Case Report: Pregnancy-associated fulminant type 1 diabetes superimposed on insulin-treated gestational diabetes with intrauterine fetal demise

Pregnancy-associated fulminant type 1 diabetes (FT1DM) is characterized by abrupt loss of endogenous insulin secretion and rapid progression to diabetic ketoacidosis (DKA). Recognition may be particularly challenging when FT1DM develops in a pregnancy already treated with insulin for gestational diabetes mellitus (GDM), because sudden glycemic deterioration may be attributed to increasing gestational insulin resistance, inadequate insulin dosing, or treatment interruption. We report a 24-year-old woman with insulin-treated GDM who developed dizziness, nausea, and vomiting at 33 weeks of gestation after one scheduled basal insulin dose was omitted. At a referring hospital, plasma glucose was 19.14 mmol/L (345 mg/dL) and urinary ketones were 3 +. Fetal cardiac activity was reportedly present initially but was absent the following day, when intrauterine fetal demise was confirmed. After transfer, plasma glucose was 20.77 mmol/L (374 mg/dL), beta-hydroxybutyrate 6.63 mmol/L (69.0 mg/dL), arterial pH was 7.235, and bicarbonate was 6.00 mmol/L (6.00 mEq/L), confirming persistent severe DKA; glycated hemoglobin was 6.1% (43 mmol/mol). Fasting and stimulated C-peptide concentrations remained profoundly reduced after metabolic stabilization, supporting the diagnosis of pregnancy-associated FT1DM. DKA improved with intravenous fluids, insulin, electrolyte replacement, and close biochemical monitoring, after which labor was induced and a stillborn female fetus was delivered. Repeated glucose and C-peptide measurements during long-term follow-up demonstrated persistent near-complete endogenous insulin deficiency. This case highlights the risk of diagnostic anchoring in insulin-treated GDM. Abrupt gastrointestinal symptoms or unexpected glycemic deterioration should prompt immediate assessment for ketosis and acidosis rather than being attributed solely to gestational insulin resistance or an isolated interruption of insulin treatment.

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Journal
Frontiers in Endocrinology
Published
2026-10-30
DOI
https://doi.org/10.3389/fendo.2026.1994868
Primary Topic
Gestational Diabetes Research and Management
Type
article
Field-Weighted Citation Impact
0.00

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article

Case Report: Pregnancy-associated fulminant type 1 diabetes superimposed on insulin-treated gestational diabetes with intrauterine fetal demise

Leweihua Lin, Huibiao Quan, Danhong Lin, Zhenshu Gao et al.
1 links
Frontiers in Endocrinology
Gestational Diabetes Research and Management
article

Case Report: Pregnancy-associated fulminant type 1 diabetes superimposed on insulin-treated gestational diabetes with intrauterine fetal demise

Leweihua Lin, Huibiao Quan, Danhong Lin, Zhenshu Gao, Dexia Li, Jiahuan Zhang
article en

Abstract

Pregnancy-associated fulminant type 1 diabetes (FT1DM) is characterized by abrupt loss of endogenous insulin secretion and rapid progression to diabetic ketoacidosis (DKA). Recognition may be particularly challenging when FT1DM develops in a pregnancy already treated with insulin for gestational diabetes mellitus (GDM), because sudden glycemic deterioration may be attributed to increasing gestational insulin resistance, inadequate insulin dosing, or treatment interruption. We report a 24-year-old woman with insulin-treated GDM who developed dizziness, nausea, and vomiting at 33 weeks of gestation after one scheduled basal insulin dose was omitted. At a referring hospital, plasma glucose was 19.14 mmol/L (345 mg/dL) and urinary ketones were 3 +. Fetal cardiac activity was reportedly present initially but was absent the following day, when intrauterine fetal demise was confirmed. After transfer, plasma glucose was 20.77 mmol/L (374 mg/dL), beta-hydroxybutyrate 6.63 mmol/L (69.0 mg/dL), arterial pH was 7.235, and bicarbonate was 6.00 mmol/L (6.00 mEq/L), confirming persistent severe DKA; glycated hemoglobin was 6.1% (43 mmol/mol). Fasting and stimulated C-peptide concentrations remained profoundly reduced after metabolic stabilization, supporting the diagnosis of pregnancy-associated FT1DM. DKA improved with intravenous fluids, insulin, electrolyte replacement, and close biochemical monitoring, after which labor was induced and a stillborn female fetus was delivered. Repeated glucose and C-peptide measurements during long-term follow-up demonstrated persistent near-complete endogenous insulin deficiency. This case highlights the risk of diagnostic anchoring in insulin-treated GDM. Abrupt gastrointestinal symptoms or unexpected glycemic deterioration should prompt immediate assessment for ketosis and acidosis rather than being attributed solely to gestational insulin resistance or an isolated interruption of insulin treatment.

Frontiers in EndocrinologyVol. 17
Hainan General Hospital (CN), Hainan Medical University (CN)
Hainan Provincial Department of Science and Technology
Good health and well-being
Openalex Percentile: Top 8%
Gestational Diabetes Research and Management
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