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Familial Risks between Pernicious Anemia and Other Autoimmune Diseases in the Population of Sweden
BACKGROUND: Pernicious anemia (PA) is an autoimmune disease (AID) which is caused by lack of vitamin B12 (cobalamin) due to its impaired uptake. PA is a multifactorial disease which is associated with a number of other AID comorbidities and which is manifested as part of autoimmune polyglandular syn...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7815416/ https://www.ncbi.nlm.nih.gov/pubmed/33505716 http://dx.doi.org/10.1155/2021/8815297 |
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author | Li, Xinjun Thomsen, Hauke Sundquist, Kristina Sundquist, Jan Försti, Asta Hemminki, Kari |
author_facet | Li, Xinjun Thomsen, Hauke Sundquist, Kristina Sundquist, Jan Försti, Asta Hemminki, Kari |
author_sort | Li, Xinjun |
collection | PubMed |
description | BACKGROUND: Pernicious anemia (PA) is an autoimmune disease (AID) which is caused by lack of vitamin B12 (cobalamin) due to its impaired uptake. PA is a multifactorial disease which is associated with a number of other AID comorbidities and which is manifested as part of autoimmune polyglandular syndrome. Due to the shortage of family studies on PA, we planned to address the problem by assessing familial risks for concordant PA between family members and for discordant PA in families of other AID patients. METHODS: We collected data on patients diagnosed with AIDs from the Swedish hospitals and family data from a population register. We calculated standardized incidence ratios (SIRs) in families for concordant and discordant risks. RESULTS: The number of PA patients in the offspring generation (for which the familial risk was calculated) was 7701; 278 (3.6%) patients had a family history of PA. The population prevalence of PA was 0.9/1000. The familial risk for PA was 3.88 when any first-degree relative was the proband, equal for men and women. The familial risk was two times higher between siblings than between offspring and parents which may be due to complex genetic background. Associations of PA with 14 discordant AIDs were significant; these included some AIDs that have previously been described as comorbidities in PA patients and several yet unreported associations, including rheumatoid arthritis and other AIDs. CONCLUSIONS: The familial risks for PA were high suggesting multifactorial genetic etiology. The results call for further population-level studies to unravel mechanisms of familial PA which may help to understand the etiology of this disease. |
format | Online Article Text |
id | pubmed-7815416 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Hindawi |
record_format | MEDLINE/PubMed |
spelling | pubmed-78154162021-01-26 Familial Risks between Pernicious Anemia and Other Autoimmune Diseases in the Population of Sweden Li, Xinjun Thomsen, Hauke Sundquist, Kristina Sundquist, Jan Försti, Asta Hemminki, Kari Autoimmune Dis Research Article BACKGROUND: Pernicious anemia (PA) is an autoimmune disease (AID) which is caused by lack of vitamin B12 (cobalamin) due to its impaired uptake. PA is a multifactorial disease which is associated with a number of other AID comorbidities and which is manifested as part of autoimmune polyglandular syndrome. Due to the shortage of family studies on PA, we planned to address the problem by assessing familial risks for concordant PA between family members and for discordant PA in families of other AID patients. METHODS: We collected data on patients diagnosed with AIDs from the Swedish hospitals and family data from a population register. We calculated standardized incidence ratios (SIRs) in families for concordant and discordant risks. RESULTS: The number of PA patients in the offspring generation (for which the familial risk was calculated) was 7701; 278 (3.6%) patients had a family history of PA. The population prevalence of PA was 0.9/1000. The familial risk for PA was 3.88 when any first-degree relative was the proband, equal for men and women. The familial risk was two times higher between siblings than between offspring and parents which may be due to complex genetic background. Associations of PA with 14 discordant AIDs were significant; these included some AIDs that have previously been described as comorbidities in PA patients and several yet unreported associations, including rheumatoid arthritis and other AIDs. CONCLUSIONS: The familial risks for PA were high suggesting multifactorial genetic etiology. The results call for further population-level studies to unravel mechanisms of familial PA which may help to understand the etiology of this disease. Hindawi 2021-01-12 /pmc/articles/PMC7815416/ /pubmed/33505716 http://dx.doi.org/10.1155/2021/8815297 Text en Copyright © 2021 Xinjun Li et al. https://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Li, Xinjun Thomsen, Hauke Sundquist, Kristina Sundquist, Jan Försti, Asta Hemminki, Kari Familial Risks between Pernicious Anemia and Other Autoimmune Diseases in the Population of Sweden |
title | Familial Risks between Pernicious Anemia and Other Autoimmune Diseases in the Population of Sweden |
title_full | Familial Risks between Pernicious Anemia and Other Autoimmune Diseases in the Population of Sweden |
title_fullStr | Familial Risks between Pernicious Anemia and Other Autoimmune Diseases in the Population of Sweden |
title_full_unstemmed | Familial Risks between Pernicious Anemia and Other Autoimmune Diseases in the Population of Sweden |
title_short | Familial Risks between Pernicious Anemia and Other Autoimmune Diseases in the Population of Sweden |
title_sort | familial risks between pernicious anemia and other autoimmune diseases in the population of sweden |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7815416/ https://www.ncbi.nlm.nih.gov/pubmed/33505716 http://dx.doi.org/10.1155/2021/8815297 |
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