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- W2005077483 abstract "While Gilbert's syndrome is extremely common and benign, its pathogenesis may not be as straightforward as once believed. It has been used as a model to examine aberrations of virtually every step in bilirubin metabolism. The clinical hallmarks are of a hereditary, chronic, mild unconjugated hyperbilirubinaemia. Not infrequently subclinical haemolysis may coexist. Liver histology is normal although some minor ultrastructural abnormalities may be evident. The universal defect appears to be a reduction in hepatic bilirubin-GT activity. However, other associated abnormalities in bilirubin metabolism, which occur less consistently, suggest that this may not be the sole defect in all patients. The syndrome is almost certainly part of a spectrum which includes the Crigler-Najjar syndromes; molecular biology data suggests that there is an absence of one (or even more) GT isoenzymes in these disorders. Whether one or more genes is consistently culpable remains open to speculation. Despite the complicated pathogenesis of Gilbert's syndrome, management remains simply reassurance alone." @default.
- W2005077483 created "2016-06-24" @default.
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- W2005077483 date "1989-04-01" @default.
- W2005077483 modified "2023-09-27" @default.
- W2005077483 title "Gilbert's syndrome" @default.
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- W2005077483 doi "https://doi.org/10.1016/0950-3528(89)90004-3" @default.
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