Gilbert syndrome, UGT1A1*28 allele, and cardiovascular disease risk: possible protective effects and therapeutic applications of bilirubin.
In April of 1995, he had an acute myocardial infarction and was also diagnosed with hepatitis B and
Gilbert syndrome.
A 61 year old male with a history of coronary artery disease, hyperlipidemia,
Gilbert syndrome, and hypothyroidism had routine laboratory studies which revealed coagulation abnormalities.
In contrast,
Gilbert syndrome (OMIM 145300), a mild inherited form of unconjugated hyperbilirubinemia that occurs in 15% of the population, is usually not treated or diagnosed because there are usually no clinical symptoms (7, 8); however,
Gilbert syndrome increases the risk of drug toxicity during cancer chemotherapy with irinotecan (Camptosar[R]; Pfizer) (9-11).
Both common and rare hereditary hepatic diseases, such as hereditary hemocliromatosis,
Gilbert syndrome (benign hyperbilirubinemia), Wilson's disease (a copper metabolism abnormality), and [alpha]1 - antitrypsin deficiency syndrome may be found in families.
We discuss the example of
Gilbert syndrome to illustrate the partitioning decision process.
Both common and rare hereditary hepatic diseases, such as hereditary hemochromatosis,
Gilbert syndrome (benign hyperbilirubinemia), Wilson's disease (a copper metabolism abnormality), and [alpha] l-antitrypsin deficiency syndrome may be found in families.
9), who found significantly lower concentrations of soluble forms of CD40 ligand and P-selectin in subjects with
Gilbert syndrome (GS).
7]TAA (allele *28, reduced transcription) and G71R (211G>A, allele *6, reduced activity), are causative factors for increased plasma bilirubin concentrations in
Gilbert syndrome (1).
Gilbert syndrome is an inborn error of bilirubin conjugation caused by mutations in the conjugating enzyme uridine diphosphate glucuronyltransferase (UGT1A1) (1).
Mild hyperbilirubinemia, usually <50 [micro]mol/L, is associated with
Gilbert syndrome (GS) and is thought to reflect a small reduction in UGT1A1 activity (1,2).
Identified causes of false positives and false negatives in the combination of FT-AT included
Gilbert syndrome, hemolysis, and inflammation (8).
