# An Adult Case of Diabetes With High Levels of GAD Antibodies Without Insulin Deficiency for More Than 10 Years

**Authors:** Hideyuki Takeuchi, Naoyuki Iso-O, Atsuko Takai, Takashi Mikamo, Kozue Nagumo, Masumi Hara

PMC · DOI: 10.1155/crie/9712659 · Case Reports in Endocrinology · 2025-02-27

## TL;DR

A 56-year-old woman with high GAD antibodies and diabetes maintained insulin production for over 10 years, challenging assumptions about autoimmune diabetes progression.

## Contribution

This case shows that high GAD antibody levels do not always lead to rapid insulin deficiency in autoimmune diabetes.

## Key findings

- The patient had high GAD antibodies but preserved insulin secretion for over a decade.
- Positive GAD antibodies alone are not reliable predictors of insulin deficiency.
- Early treatment should focus on weight management and CVD prevention when insulin secretion is preserved.

## Abstract

Latent autoimmune diabetes in adults (LADA) or slowly progressive insulin-dependent diabetes mellitus (SPIDDM) is a form of autoimmune diabetes characterized by autoimmune destruction of pancreatic beta cells, leading to deficient insulin secretion. Here, we report a case of diabetes and obesity in a 56-year-old woman. She was diagnosed with severe obesity, impaired glucose tolerance (IGT), and a positive antiglutamic acid decarboxylase antibody (GADA) test result at the age of 39 years. She developed diabetes 7 years later, meeting the diagnostic criteria for SPIDDM (probable). Despite high GADA levels, her endogenous insulin secretion has been preserved for over a decade. GADA has been regarded as a marker of autoimmune destruction of pancreatic beta cells, and high levels of GADA are considered a risk factor for future insulin deficiency. However, the role of GADA in its pathogenesis remains unclear. GADA is not a specific indicator of autoimmune diabetes, as it is also positive for autoimmune diseases such as autoimmune thyroid diseases (AITDs) and stiff-person syndrome. Therefore, a positive GADA test alone is not sufficient to predict insulin deficiency in an individual case, even if the titer is high. In the early stages, autoimmune diabetes presents clinical features similar to those of type 2 diabetes, particularly obesity. Although insulin therapy is often started early in the treatment of autoimmune diabetes, as the consensus statement indicates, when endogenous insulin secretion is preserved and the risk of insulin deficiency is low, efforts should be made to prevent body weight gain and the development of cardiovascular diseases (CVD) by following treatment guidelines for type 2 diabetes, with the exception of the use of sulfonylurea agents.

## Linked entities

- **Diseases:** diabetes (MONDO:0005015), obesity (MONDO:0011122), stiff-person syndrome (MONDO:0008491)

## Full-text entities

- **Genes:** INS (insulin) [NCBI Gene 3630] {aka IDDM, IDDM1, IDDM2, ILPR, IRDN, MODY10}, GAD1 (glutamate decarboxylase 1) [NCBI Gene 2571] {aka CPSQ1, DEE89, GAD, GAD-67, SCP}
- **Diseases:** CVD (MESH:D002318), slowly progressive (MESH:D018450), Diabetes (MESH:D003920), IGT (MESH:D018149), Latent autoimmune diabetes in (MESH:D000071698), SPIDDM (MESH:D003922), stiff-person syndrome (MESH:D016750), autoimmune (MESH:D001327), AITDs (MESH:D013967), weight gain (MESH:D015430), type 2 diabetes (MESH:D003924), Insulin Deficiency (MESH:D007333), obesity (MESH:D009765)
- **Chemicals:** GADA (-)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

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## References

31 references — full list in the complete paper: https://tomesphere.com/paper/PMC11987071/full.md

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Source: https://tomesphere.com/paper/PMC11987071