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Updated: Apr 17, 2026
Electrochemiluminescence Assays for Human Islet Autoantibodies
Published on: March 23, 2018
Serum thyroid hormone autoantibodies in type 1 diabetes mellitus
Salvatore Benvenga1, Basilio Pintaudi, Roberto Vita
1Department of Clinical and Experimental Medicine (R.V.), Master Program on Childhood, Adolescent and Women's Endocrine Health (S.B.), University of Messina School of Medicine, 98125 Messina, Italy; Interdepartmental Program on Molecular & Clinical Endocrinology (S.B.) and Women's Endocrine Health, University Hospital, University of Messina, 98125 Messina, Italy; Department of Clinical Pharmacology and Epidemiology (B.P.), Fondazione Mario Negri Sud, 66030 Santa Maria Imbaro (CH), Italy; and Department of Clinical and Experimental Medicine (G.D.V., A.D.B.), University of Messina, 98125 Messina, Italy.
Context:
Autoimmune thyroid diseases (AITDs) can be associated with type 1 diabetes (DM1). The prevalence of serum antibodies against thyroid hormones (THAb) in subjects with autoimmune diseases other than DM1 is increasing. No data are available for DM1.
Objective:
The objectives were evaluate the rate of associated AITD; the rate of positiveness for serum THAb; the panel of THAb based on thyroid hormone interaction and on Ig class; and the association of AITD alone, THAb alone, or AITD plus THAb with diabetes-related complications.
Design:
This was an observational, prospective study with 6-year (2005-2011) follow-up.
Setting:
The setting was an outpatient diabetes clinic.
Patients:
Fifty-two consecutive subjects (53.8% males; mean age, 37.4 ± 7.4 y; diabetes duration, 19.9 ± 8.2 y) with DM1. All participants completed the study.
Main Outcome Measures:
Main outcome measures were AITD rate; THAb positivity according to hormone interaction and Ig class; association of AITD and THAb with diabetes-related complications.
Results:
AITD rate increased from baseline (34.6%) to follow-up (38.5%). Subjects with DM1 had a high prevalence of THAb (92.3%). The presence of AITD at baseline was associated with subsequent development of macroangiopathy (0 vs 33% at baseline and follow-up, respectively; P = .029). Some THAb patterns, the majority having T3 binding in common, were associated with the progression and development of diabetes-related complications.
Conclusions:
THAb synthesis in DM1 might be driven by increased glycosylation of thyroglobulin. Anti T3-THAb may cause a relative "tissue hypothyroidism" by sequestering thyroid hormone, this at least partially contributing to worsening diabetes-related vascular complications. In a clinical setting THAb positivity could identify subjects more likely to develop diabetes complications.
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