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Gilbert syndrome (GS) is a syndrome in which the liver of affected individuals processes bilirubin more slowly than the majority. [1] Many people never have symptoms. [ 1 ] Occasionally jaundice (a slight yellowish color of the skin or whites of the eyes) may occur.
Gilbert Syndrome, a hereditary disease affecting 5% of the US population, leads to stress-induced mild hyperbilirubinemia. [9] The mutated UGT1 gene produces defective UGT1A1 enzymes vital for bilirubin conjugation.
Gilbert Syndrome is a partial reduction in UGT1A1's activity which causes transient hyperbilirubinemia during various stressors, like fasting or acute illness. Gilbert syndrome is inherited in both autosomal dominant and autosomal recession nature. Crigler-Najjar syndrome is much more severe and presents in newborns.
Grisel's syndrome; Growing teratoma syndrome; Gilbert's syndrome; Gulf War syndrome; H. Haber syndrome; Hagemoser–Weinstein–Bresnick syndrome; Haglund's syndrome;
UGT1A1, UGT1A6, and UGT1A7 (enzymes deficient in most people with Gilbert's syndrome) deal with much more than just bilirubin. This wiki page is outdated and inaccurate because it fails to mention what other substances the enzymes process and the effects of their deficiency in people with Gilbert's syndrome, theoretically speaking.
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Gilbert's syndrome – a genetic disorder of bilirubin metabolism that can result in mild jaundice, found in about 5% of the population; Rotor syndrome: non-itching jaundice, with rise of bilirubin in the patient's serum, mainly of the conjugated type; Dubin–Johnson syndrome; Crigler–Najjar syndrome
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