Improving coeliac disease risk prediction by testing non-HLA variants additional to HLA variants

نویسندگان

  • Jihane Romanos
  • Anna Rosén
  • Vinod Kumar
  • Gosia Trynka
  • Lude Franke
  • Agata Szperl
  • Javier Gutierrez-Achury
  • Cleo C van Diemen
  • Roan Kanninga
  • Soesma A Jankipersadsing
  • Andrea Steck
  • Georges Eisenbarth
  • David A van Heel
  • Bozena Cukrowska
  • Valentina Bruno
  • Maria Cristina Mazzilli
  • Concepcion Núñez
  • Jose Ramon Bilbao
  • M Luisa Mearin
  • Donatella Barisani
  • Marian Rewers
  • Jill M Norris
  • Anneli Ivarsson
  • H Marieke Boezen
  • Edwin Liu
  • Cisca Wijmenga
  • Cristian Scerri
  • Tunde Koltai
  • Sanja Kolaček
  • Zrinka Mišak
  • Slaven Abdović
  • Sibylle Koletzko
  • Gertraud Osiander
  • Katharina Werkstetter
  • Eckart Mummert
  • Ilma R Korponay-Szabo
  • Judit Gyimesi
  • Raanan Shamir
  • Corina Hartman
  • Enzo Bravi
  • Marco Poles
  • Renata Auricchio
  • G Gianna Giovamma Limongelli
  • Luigi Greco
  • Riccardo Troncone
  • Vincenzo Villanacci
  • Jacques G Bindels
  • Ronald Brand
  • Bibi Funke Kupper
  • Caroline E Hogen Esch
  • Erica G Hopman
  • Frits Koning
  • Yvonne Kooy-Winkelaar
  • Chantal te Marvelde
  • Hein Putter
  • Els Stoopman
  • Sabine Vriezinga
  • Ludvig M Sollid
  • Melinda Ráki
  • Ania Chmielewska
  • Piotr Dziechciarz
  • Małgorzata Pieścik-Lech
  • Hania Szajewska
  • Anna Szaflarska-Szczepanik
  • Gemma Castillejo
  • Amalia Capilla
  • Vicente Varea
  • Carmen Ribes-Koninckx
  • Anna Lopez
  • Paula Crespo
  • Eva Martinez
  • Isabel Polanco
  • Lotta Högberg
  • Lars Stenhammar
  • Annelie Carlsson
  • Charlotta Webb
  • Solveig Hammarroth
  • Olle Hernell
  • Carina Lagerqvist
  • Anna Myléus
  • Katrina Nordyke
  • Fredrik Norström
  • Olof Sandström
  • Stig Wall
  • Eva Karlsson
چکیده

BACKGROUND The majority of coeliac disease (CD) patients are not being properly diagnosed and therefore remain untreated, leading to a greater risk of developing CD-associated complications. The major genetic risk heterodimer, HLA-DQ2 and DQ8, is already used clinically to help exclude disease. However, approximately 40% of the population carry these alleles and the majority never develop CD. OBJECTIVE We explored whether CD risk prediction can be improved by adding non-HLA-susceptible variants to common HLA testing. DESIGN We developed an average weighted genetic risk score with 10, 26 and 57 single nucleotide polymorphisms (SNP) in 2675 cases and 2815 controls and assessed the improvement in risk prediction provided by the non-HLA SNP. Moreover, we assessed the transferability of the genetic risk model with 26 non-HLA variants to a nested case-control population (n=1709) and a prospective cohort (n=1245) and then tested how well this model predicted CD outcome for 985 independent individuals. RESULTS Adding 57 non-HLA variants to HLA testing showed a statistically significant improvement compared to scores from models based on HLA only, HLA plus 10 SNP and HLA plus 26 SNP. With 57 non-HLA variants, the area under the receiver operator characteristic curve reached 0.854 compared to 0.823 for HLA only, and 11.1% of individuals were reclassified to a more accurate risk group. We show that the risk model with HLA plus 26 SNP is useful in independent populations. CONCLUSIONS Predicting risk with 57 additional non-HLA variants improved the identification of potential CD patients. This demonstrates a possible role for combined HLA and non-HLA genetic testing in diagnostic work for CD.

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عنوان ژورنال:

دوره 63  شماره 

صفحات  -

تاریخ انتشار 2014