Anti-nuclear autoantibodies in Graves' disease and Graves' orbitopathy.
Anti-nuclear autoantibodies
Graves’ disease
Graves’ ophthalmopathy
Graves’ orbitopathy
Non-organ-specific autoantibodies
Thyroid eye disease
Journal
Journal of endocrinological investigation
ISSN: 1720-8386
Titre abrégé: J Endocrinol Invest
Pays: Italy
ID NLM: 7806594
Informations de publication
Date de publication:
Feb 2023
Feb 2023
Historique:
received:
22
03
2022
accepted:
18
08
2022
pubmed:
28
8
2022
medline:
25
1
2023
entrez:
27
8
2022
Statut:
ppublish
Résumé
A relationship between thyroid and non-organ-specific autoimmunity could be relevant for Graves' orbitopathy (GO), which affects connective tissue. We investigated the association between GO and anti-nuclear antibodies (ANAs). Retrospective investigation was conducted in 265 patients with Graves' disease (GD), 158 with and 107 without GO. Primary outcome was: prevalence of ANAs in GO vs no-GO. Secondary outcomes were: (1) relationship between ANAs and GO features; (2) prevalence of ANAs in GD compared with non-autoimmune hyperthyroidism [(78 patients with toxic nodular goiter (TNG)]; (3) distribution of ANA patterns. ANAs were detected in 212 (80%) GD patients, but prevalence did not differ between GO (79.7%) and no-GO (80.3%). Higher ANA titers (1:160) were more common in GO (51.5 vs 38.3%), but only nearly significantly (OR 0.5; 95% CI: 0.3-1; P = 0.059). Proptosis was lower in ANA-positive patients (mean difference: - 1.4 mm; 95% CI from - 2.5 to - 0.3; P = 0.011), in whom nearly significantly lower CAS (Mann-Whitney U: 1.5; P = 0.077) and eyelid aperture (mean difference: - 0.9 mm; 95% CI from - 2 to 0; P = 0.062) were observed. Prevalence of ANAs in GD was lower than in TNG (80 vs 91%; OR 0.3; 95% CI: 0.1-0.9; P = 0.028), but nuclear speckled pattern was more frequent (OR 22.9; 95% CI 1.3-381.3; P = 0.028). Although ANAs are not more frequent in GO, they seem to exert a protective role on its severity and on development of GD. A switch of T cell population in ANA-positive patients, resulting in a different phenotype, may be responsible. Further studies are needed to investigate the mechanisms.
Identifiants
pubmed: 36030301
doi: 10.1007/s40618-022-01906-3
pii: 10.1007/s40618-022-01906-3
pmc: PMC9859920
doi:
Substances chimiques
Autoantibodies
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
337-344Subventions
Organisme : University of Pisa
ID : 539901
Informations de copyright
© 2022. The Author(s).
Références
Autoimmun Rev. 2016 Feb;15(2):162-6
pubmed: 26524640
Ann Rheum Dis. 2019 Jul;78(7):879-889
pubmed: 30862649
Indian J Endocrinol Metab. 2012 Jul;16(4):569-74
pubmed: 22837918
J Endocrinol Invest. 2016 Apr;39(4):357-73
pubmed: 26392367
Med Princ Pract. 2018;27(4):332-336
pubmed: 29864750
Nat Rev Rheumatol. 2020 Dec;16(12):715-726
pubmed: 33154583
J Endocrinol Invest. 2020 Dec;43(12):1759-1768
pubmed: 32583374
J Endocrinol Invest. 2022 Mar;45(3):563-572
pubmed: 34671950
Best Pract Res Clin Endocrinol Metab. 2005 Mar;19(1):17-32
pubmed: 15826920
Best Pract Res Clin Rheumatol. 2020 Feb;34(1):101462
pubmed: 31848055
J Endocrinol Invest. 2022 Feb;45(2):235-259
pubmed: 34417736
J Endocrinol Invest. 2021 Dec;44(12):2575-2579
pubmed: 33844165
Int J Mol Sci. 2020 Feb 18;21(4):
pubmed: 32085664
Clin Ter. 1992 Sep;141(9 Pt 2):49-54
pubmed: 1468198
Ann Rheum Dis. 2014 Jan;73(1):17-23
pubmed: 24126457
Eur J Endocrinol. 2021 Aug 27;185(4):G43-G67
pubmed: 34297684
Pol Arch Med Wewn. 2012;122 Suppl 1:55-9
pubmed: 23222800
Medicine (Baltimore). 2016 Sep;95(38):e4336
pubmed: 27661011
J Clin Endocrinol Metab. 2021 Apr 23;106(5):e2176-e2190
pubmed: 33484567
J Immunol Res. 2018 Dec 17;2018:6895146
pubmed: 30911555
Lab Med. 2018 Jul 5;49(3):e62-e73
pubmed: 29868860
J Endocrinol Invest. 2022 Jan;45(1):189-197
pubmed: 34324163
J Endocrinol Invest. 2021 Apr;44(4):703-712
pubmed: 32749654
J Endocrinol Invest. 2021 Mar;44(3):581-585
pubmed: 32648002
J Immunol Res. 2014;2014:150239
pubmed: 24741574
Lupus. 2004;13(6):450-4
pubmed: 15303572