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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.
According to the Mayo Clinic, Gilbert syndrome is a common and harmless liver condition caused by a modified gene inherited from parents.
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.
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Gilbert's syndrome and Crigler–Najjar syndrome have defects in the UDP-glucuronyl-transferase enzyme, affecting bilirubin conjugation. [6] The degree of rise in conjugated bilirubin is directly proportional to the degree of hepatocyte injury. Viral hepatitis can also cause the rise in conjugated bilirubin.
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