Atopic dermatitis is associated with an increased risk for rheumatoid arthritis and inflammatory bowel disease, and a decreased risk for type 1 diabetes - 07/01/16
, Kristin Schwarz, MSc a, Hansjörg Baurecht, MSc c, Melanie Hotze, MSc c, Regina Fölster-Holst, MD c, Elke Rodríguez, PhD c, Young A.E. Lee, MD d, e, Andre Franke, PhD f, Frauke Degenhardt, MSc c, f, Wolfgang Lieb, PhD g, Christian Gieger, PhD h, Michael Kabesch, MD i, Markus M. Nöthen, MD j, k, Alan D. Irvine, MD l, m, n, W.H. Irwin McLean, PhD o, Stefanie Deckert, MPH a, Victoria Stephan a, Peter Schwarz, MD p, Martin Aringer, MD p, Natalija Novak, MD q, Stephan Weidinger, MD, MaHM cAbstract |
Background |
Atopic dermatitis (AD) is characterized by epidermal barrier failure and immune-mediated inflammation. Evidence on AD as a potential risk factor for inflammatory comorbidities is scarce.
Objectives |
We sought to test the hypothesis that prevalent AD is a risk factor for incident rheumatoid arthritis (RA) and inflammatory bowel disease (IBD; Crohn disease [CD], ulcerative colitis [UC]) and is inversely related to type 1 diabetes (T1D) and to investigate established RA, IBD, and T1D susceptibility loci in AD.
Methods |
This cohort study used data from German National Health Insurance beneficiaries aged 40 years or younger (n = 655,815) from 2005 through 2011. Prevalent AD in the period 2005 to 2006 was defined as primary exposure, and incident RA, IBD, and T1D in the period 2007 to 2011 were defined as primary outcomes. Risk ratios were calculated with generalized linear models. Established RA, IBD, and T1D loci were explored in high-density genotyping data from 2,425 cases with AD and 5,449 controls.
Results |
Patients with AD (n = 49,847) were at increased risk for incident RA (risk ratio [RR], 1.72; 95% CI, 1.25-2.37) and/or IBD (CD: RR, 1.34; 95% CI, 1.11-1.61; UC: RR, 1.25; 95% CI, 1.03-1.53). After adjusting for health care utilization, there was a nominally significant inverse effect on T1D risk (RR, 0.72; 95% CI, 0.53-0.998). There was no disproportionate occurrence of known RA, CD, UC, or T1D risk alleles in AD.
Conclusions |
AD is a risk factor for the development of RA and IBD. This excess comorbidity cannot be attributed to major known IBD and RA genetic risk factors.
Le texte complet de cet article est disponible en PDF.Key words : Atopic dermatitis, cohort study, epidemiology, inflammatory bowel disease, rheumatoid arthritis, type 1 diabetes
Abbreviations used : AD, CD, IBD, ICD-10, IMID, RA, RR, SNP, T1D, UC
Plan
| The project received infrastructure support through the DFG Clusters of Excellence “Inflammation at Interfaces” (grant nos EXC306 and EXC306/2), and was supported by the German Federal Ministry of Education and Research (BMBF) within the framework of the e:Med research and funding concept (sysINFLAME, grant no. 01ZX1306A), and the PopGen 2.0 network (grant no. 01EY1103). N.N. was supported by the German National Research Council (DFG) through SFB704, the Cluster of Excellence “ImmunoSensation,” and the Christine Kühne Stiftung Center for Allergy Research and Education. |
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| Disclosure of potential conflict of interest: J. Schmitt has received research support from Sanofi, Novartis, and Pfizer. M. Kabesch has received research support from the European Union, the German Ministry of Education and Research, and the German Research Foundation and has received payment for lectures from the European Respiratory Society, the European Academy of Allergy and Clinical Immunology, the American Thoracic Society, Novartis, and GlaxoSmithKline. A. D. Irvine has consultant arrangements with Regeneron. N. Novak has received research support from the German Research Council, Bonfor, Christine Kühne Stiftung Center for Allergy Research and Education, and ALK Abello; has consultant arrangements with Leti Pharma and HAL Allergy; and has received payment for lectures from Astella, Bencard Allergy Therapeutics, MSD, GlaxoSmithKline, HAL Allergy, Astellas, Leo, and Jenapharm. The rest of the authors declare that they have no relevant conflicts of interest. |
Vol 137 - N° 1
P. 130-136 - janvier 2016 Retour au numéro
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