Glucuronide Formation in Patients with Constitutional Hepatic Dysfunction (Gilbert's Disease)

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Abstract
IT has been shown that bilirubin has to be converted to its glucuronide or sulfate1 2 3 4 before it can be excreted in the bile. Retention of nonconjugated bilirubin in the plasma, associated with an enzymatic defect in glucuronide formation in the liver, has been demonstrated in a strain of rats with congenital icterus.5 , 6 A similar defect in glucuronide formation has been found in children with severe congenital nonhemolytic jaundice (Crigler–Najjar syndrome).7 8 9 It has been suggested that, in patients with constitutional hepatic dysfunction or so-called Gilbert disease,10 the mild and intermittent icterus may be the result of a similar but less severe . . .