Case Report: Pregnancy-associated fulminant type 1 diabetes superimposed on insulin-treated gestational diabetes with intrauterine fetal demise
- 1Department of Endocrinology, Hainan General Hospital, Affiliated Hainan Hospital of Hainan Medical University
- 2Department of Hematology, The Second Affiliated Hospital of Hainan Medical University
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.
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BibTeX
@article{li2026case,
title = {{Case Report: Pregnancy-associated fulminant type 1 diabetes superimposed on insulin-treated gestational diabetes with intrauterine fetal demise}},
author = {Dexia Li and Leweihua Lin and Zhenshu Gao and Danhong Lin and Jiahuan Zhang and Huibiao Quan},
journal = {Frontiers in Endocrinology},
year = {2026},
month = oct,
doi = {10.3389/fendo.2026.1994868},
url = {https://www.frontiersin.org/articles/10.3389/fendo.2026.1994868/full},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Case Report: Pregnancy-associated fulminant type 1 diabetes superimposed on insulin-treated gestational diabetes with intrauterine fetal demise
AU - Dexia Li
AU - Leweihua Lin
AU - Zhenshu Gao
AU - Danhong Lin
AU - Jiahuan Zhang
AU - Huibiao Quan
PY - 2026
DA - 2026/10/30
JO - Frontiers in Endocrinology
DO - 10.3389/fendo.2026.1994868
UR - https://www.frontiersin.org/articles/10.3389/fendo.2026.1994868/full
AB - 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.
SN - 1664-2392
ER -