Genetic Overlap Across Allergic Diseases

By combining information from asthma, hay fever and eczema in the
case-control definition used in our GWAS, we expected our study design to
improve power to identify risk variants shared between, but not specific to any
of, the three diseases 6 (link). To understand if
the associations discovered in our GWAS were indeed likely to represent risk
factors shared across allergic diseases, we took advantage of the observation
that not all affected individuals report allergic co-morbidities 1 (link),22 (link),23 (link), and compared allele
frequencies between three groups of adults: asthma-only cases
(n=12,268), hay fever-only cases
(n=33,305) and eczema-only cases (n=6,276).
The studies that contributed to this analysis are indicated in Supplementary Table 1 and
described in detail in the Supplementary Note. We performed three sets of association analyses
contrasting three non-overlapping groups of individuals: asthma-only (g1) vs.
hay fever-only (g2); asthma-only (g1) vs. eczema-only (g3); and hay fever-only
(g2) vs. eczema-only (g3). These analyses are statistically independent from the
case-control analysis carried out as part of the GWAS, which facilitates
interpretation of the results. For a given sentinel SNP, results from these
analyses indicate if the risk allele is more (odds ratio [OR] >1) or less
(OR<1) common in e.g. group 1 (g1) when compared to group 2 (g2). For
example, if a SNP contributed similarly to the risks of asthma and hay fever but
not eczema, then one would expect an OR~1 in the asthma-only vs. hay
fever-only comparison, but an OR>1 in the asthma vs. eczema and hay fever vs.
eczema analyses. The significance threshold for these analyses was set at
1.2x10^-4, which corresponds to a Bonferroni correction for the
136 SNPs and three sets of analyses performed (i.e.
P<0.05/(136x3)).

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Ferreira M.A., Vonk J.M., Baurecht H., Marenholz I., Tian C., Hoffman J.D., Helmer Q., Tillander A., Ullemar V., van Dongen J., Lu Y., Rüschendorf F., Esparza-Gordillo J., Medway C.W., Mountjoy E., Burrows K., Hummel O., Grosche S., Brumpton B.M., Witte J.S., Hottenga J.J., Willemsen G., Zheng J., Rodríguez E., Hotze M., Franke A., Revez J.A., Beesley J., Matheson M.C., Dharmage S.C., Bain L.M., Fritsche L.G., Gabrielsen M.E., Balliu B., Nielsen J.B., Zhou W., Hveem K., Langhammer A., Holmen O.L., Løset M., Abecasis G.R., Willer C.J., Arnold A., Homuth G., Schmidt C.O., Thompson P.J., Martin N.G., Duffy D.L., Novak N., Schulz H., Karrasch S., Gieger C., Strauch K., Melles R.B., Hinds D.A., Hübner N., Weidinger S., Magnusson P.K., Jansen R., Jorgenson E., Lee Y.A., Boomsma D.I., Almqvist C., Karlsson R., Koppelman G.H, & Paternoster L. (2017). Shared genetic origin of asthma, hay fever and eczema elucidates allergic disease biology. Nature genetics, 49(12), 1752-1757.

Publication 2017

Adults Allele Allergic diseases Asthma Diseases 6 Eczema Gwas Hay fever Snps

Corresponding Organization : QIMR Berghofer Medical Research Institute

Other organizations : University Medical Center Groningen, University of Groningen, University Hospital Schleswig-Holstein, University of Lübeck, Max Delbrück Center, 23andMe (United States), University of California, San Francisco, Karolinska Institutet, University of Bristol, Charité - Universitätsmedizin Berlin, Kiel University, University of Melbourne, Norwegian University of Science and Technology, Stanford University, University of Michigan–Ann Arbor, Universitätsmedizin Greifswald, Universität Greifswald, Harry Perkins Institute of Medical Research, University of Western Australia, Institute for Respiratory Health, University Hospital Bonn, Helmholtz Zentrum München, Kaiser Permanente, Amsterdam UMC Location VUmc, Karolinska University Hospital, GlaxoSmithKline (United Kingdom), Age UK

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Variable analysis

independent variables

Asthma-only cases (n=12,268)
Hay fever-only cases (n=33,305)
Eczema-only cases (n=6,276)

dependent variables

Allele frequencies between the three groups of adults

control variables

The studies that contributed to this analysis are indicated in Supplementary Table 1 and described in detail in the Supplementary Note.

controls

The analyses are statistically independent from the case-control analysis carried out as part of the GWAS, which facilitates interpretation of the results.

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