Gallstone disease in Swedish twins is associated with the Gilbert variant of UGT1A1.

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Fältnamn	Indikatorer	Metadata
000		03653naa a2200409 4500
001		oai:gup.ub.gu.se/176523
003		SwePub
008		240528s2013 \| \|\|\|\|\|\|\|\|\|\|\|000 \|\|eng\|
009		oai:prod.swepub.kib.ki.se:126874439
024	7	a https://gup.ub.gu.se/publication/1765232 URI
024	7	a https://doi.org/10.1111/liv.121412 DOI
024	7	a http://kipublications.ki.se/Default.aspx?queryparsed=id:1268744392 URI
040		a (SwePub)gud (SwePub)ki
041		a eng
042		9 SwePub
072	7	a ref2 swepub-contenttype
072	7	a art2 swepub-publicationtype
100	1	a Marschall, Hanns-Ulrich,d 1954u Gothenburg University,Göteborgs universitet,Institutionen för medicin, avdelningen för molekylär och klinisk medicin,Institute of Medicine, Department of Molecular and Clinical Medicine4 aut0 (Swepub:gu)xmarsh
245	1 0	a Gallstone disease in Swedish twins is associated with the Gilbert variant of UGT1A1.
264		c 2013-03-20
264	1	b Wiley,c 2013
520		a BACKGROUND & AIMS: The Gilbert syndrome-associated functional TATA box variant UGT1A128 (A(TA)7 TAA) was found to increase susceptibility to pigment gallstone formation in patients with haemolytic anaemia. Further studies in extensive cohorts demonstrated an increased risk of this variant for cholesterol gallstone disease (GD). We now investigated this polymorphism as a determinant of symptomatic GD in Swedish twins. METHODS: The Swedish Twin Registry was merged with the Hospital Discharge and Causes of Death Registries and searched for GD-related diagnoses among monozygotic (MZ) twins living in the Stockholm area. In addition, we screened the TwinGene database for GD. In total, we found 44 MZ twin pairs with and eight MZ twins without GD to be evaluable. GD-free twins from TwinGene (109 concordantly MZ and 126 independent DZ) served as controls. UGT1A128 genotyping was performed using TaqMan assays. RESULTS: Overall, 58 and 8 of 106 twins with GD were hetero- and homozygous UGT1A1 risk allele carriers respectively. The case-control association tests showed a significantly (P<0.05) increased risk of developing GD (OR=1.62, 95% CI 1.00-2.63) in heterozygotes carriers and in addition, a trend (P=0.075) for an increased risk among carriers (OR=1.52, 95% CI 0.97-2.44) of the risk allele. CONCLUSION: These data from Swedish twins confirm the Gilbert variant as risk factor for GD. Our observation is in line with nucleation in bilirubin supersaturated bile representing an initial step in cholelithogenesis.
650	7	a MEDICIN OCH HÄLSOVETENSKAPx Klinisk medicin0 (SwePub)3022 hsv//swe
650	7	a MEDICAL AND HEALTH SCIENCESx Clinical Medicine0 (SwePub)3022 hsv//eng
650	7	a MEDICIN OCH HÄLSOVETENSKAPx Klinisk medicinx Gastroenterologi0 (SwePub)302132 hsv//swe
650	7	a MEDICAL AND HEALTH SCIENCESx Clinical Medicinex Gastroenterology and Hepatology0 (SwePub)302132 hsv//eng
700	1	a Krawczyk, Marcin4 aut
700	1	a Grünhage, Frank4 aut
700	1	a Katsika, Despina4 aut
700	1	a Einarsson, Curt4 aut
700	1	a Lammert, Frank4 aut
710	2	a Göteborgs universitetb Institutionen för medicin, avdelningen för molekylär och klinisk medicin4 org
773	0	t Liver international : official journal of the International Association for the Study of the Liverd : Wileyg 33:6, s. 904-8q 33:6<904-8x 1478-3231
773	0	t Liver Internationald : Wileyg 33:6, s. 904-8q 33:6<904-8x 1478-3223
856	4 8	u https://gup.ub.gu.se/publication/176523
856	4 8	u https://doi.org/10.1111/liv.12141
856	4 8	u http://kipublications.ki.se/Default.aspx?queryparsed=id:126874439

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