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@ARTICLE{Li:167249,
      author       = {X. Li and H. Thomsen$^*$ and K. Sundquist and J. Sundquist
                      and A. Försti$^*$ and K. Hemminki$^*$},
      title        = {{F}amilial {R}isks between {P}ernicious {A}nemia and
                      {O}ther {A}utoimmune {D}iseases in the {P}opulation of
                      {S}weden.},
      journal      = {Autoimmune diseases},
      volume       = {2021},
      issn         = {2090-0430},
      address      = {London [u.a.]},
      publisher    = {Sage-Hindawi},
      reportid     = {DKFZ-2021-00222},
      pages        = {8815297},
      year         = {2021},
      note         = {#LA:C050# / 2021 Jan 12;2021:8815297},
      abstract     = {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.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.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.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.},
      cin          = {B062 / HD01 / C050},
      ddc          = {610},
      cid          = {I:(DE-He78)B062-20160331 / I:(DE-He78)HD01-20160331 /
                      I:(DE-He78)C050-20160331},
      pnm          = {313 - Krebsrisikofaktoren und Prävention (POF4-313)},
      pid          = {G:(DE-HGF)POF4-313},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:33505716},
      pmc          = {pmc:PMC7815416},
      doi          = {10.1155/2021/8815297},
      url          = {https://inrepo02.dkfz.de/record/167249},
}