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Gout: HELP
Articles by Grant W. Montgomery
Based on 4 articles published since 2009
(Why 4 articles?)
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Between 2009 and 2019, G. Montgomery wrote the following 4 articles about Gout.
 
+ Citations + Abstracts
1 Article Twenty-eight loci that influence serum urate levels: analysis of association with gout. 2016

Phipps-Green, A J / Merriman, M E / Topless, R / Altaf, S / Montgomery, G W / Franklin, C / Jones, G T / van Rij, A M / White, D / Stamp, L K / Dalbeth, N / Merriman, T R. ·Department of Biochemistry, University of Otago, Dunedin, New Zealand. · Queensland Institute of Medical Research, Brisbane, Queensland, Australia. · Department of Medicine, University of Auckland, Auckland, New Zealand. · Department of Medicine, University of Otago, Dunedin, New Zealand. · Waikato District Health Board, Hamilton, New Zealand. · Department of Medicine, University of Otago, Christchurch, New Zealand. ·Ann Rheum Dis · Pubmed #25187157.

ABSTRACT: OBJECTIVES: Twenty-eight genetic loci are associated with serum urate levels in Europeans. Evidence for association with gout at most loci is absent, equivocal or not replicated. Our aim was to test the loci for association with gout meeting the American College of Rheumatology gout classification criteria in New Zealand European and Polynesian case-control sample sets. METHODS: 648 European cases and 1550 controls, and 888 Polynesian (Ma¯ori and Pacific) cases and 1095 controls were genotyped. Association with gout was tested by logistic regression adjusting for age and sex. Power was adequate (>0.7) to detect effects of OR>1.3. RESULTS: We focused on 24 loci without previous consistent evidence for association with gout. In Europeans, we detected association at seven loci, one of which was the first report of association with gout (IGF1R). In Polynesian, association was detected at three loci. Meta-analysis revealed association at eight loci-two had not previously been associated with gout (PDZK1 and MAF). In participants with higher Polynesian ancestry, there was association in an opposing direction to Europeans at PRKAG2 and HLF (HLF is the first report of association with gout). There was obvious inconsistency of gout association at four loci (GCKR, INHBC, SLC22A11, SLC16A9) that display very similar effects on urate levels. CONCLUSIONS: We provide the first evidence for association with gout at four loci (IGF1R, PDZK1, MAF, HLF). Understanding why there is lack of correlation between urate and gout effect sizes will be important in understanding the aetiology of gout.

2 Article Association analysis of the SLC22A11 (organic anion transporter 4) and SLC22A12 (urate transporter 1) urate transporter locus with gout in New Zealand case-control sample sets reveals multiple ancestral-specific effects. 2013

Flynn, Tanya J / Phipps-Green, Amanda / Hollis-Moffatt, Jade E / Merriman, Marilyn E / Topless, Ruth / Montgomery, Grant / Chapman, Brett / Stamp, Lisa K / Dalbeth, Nicola / Merriman, Tony R. · ·Arthritis Res Ther · Pubmed #24360580.

ABSTRACT: INTRODUCTION: There is inconsistent association between urate transporters SLC22A11 (organic anion transporter 4 (OAT4)) and SLC22A12 (urate transporter 1 (URAT1)) and risk of gout. New Zealand (NZ) Māori and Pacific Island people have higher serum urate and more severe gout than European people. The aim of this study was to test genetic variation across the SLC22A11/SLC22A12 locus for association with risk of gout in NZ sample sets. METHODS: A total of 12 single nucleotide polymorphism (SNP) variants in four haplotype blocks were genotyped using TaqMan® and Sequenom MassArray in 1003 gout cases and 1156 controls. All cases had gout according to the 1977 American Rheumatism Association criteria. Association analysis of single markers and haplotypes was performed using PLINK and Stata. RESULTS: A haplotype block 1 SNP (rs17299124) (upstream of SLC22A11) was associated with gout in less admixed Polynesian sample sets, but not European Caucasian (odds ratio; OR = 3.38, P = 6.1 × 10-4; OR = 0.91, P = 0.40, respectively) sample sets. A protective block 1 haplotype caused the rs17299124 association (OR = 0.28, P = 6.0 × 10-4). Within haplotype block 2 (SLC22A11) we could not replicate previous reports of association of rs2078267 with gout in European Caucasian (OR = 0.98, P = 0.82) sample sets, however this SNP was associated with gout in Polynesian (OR = 1.51, P = 0.022) sample sets. Within haplotype block 3 (including SLC22A12) analysis of haplotypes revealed a haplotype with trans-ancestral protective effects (OR = 0.80, P = 0.004), and a second haplotype conferring protection in less admixed Polynesian sample sets (OR = 0.63, P = 0.028) but risk in European Caucasian samples (OR = 1.33, P = 0.039). CONCLUSIONS: Our analysis provides evidence for multiple ancestral-specific effects across the SLC22A11/SLC22A12 locus that presumably influence the activity of OAT4 and URAT1 and risk of gout. Further fine mapping of the association signal is needed using trans-ancestral re-sequence data.

3 Article Genome-wide association analyses identify 18 new loci associated with serum urate concentrations. 2013

Köttgen, Anna / Albrecht, Eva / Teumer, Alexander / Vitart, Veronique / Krumsiek, Jan / Hundertmark, Claudia / Pistis, Giorgio / Ruggiero, Daniela / O'Seaghdha, Conall M / Haller, Toomas / Yang, Qiong / Tanaka, Toshiko / Johnson, Andrew D / Kutalik, Zoltán / Smith, Albert V / Shi, Julia / Struchalin, Maksim / Middelberg, Rita P S / Brown, Morris J / Gaffo, Angelo L / Pirastu, Nicola / Li, Guo / Hayward, Caroline / Zemunik, Tatijana / Huffman, Jennifer / Yengo, Loic / Zhao, Jing Hua / Demirkan, Ayse / Feitosa, Mary F / Liu, Xuan / Malerba, Giovanni / Lopez, Lorna M / van der Harst, Pim / Li, Xinzhong / Kleber, Marcus E / Hicks, Andrew A / Nolte, Ilja M / Johansson, Asa / Murgia, Federico / Wild, Sarah H / Bakker, Stephan J L / Peden, John F / Dehghan, Abbas / Steri, Maristella / Tenesa, Albert / Lagou, Vasiliki / Salo, Perttu / Mangino, Massimo / Rose, Lynda M / Lehtimäki, Terho / Woodward, Owen M / Okada, Yukinori / Tin, Adrienne / Müller, Christian / Oldmeadow, Christopher / Putku, Margus / Czamara, Darina / Kraft, Peter / Frogheri, Laura / Thun, Gian Andri / Grotevendt, Anne / Gislason, Gauti Kjartan / Harris, Tamara B / Launer, Lenore J / McArdle, Patrick / Shuldiner, Alan R / Boerwinkle, Eric / Coresh, Josef / Schmidt, Helena / Schallert, Michael / Martin, Nicholas G / Montgomery, Grant W / Kubo, Michiaki / Nakamura, Yusuke / Tanaka, Toshihiro / Munroe, Patricia B / Samani, Nilesh J / Jacobs, David R / Liu, Kiang / D'Adamo, Pio / Ulivi, Sheila / Rotter, Jerome I / Psaty, Bruce M / Vollenweider, Peter / Waeber, Gerard / Campbell, Susan / Devuyst, Olivier / Navarro, Pau / Kolcic, Ivana / Hastie, Nicholas / Balkau, Beverley / Froguel, Philippe / Esko, Tõnu / Salumets, Andres / Khaw, Kay Tee / Langenberg, Claudia / Wareham, Nicholas J / Isaacs, Aaron / Kraja, Aldi / Zhang, Qunyuan / Wild, Philipp S / Scott, Rodney J / Holliday, Elizabeth G / Org, Elin / Viigimaa, Margus / Bandinelli, Stefania / Metter, Jeffrey E / Lupo, Antonio / Trabetti, Elisabetta / Sorice, Rossella / Döring, Angela / Lattka, Eva / Strauch, Konstantin / Theis, Fabian / Waldenberger, Melanie / Wichmann, H-Erich / Davies, Gail / Gow, Alan J / Bruinenberg, Marcel / Anonymous4691162 / Stolk, Ronald P / Kooner, Jaspal S / Zhang, Weihua / Winkelmann, Bernhard R / Boehm, Bernhard O / Lucae, Susanne / Penninx, Brenda W / Smit, Johannes H / Curhan, Gary / Mudgal, Poorva / Plenge, Robert M / Portas, Laura / Persico, Ivana / Kirin, Mirna / Wilson, James F / Mateo Leach, Irene / van Gilst, Wiek H / Goel, Anuj / Ongen, Halit / Hofman, Albert / Rivadeneira, Fernando / Uitterlinden, Andre G / Imboden, Medea / von Eckardstein, Arnold / Cucca, Francesco / Nagaraja, Ramaiah / Piras, Maria Grazia / Nauck, Matthias / Schurmann, Claudia / Budde, Kathrin / Ernst, Florian / Farrington, Susan M / Theodoratou, Evropi / Prokopenko, Inga / Stumvoll, Michael / Jula, Antti / Perola, Markus / Salomaa, Veikko / Shin, So-Youn / Spector, Tim D / Sala, Cinzia / Ridker, Paul M / Kähönen, Mika / Viikari, Jorma / Hengstenberg, Christian / Nelson, Christopher P / Anonymous4701162 / Anonymous4711162 / Anonymous4721162 / Anonymous4731162 / Meschia, James F / Nalls, Michael A / Sharma, Pankaj / Singleton, Andrew B / Kamatani, Naoyuki / Zeller, Tanja / Burnier, Michel / Attia, John / Laan, Maris / Klopp, Norman / Hillege, Hans L / Kloiber, Stefan / Choi, Hyon / Pirastu, Mario / Tore, Silvia / Probst-Hensch, Nicole M / Völzke, Henry / Gudnason, Vilmundur / Parsa, Afshin / Schmidt, Reinhold / Whitfield, John B / Fornage, Myriam / Gasparini, Paolo / Siscovick, David S / Polašek, Ozren / Campbell, Harry / Rudan, Igor / Bouatia-Naji, Nabila / Metspalu, Andres / Loos, Ruth J F / van Duijn, Cornelia M / Borecki, Ingrid B / Ferrucci, Luigi / Gambaro, Giovanni / Deary, Ian J / Wolffenbuttel, Bruce H R / Chambers, John C / März, Winfried / Pramstaller, Peter P / Snieder, Harold / Gyllensten, Ulf / Wright, Alan F / Navis, Gerjan / Watkins, Hugh / Witteman, Jacqueline C M / Sanna, Serena / Schipf, Sabine / Dunlop, Malcolm G / Tönjes, Anke / Ripatti, Samuli / Soranzo, Nicole / Toniolo, Daniela / Chasman, Daniel I / Raitakari, Olli / Kao, W H Linda / Ciullo, Marina / Fox, Caroline S / Caulfield, Mark / Bochud, Murielle / Gieger, Christian. ·Renal Division, Freiburg University Hospital, Freiburg, Germany. anna.koettgen@uniklinik-freiburg.de ·Nat Genet · Pubmed #23263486.

ABSTRACT: Elevated serum urate concentrations can cause gout, a prevalent and painful inflammatory arthritis. By combining data from >140,000 individuals of European ancestry within the Global Urate Genetics Consortium (GUGC), we identified and replicated 28 genome-wide significant loci in association with serum urate concentrations (18 new regions in or near TRIM46, INHBB, SFMBT1, TMEM171, VEGFA, BAZ1B, PRKAG2, STC1, HNF4G, A1CF, ATXN2, UBE2Q2, IGF1R, NFAT5, MAF, HLF, ACVR1B-ACVRL1 and B3GNT4). Associations for many of the loci were of similar magnitude in individuals of non-European ancestry. We further characterized these loci for associations with gout, transcript expression and the fractional excretion of urate. Network analyses implicate the inhibins-activins signaling pathways and glucose metabolism in systemic urate control. New candidate genes for serum urate concentration highlight the importance of metabolic control of urate production and excretion, which may have implications for the treatment and prevention of gout.

4 Article The renal urate transporter SLC17A1 locus: confirmation of association with gout. 2012

Hollis-Moffatt, Jade E / Phipps-Green, Amanda J / Chapman, Brett / Jones, Gregory T / van Rij, Andre / Gow, Peter J / Harrison, Andrew A / Highton, John / Jones, Peter B / Montgomery, Grant W / Stamp, Lisa K / Dalbeth, Nicola / Merriman, Tony R. ·Department of Biochemistry, University of Otago, 710 Cumberland Street, Dunedin 9054, New Zealand. ·Arthritis Res Ther · Pubmed #22541845.

ABSTRACT: INTRODUCTION: Two major gout-causing genes have been identified, the urate transport genes SLC2A9 and ABCG2. Variation within the SLC17A1 locus, which encodes sodium-dependent phosphate transporter 1, a renal transporter of uric acid, has also been associated with serum urate concentration. However, evidence for association with gout is equivocal. We investigated the association of the SLC17A1 locus with gout in New Zealand sample sets. METHODS: Five variants (rs1165196, rs1183201, rs9358890, rs3799344, rs12664474) were genotyped across a New Zealand sample set totaling 971 cases and 1,742 controls. Cases were ascertained according to American Rheumatism Association criteria. Two population groups were studied: Caucasian and Polynesian. RESULTS: At rs1183201 (SLC17A1), evidence for association with gout was observed in both the Caucasian (odds ratio (OR) = 0.67, P = 3.0 × 10-6) and Polynesian (OR = 0.74, P = 3.0 × 10-3) groups. Meta-analysis confirmed association of rs1183201 with gout at a genome-wide level of significance (OR = 0.70, P = 3.0 × 10-8). Haplotype analysis suggested the presence of a common protective haplotype. CONCLUSION: We confirm the SLC17A1 locus as the third associated with gout at a genome-wide level of significance.