# Type 1 diabetes, celiac disease, and autoimmune thyroiditis autoantibodies in population-based type 2 diabetes patients

**Authors:** Lind Alexander, Tsai Cheng-ting, Lernmark Åke, Jendle Johan

PMC · DOI: 10.1016/j.jcte.2024.100367 · Journal of Clinical & Translational Endocrinology · 2024-09-06

## TL;DR

The study found that some people diagnosed with type 2 diabetes may have autoantibodies linked to other autoimmune diseases, suggesting the need for more detailed testing.

## Contribution

The study reveals that GADA and TPOA autoantibodies are more common in T2D patients than previously recognized, suggesting improved diagnostic approaches.

## Key findings

- GADA autoantibodies were present in 6.2% of T2D individuals, significantly higher than in controls.
- TPOA autoantibodies were more frequent in GADA-positive T2D individuals compared to GADA-negative ones.
- Analyzing both GADA and TPOA could improve diagnostic precision in T2D patients.

## Abstract

•Autoantibodies associated with T1D, CD and AITD were determined in individuals living with T1D, T2D and matched controls.•GADA were increased in T2D individuals, 6.2%, compared to matched controls, 2.6%.•TPOA were increased in GADA positive, 34.8%, compared to negative, 13.5%, T2D individuals.•Individuals classified and treated as T2D may benefit from analyzing not only GADA but also TPOA to increase the diagnostic precision.

Autoantibodies associated with T1D, CD and AITD were determined in individuals living with T1D, T2D and matched controls.

GADA were increased in T2D individuals, 6.2%, compared to matched controls, 2.6%.

TPOA were increased in GADA positive, 34.8%, compared to negative, 13.5%, T2D individuals.

Individuals classified and treated as T2D may benefit from analyzing not only GADA but also TPOA to increase the diagnostic precision.

The study aims were to determine autoantibodies associated with type 1 diabetes (T1D), celiac disease (CD) and autoimmune thyroid disease (AITD) in individuals living with type 2 diabetes (T2D) compared to T1D and matched controls.

Individuals with T1D and T2D were randomly identified in health-care registers. Blood was collected through home-capillary sampling and autoantibodies associated with either T1D against glutamic acid decarboxylase (GADA), insulin (IAA), insulinoma antigen-2 (IA-2A), and zinc transporter 8 (ZnT8A), CD against tissue transglutaminase (tTGA) or AITD against thyroid peroxidase (TPOA) were determined in an automated, multiplex Antibody Detection by Agglutination-PCR (ADAP) assay.

GADA were detected in 46 % (88/191) of T1D and increased to 6.2 % (23/372) in T2D compared to 2.6 % (7/259) of controls (p = 0.0367). tTGA was low (1.1–2.6 %) and not different in between the study cohorts, nonetheless, in T1D tTGA was associated to islet autoantibodies. TPOA was more frequent in T1D, 27.1 % (53/191), compared to either T2D, 14.8 % (55/372; p = 0.0002) or controls, 14.3 % (37/259) (p = 0.0004). Overall, TPOA was more frequent in GADA positive (34.8 %; 8/23) than negative (13.5 %; 47/349; p = 0.0053) T2D individuals.

It’s suggested that analyzing GADA and TPOA may refine the autoimmune landscape in individuals clinically classified as T2D.

## Linked entities

- **Proteins:** PIN (insulin precursor)
- **Diseases:** type 1 diabetes (MONDO:0005147), celiac disease (MONDO:0005130), autoimmune thyroiditis (MONDO:0005623), type 2 diabetes (MONDO:0005148)

## Full-text entities

- **Genes:** SLC30A8 (solute carrier family 30 member 8) [NCBI Gene 169026] {aka ZNT8, ZnT-8}, INS (insulin) [NCBI Gene 3630] {aka IDDM, IDDM1, IDDM2, ILPR, IRDN, MODY10}, TGM2 (transglutaminase 2) [NCBI Gene 7052] {aka G(h), TG(C), TGC, hTG2, tTG}, TPO (thyroid peroxidase) [NCBI Gene 7173] {aka MSA, TDH2A, TPX}
- **Diseases:** CD (MESH:D002446), T1D (MESH:D003922), T2D (MESH:D003924), AITD (MESH:D013967)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

8 figures with captions in the complete paper: https://tomesphere.com/paper/PMC11416225/full.md

## References

50 references — full list in the complete paper: https://tomesphere.com/paper/PMC11416225/full.md

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Source: https://tomesphere.com/paper/PMC11416225