Case report describes rapid diabetes progression in a patient with high anti-GAD antibodies, suggesting autoimmune triggers.
A 61-year-old man visited our hospital with a sudden onset of polydipsia and polyuria occurring 5 days prior, accompanied by a 5-kg weight loss. A month prior, his glycated hemoglobin level was 6.2%. Precisely 8 days before the first visit, he had a fever, and hyperglycemic symptoms began shortly thereafter. At the first visit, he had a blood glucose level of 465 mg/dL, a glycated hemoglobin level of 7.7%, and ketosis. He was diagnosed with fulminant type 1 diabetes mellitus. The antiglutamic acid decarboxylase (GAD) antibodies were >2000 IU/mL, without other pancreatic islet-related autoantibodies. The human leukocyte antigen haplotype was DRB1*09:01-DQB1*03:03 and DRB1*13:02-DQB1*06:04. Intensive insulin therapy was initiated, and the patient was admitted for monitoring the blood glucose profile. The anti-GAD antibody turned negative approximately 7 months later. Some infections may have triggered rapid pancreatic islet destruction in an autoimmunity-induced impaired glucose tolerance state.
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Sato et al. (2026) studied this question.
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