Familial risks between Graves disease and Hashimoto thyroiditis and other autoimmune diseases in the population of Sweden
Status PubMed-not-MEDLINE Jazyk angličtina Země Nizozemsko Médium electronic-ecollection
Typ dokumentu časopisecké články
PubMed
32743538
PubMed Central
PMC7388361
DOI
10.1016/j.jtauto.2020.100058
PII: S2589-9090(20)30025-3
Knihovny.cz E-zdroje
- Klíčová slova
- Discordant risks, Genetics, Polyautoimmunity, Risk between spouses,
- Publikační typ
- časopisecké články MeSH
Genetic and family studies have indicated that Graves disease and Hashimoto thyroiditis have a heritable component which appears to be shared to some extend also with some other autoimmune diseases (AIDs). In the present nation-wide study we describe familial risk for Graves disease and Hashimoto thyroiditis identified from the Swedish Hospital Discharge Register (years 1964 through 2012) and the Outpatient Register (2001 through 2012). Family relationships were obtained from the Multigeneration Register and cancers from the Cancer Registry. Familial standardized incidence ratios (SIRs) were calculated for 29,005 offspring with Graves disease and for 25,607 offspring with Hashimoto thyroiditis depending on any of 43 AIDs in parents or siblings. The concordant familial risks for Graves disease and Hashimoto thyroiditis were 3.85 and 4.75, higher for men than for women. The familial risks were very high (11.35, Graves and 22.06, Hashimoto) when both a parent and a sibling were affected. Spousal familial risks were higher for Hashimoto thyroiditis (1.98/1.93) than for Graves disease (1.48/1.50). For Graves disease, 24 discordant AIDs showed a significant association; for Hashimoto thyroiditis, 20 discordant associations were significant. All significant discordant associations were positive for the two thyroid AIDs, with the exception of Hashimoto thyroiditis with Reiter disease. Overall 8 associations were significant only for Graves disease and 6 Hashimoto thyroiditis. The overall high concordant familial risks for Graves disease and Hashimoto thyroiditis suggest a strong genetic contribution to the familial risk. Significant familial associations among more than half of the 43 AIDs attest to the extensive polyautoimmunity among thyroid AIDs.
Center for Primary Health Care Research Lund University Malmö Sweden
Division of Cancer Epidemiology German Cancer Research Centre 69120 Heidelberg Germany
Division of Molecular Genetic Epidemiology German Cancer Research Centre 69120 Heidelberg Germany
Division of Pediatric Neurooncology German Cancer Research Center Heidelberg Germany
GeneWerk GmbH 69120 Heidelberg Germany
Zobrazit více v PubMed
Bliddal S., Nielsen C.H., Feldt-Rasmussen U. Recent advances in understanding autoimmune thyroid disease: the tallest tree in the forest of polyautoimmunity. F1000Res. 2017;6:1776. PubMed PMC
Antonelli A., Fallahi P., Elia G., Ragusa F., Paparo S.R., Ruffilli I. Graves’ disease: clinical manifestations, immune pathogenesis (cytokines and chemokines) and therapy. Best Pract. Res. Clin. Endocrinol. Metabol. 2020:101388. PubMed
Ragusa F., Fallahi P., Elia G., Gonnella D., Paparo S.R., Giusti C. Hashimotos’ thyroiditis: epidemiology, pathogenesis, clinic and therapy. Best Pract. Res. Clin. Endocrinol. Metabol. 2019:101367. PubMed
Fallahi P., Elia G., Ragusa F., Ruffilli I., Camastra S., Giusti C. The aggregation between AITD with rheumatologic, or dermatologic, autoimmune diseases. Best Pract. Res. Clin. Endocrinol. Metabol. 2019:101372. PubMed
Shukla S.K., Singh G., Ahmad S., Pant P. Infections, genetic and environmental factors in pathogenesis of autoimmune thyroid diseases. Microb. Pathog. 2018;116:279–288. PubMed
Luty J., Ruckemann-Dziurdzinska K., Witkowski J.M., Bryl E. Immunological aspects of autoimmune thyroid disease - complex interplay between cells and cytokines. Cytokine. 2019;116:128–133. PubMed
Dougan M., Pietropaolo M. Time to dissect the autoimmune etiology of cancer antibody immunotherapy. J. Clin. Invest. 2020;130:51–61. PubMed PMC
Hwangbo Y., Park Y.J. Genome-wide association studies of autoimmune thyroid diseases, thyroid function, and thyroid cancer. Endocrinol. Metab. (Seoul) 2018;33:175–184. PubMed PMC
Vejrazkova D., Vcelak J., Vaclavikova E., Vankova M., Zajickova K., Duskova M. Genetic predictors of the development and recurrence of Graves’ disease. Physiol. Res. 2018;67 S431-s9. PubMed
Hemminki K., Li X., Sundquist J., Sundquist K. The epidemiology of Graves’ disease: evidence of a genetic and an environmental contribution. J. Autoimmun. 2010;34:J307–J313. PubMed
Dittmar M., Libich C., Brenzel T., Kahaly G.J. Increased familial clustering of autoimmune thyroid diseases. Hormone Metab. Res. = Hormon- und Stoffwechselforschung = Hormones et metabolisme. 2011;43:200–204. PubMed
Hemminki K., Forsti A., Sundquist K., Sundquist J., Li X. Familial associations of monoclonal gammopathy of unknown significance with autoimmune diseases. Leukemia. 2016;30:1766–1769. PubMed
Hemminki K., Ji J., Brandt A., Mousavi S.M., Sundquist J. The Swedish Family-Cancer Database 2009: prospects for histology-specific and immigrant studies. Int. J. Canc. 2010;126:2259–2267. PubMed
Abraham-Nordling M., Byström K., Törring O., Lantz M., Berg G., Calissendorff J. Incidence of hyperthyroidism in Sweden. Eur. J. Endocrinol. 2011;165:899–905. PubMed
Ludvigsson J.F., Andersson E., Ekbom A., Feychting M., Kim J.L., Reuterwall C. External review and validation of the Swedish national inpatient register. BMC Publ. Health. 2011;11:450. PubMed PMC
Carter C. The inheritance of congenital pyloric stenosis. Br. Med. Bull. 1961;17:251–254. PubMed
Vogel F., Motulsky A. Springer; Heidelberg: 1996. Human Genetics: Problems and Approaches.
Frank C., Fallah M., Sundquist J., Hemminki A., Hemminki K. Population landscape of familial cancer. Sci. Rep. 2015;5:12891. PubMed PMC
Hemminki K., Li X., Sundquist K., Sundquist J. Familial risks for common diseases: etiologic clues and guidance to gene identification Mutat. Res. Rev. 2008;658:247–258. PubMed
Weires M., Bermejo J.L., Sundquist J., Hemminki K. Clustering of concordant and discordant cancer types in Swedish couples is rare. Eur. J. Canc. 2011;47:98–106. PubMed
Cho J.H., Gregersen P.K. Genomics and the multifactorial nature of human autoimmune disease. N. Engl. J. Med. 2011;365:1612–1623. PubMed
Ramos P.S., Criswell L.A., Moser K.L., Comeau M.E., Williams A.H., Pajewski N.M. A comprehensive analysis of shared loci between systemic lupus erythematosus (SLE) and sixteen autoimmune diseases reveals limited genetic overlap. PLoS Genet. 2011;7 PubMed PMC
Li Y.R., Li J., Zhao S.D., Bradfield J.P., Mentch F.D., Maggadottir S.M. Meta-analysis of shared genetic architecture across ten pediatric autoimmune diseases. Nat. Med. 2015;21:1018–1027. PubMed PMC
Tajuddin S.M., Schick U.M., Eicher J.D., Chami N., Giri A., Brody J.A. Large-scale exome-wide association analysis identifies loci for white blood cell traits and pleiotropy with immune-mediated diseases. Am. J. Hum. Genet. 2016;99:22–39. PubMed PMC
Law P.J., Sud A., Mitchell J.S., Henrion M., Orlando G., Lenive O. Genome-wide association analysis of chronic lymphocytic leukaemia, Hodgkin lymphoma and multiple myeloma identifies pleiotropic risk loci. Sci. Rep. 2017;7:41071. PubMed PMC
Wu I.B., Schwartz R.A. Reiter’s syndrome: the classic triad and more. J. Am. Acad. Dermatol. 2008;59:113–121. PubMed
Brent G.A. Environmental exposures and autoimmune thyroid disease. Thyroid. 2010;20:755–761. PubMed PMC
Familial Risks between Pernicious Anemia and Other Autoimmune Diseases in the Population of Sweden