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Autoantibodies against the calcium‐sensing receptor and cytokines in autoimmune polyglandular syndromes types 2, 3 and 4
Author(s) -
Kemp E. Helen,
Kahaly George J.,
Porter Julie A.,
Frommer Lara,
Weetman Anthony P.
Publication year - 2018
Publication title -
clinical endocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.055
H-Index - 147
eISSN - 1365-2265
pISSN - 0300-0664
DOI - 10.1111/cen.13482
Subject(s) - autoantibody , autoimmunity , medicine , immunology , endocrinology , calcium sensing receptor , autoimmune gastritis , antibody , calcium metabolism , calcium
Summary Objective The frequency of autoimmunity against the parathyroid glands in patients with polyglandular autoimmunity that is not due to autoimmune polyendocrine syndrome type 1 ( APS 1) is unclear. To investigate this, this study aimed to determine the prevalence of autoantibodies against parathyroid autoantigens, calcium‐sensing receptor (Ca SR ) and NACHT leucine‐rich‐repeat protein 5 ( NALP 5), in a large group of patients with non‐ APS 1 polyendocrine autoimmunity. Possible occult APS 1 was investigated by cytokine autoantibody measurement and AIRE gene analysis. Design, Subjects and Measurements Subjects were 178 patients with APS 2, 3 or 4, and 80 healthy blood donors. Autoantibodies against the Ca SR , NALP 5 and cytokines were measured by immunoprecipitation, radioligand binding assays or ELISA , respectively. Results Four patient samples (2.2%), but none of the controls, were positive for Ca SR autoantibodies. NALP 5 autoantibodies were not detected in any participant. Eleven patients (6.2%) had cytokine autoantibodies, but none of the control samples was positive. None of the patients with cytokine autoantibodies had any known or novel mutations in the AIRE gene. Conclusions The low prevalence of Ca SR autoantibodies indicate a very low level of subclinical parathyroid autoimmunity in APS types 2, 3 and 4. In addition, autoantibodies against cytokines constitute an uncommon feature of non‐ APS 1 polyglandular autoimmunity.