Genetic immune and inflammatory markers associated with diabetes in solid organ transplant recipients.

TitreGenetic immune and inflammatory markers associated with diabetes in solid organ transplant recipients.
Publication TypeJournal Article
Year of Publication2019
AuthorsQuteineh, L, Wojtowicz, A, Bochud, P-Y, Crettol, S, Vandenberghe, F, Venetz, J-P, Manuel, O, Golshayan, D, Lehmann, R, Mueller, NJ, Binet, I, van Delden, C, Steiger, J, Mohacsi, P, Dufour, J-F, Soccal, PM, Kutalik, Z, Marques-Vidal, P, Vollenweider, P, Recher, M, Hess, C, Pascual, M, Eap, CB
Corporate AuthorsSwiss Transplant Cohort Study
JournalAmerican journal of transplantation
Volume19
Pagination238-246
Date Published01/2019
DOI10.1111/ajt.14971
ISSN1600-6143
Mots-clésclinical research/practice, Diabetes, genetics, new onset/posttransplant
Abstract

New-onset diabetes after transplantation (NODAT) is a complication following solid organ transplantation (SOT) and may be related to immune or inflammatory responses. We investigated whether single nucleotide polymorphisms (SNPs) within 158 immune- or inflammation-related genes contribute to NODAT in SOT recipients. The association between 263 SNPs and NODAT were investigated in a discovery sample of SOT recipients from the Swiss Transplant Cohort Study (STCS, n =696). Positive results were tested in a first STCS replication sample (n =489) and SNPs remaining significant after multiple test corrections were tested in a second SOT replication sample (n =156). Associations with diabetic traits were further tested in several large general population-based samples (n>480'000). Only SP110 rs2114592C>T remained associated with NODAT in the STCS replication sample. Carriers of rs2114592-TT had 9.9 times (95%C.I.:3.22-30.5, p=0.00006) higher risk for NODAT in the combined STCS samples (n=1184). rs2114592C>T was further associated with NODAT in the second SOT sample (OR:4.8, 95%C.I.:1.55-14.6, p=0.006). On the other hand, SP110 rs2114592C>T was not associated with diabetic traits in population-based samples, suggesting a specific gene-environment interaction, possibly due to the use of specific medications (i.e. immunosuppressants) in transplant patients and/or to the illness that may unmask the gene effect. This article is protected by copyright. All rights reserved.

Alternate URL

http://www.ncbi.nlm.nih.gov/pubmed/29920932?dopt=Abstract

First publication date (online)

06/2018

WOS ID (UT)

000454512600028

Alternate JournalAm. J. Transplant.
Citation Key / SERVAL ID8953
Peer reviewRefereed
PubMed ID29920932

                         

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