Hyperbilirubinemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
ATV/rit-related hyperbilirubinemia has been previously associated with genetic characteristics in uridine diphosphate glucuronosyltransferase (UGT) enzyme.
|
28790862 |
2017 |
Hyperbilirubinemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
This study aimed to characterise the role of UGT1A1 inhibition in hyperbilirubinemia and assess the broader potential of these drugs to perpetrate drug-drug interactions arising from UGT enzyme inhibition.
|
28065859 |
2017 |
Hyperbilirubinemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Here we use a new mouse model that targets deletion of the Ugt1 locus and the Ugt1a1 gene in liver to promote hyperbilirubinemia-induced seizures and central nervous system toxicity.
|
26480925 |
2016 |
Hyperbilirubinemia
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Reduced expression of UGT1A1 in intestines of humanized UGT1 mice via inactivation of NF-κB leads to hyperbilirubinemia.
|
21983082 |
2012 |
Hyperbilirubinemia
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Genetic polymorphisms affecting the activity and/or the expression of cytochromes P450 or UGT isozymes and membrane drug transport proteins are highlighted and include such examples as the association of neurotoxicity with efavirenz, nephrotoxicity with tenofovir, hepatotoxicity with nevirapine, and hyperbilirubinemia with indinavir and atazanavir.
|
22759796 |
2012 |
Hyperbilirubinemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Adult Tg(UGT1(A1*28))Ugt1(-/-) mice expressed elevated levels of total bilirubin (TB) compared with Tg(UGT1(A1*1))Ugt1(-/-) mice, confirming that the promoter polymorphism associated with the UGT1A1*28 allele contributes to hyperbilirubinemia in mice.
|
20194756 |
2010 |
Hyperbilirubinemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Variations in B-UGT gene (UGT-1A1) have been related to disorders characterised by hyperbilirubinaemia.
|
16623861 |
2006 |
Hyperbilirubinemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Both within and between the G-6-PD-deficient and control groups, our data demonstrate changing and differing contributions of hemolysis and UGT promoter polymorphism to bilirubinemia during the first 3 d of life.
|
11568299 |
2001 |
Hyperbilirubinemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Whereas G-6-PD deficiency or Gilbert's Syndrome, alone, did not predispose to hyperbilirubinemia, G-6-PD-deficient neonates who also were heterozygotes or homozygotes for the variant UGT gene promoter did have significantly increased incidences of hyperbilirubinemia.
|
11803413 |
2001 |
Hyperbilirubinemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
The incidence of hyperbilirubinaemia was significantly higher only in the former who were also homozygotes for the variant UGT promoter, compared with ABO-incompatible babies homozygous for the normal UGT promoter (43% vs 0, p=0.02), and with ABO-compatible controls of all UGT genotypes combined (relative risk 5.65, 95% CI 2.23-14.31).
|
10968441 |
2000 |
Hyperbilirubinemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
We have previously reported that the Gly71Arg mutation of the B-UGT gene associated with Gilbert syndrome is prevalent in Japanese, Korean, and Chinese populations and was more frequently detected in neonates with severe hyperbilirubinemia than in control subjects.
|
9929972 |
1999 |
Hyperbilirubinemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Elucidation of both the structure of the UGT1 gene complex, and the Mrp2 (cMoat) gene which encodes the canalicular conjugate export pump, has led to a greater understanding of the genetic basis of hyperbilirubinemia.
|
9748558 |
1998 |