilirubin Glucuronosyltransferase Deficiency Kind I.
  • Uridine Diphosphate Glucuronosyltransferase, Severe Def. Type I.
  • Congenital Familial Nonhemolytic Jaundice Kind I.
  • Congenital Familial Nonhemolytic Jaundice Type.

General Conversation
Crigler-Najjar disorder is a rare genetic disorder identified by elevated degrees of bilirubin in the blood (hyperbilirubinemia). Bilirubin is a yellow-colored waste item that is developed when the liver breaks down old or worn out red blood cells (hemolysis). Individuals with Crigler-Najjar disorder create hyperbilirubinemia in the lack of hemolysis. The elevated bilirubin degrees occur considering that affected people do not have a certain liver enzyme required to break down (metabolize) bilirubin. The trademark finding of Crigler-Najjar disorder is persistent yellowing of the skin, mucous membranes and whites of the eyes (jaundice). There are 2 kinds of this condition: Crigler-Najjar disorder kind I, characterized by an almost full absence of enzyme task and severe signs; and also Crigler-Najjar syndrome type II, identified by partial enzyme activity as well as milder signs and symptoms. A lot of cases of Crigler-Najjar syndrome are acquired as autosomal recessive characteristics and also are due to mistakes or disruptions (anomalies) of the UGT1 gene positioned on chromosome 2.

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