title: Yersinia enterocolitica infection does not confer an increased risk of thyroid antibodies: evidence from a Danish twin study.
abstract: Understanding of the aetiological basis of thyroid autoimmunity may be gained by studying the early stages of the disease process. We aimed to (1) investigate the relationship between thyroid antibody status and Yersinia enterocolitica (YE) infection in euthyroid subjects and (2) explore the relative importance of genetic and environmental risk factors in the acquisition of YE infection. The association between thyroid antibody status and YE infection was explored using a case-control design. Furthermore, thyroid antibody-positive twins were compared with their thyroid antibody-negative co-twin. In 468 twins, IgA and IgG antibodies to virulence-associated outer-membrane proteins (YOPs) of YE were measured. Of these, 147 were thyroid antibody-positive (cases). A total of 147 age- and gender-matched twins were chosen as controls. The prevalence of YOP antibodies was lower among thyroid antibody-positive individuals than among controls. Yersinia infection was not associated with a positive thyroid antibody status: the odds ratio (with 95% CI) for YOP IgA-ab was 0.66 (0.42-1.05), P = 0.078 and for YOP IgG-ab it was 0.95 (0.60-1.50), P = 0.816. Within discordant twin pairs, the thyroid antibody-positive twin did not have an increased risk of Yersinia infection compared to the thyroid antibody-negative co-twin [odds ratio: YOP IgA-Ab: 0.94 (0.49-1.83), P = 0.866, and YOP IgG-Ab: 1.35 (0.72-2.53), P = 0.345]; 41% (95% CI 10-67% of the liability of being YOP antibody-positive was due to genetic effects. In conclusion, Yersinia infection does not confer an increased risk of thyroid antibodies. The genetic contribution in the acquisition of Yersinia infection is modest.
authors.affiliation: Department of Endocrinology and Metabolism, Odense University Hospital, Odense, Denmark. piaskovhansen@dadlnet.dk
authors.forename: P S
authors.initials: PS
authors.lastname: Hansen
authors.forename: B E
authors.initials: BE
authors.lastname: Wenzel
authors.forename: T H
authors.initials: TH
authors.lastname: Brix
authors.forename: L
authors.initials: L
authors.lastname: Hegedüs
mesh_terms: D000328:Adult; D000907:Antibodies, Bacterial / Q000097:blood; D001323:Autoantibodies / Q000097:blood*; D015551:Autoimmunity; D016022:Case-Control Studies; D004200:Diseases in Twins / Q000276:immunology*; D005260:Female; D020022:Genetic Predisposition to Disease; D006801:Humans; D007070:Immunoglobulin A / Q000097:blood; D007074:Immunoglobulin G / Q000097:blood; D008297:Male; D008875:Middle Aged; D012307:Risk Factors; D013961:Thyroid Gland / Q000276:immunology*; D015007:Yersinia / Q000276:immunology / Q000302:isolation & purification; D015009:Yersinia Infections / Q000209:etiology / Q000235:genetics / Q000276:immunology*
chemical_list: D000907:Antibodies, Bacterial; D001323:Autoantibodies; D007070:Immunoglobulin A; D007074:Immunoglobulin G