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Peer-reviewedCC BYCureus

Hyperosmolar Hyperglycemic State As the Initial Presentation of Type 1 Diabetes Mellitus in an Adolescent: A Case Report.

5 affiliations
  1. 1Pediatric Intensive Care Unit, Almoosa Specialist Hospital, Al-Ahsa, SAU.
  2. 2Pediatric Intensive Care Unit, King Fahad Medical City, Riyadh, SAU.
  3. 3Pediatric Critical Care Medicine, Almoosa Specialist Hospital, Al-Ahsa, SAU.
  4. 4Pediatric Endocrinology, Almoosa Specialist Hospital, Al-Ahsa, SAU.
  5. 5Pediatrics, Almoosa Specialist Hospital, Al-Ahsa, SAU.

Abstract

Hyperosmolar hyperglycemic state (HHS) is an uncommon but life-threatening hyperglycemic emergency in children and is more often associated with type 2 diabetes mellitus. We report a 13-year-old boy with a lean habitus and no previously diagnosed chronic illnesses who presented after three weeks of polyuria, polydipsia, fatigue, and weight loss. On admission, serum glucose was 1,080 mg/dL (60 mmol/L), hemoglobin A1c was 13.8%, measured serum osmolality was 331 mOsm/kg, calculated effective osmolality was 324 mOsm/kg, venous pH was 7.29, bicarbonate was 23.1 mmol/L, beta-hydroxybutyrate was 0.7 mmol/L, and urine ketones were negative. The biochemical profile met pediatric HHS criteria without significant ketoacidosis. He received an initial 20 mL/kg bolus of 0.9% sodium chloride followed by controlled deficit replacement. Intravenous insulin at 0.05 units/kg/hour was deliberately delayed until four hours after the initiation of fluid therapy, when the decline in glucose with fluids alone slowed to <50 mg/dL/hour. Glucose and effective osmolality then declined in a controlled fashion, while measured sodium rose gradually as hyperglycemia corrected; dextrose was added when glucose reached 275 mg/dL. No neurologic, thrombotic, renal, or major electrolyte complications occurred. Strongly positive GAD65 antibodies and a low C-peptide concentration obtained during concurrent hyperglycemia supported autoimmune type 1 diabetes mellitus (T1DM). The patient transitioned to subcutaneous basal-bolus insulin and was discharged on day 3. At three months, hemoglobin A1c was 7.0%. This case illustrates that HHS may be the first manifestation of autoimmune T1DM even in a lean adolescent and emphasizes the importance of interpreting glucose, sodium, and effective osmolality together while prioritizing controlled fluid replacement before insulin.

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BibTeX
@article{alamer2026hyperosmolar,
  title = {{Hyperosmolar Hyperglycemic State As the Initial Presentation of Type 1 Diabetes Mellitus in an Adolescent: A Case Report.}},
  author = {Ali T Alamer and Sajjad M AlKadhem and Osama Kattih and Ahmed A Al-Amoudi and Aida S AlJabri and Zainab M Almeftah and Husain A Althani},
  journal = {Cureus},
  year = {2026},
  month = sep,
  doi = {10.7759/cureus.116797},
  url = {https://europepmc.org/article/MED/42921622},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Hyperosmolar Hyperglycemic State As the Initial Presentation of Type 1 Diabetes Mellitus in an Adolescent: A Case Report.
AU  - Ali T Alamer
AU  - Sajjad M AlKadhem
AU  - Osama Kattih
AU  - Ahmed A Al-Amoudi
AU  - Aida S AlJabri
AU  - Zainab M Almeftah
AU  - Husain A Althani
PY  - 2026
DA  - 2026/09/23
JO  - Cureus
DO  - 10.7759/cureus.116797
UR  - https://europepmc.org/article/MED/42921622
AB  - Hyperosmolar hyperglycemic state (HHS) is an uncommon but life-threatening hyperglycemic emergency in children and is more often associated with type 2 diabetes mellitus. We report a 13-year-old boy with a lean habitus and no previously diagnosed chronic illnesses who presented after three weeks of polyuria, polydipsia, fatigue, and weight loss. On admission, serum glucose was 1,080 mg/dL (60 mmol/L), hemoglobin A1c was 13.8%, measured serum osmolality was 331 mOsm/kg, calculated effective osmolality was 324 mOsm/kg, venous pH was 7.29, bicarbonate was 23.1 mmol/L, beta-hydroxybutyrate was 0.7 mmol/L, and urine ketones were negative. The biochemical profile met pediatric HHS criteria without significant ketoacidosis. He received an initial 20 mL/kg bolus of 0.9% sodium chloride followed by controlled deficit replacement. Intravenous insulin at 0.05 units/kg/hour was deliberately delayed until four hours after the initiation of fluid therapy, when the decline in glucose with fluids alone slowed to <50 mg/dL/hour. Glucose and effective osmolality then declined in a controlled fashion, while measured sodium rose gradually as hyperglycemia corrected; dextrose was added when glucose reached 275 mg/dL. No neurologic, thrombotic, renal, or major electrolyte complications occurred. Strongly positive GAD65 antibodies and a low C-peptide concentration obtained during concurrent hyperglycemia supported autoimmune type 1 diabetes mellitus (T1DM). The patient transitioned to subcutaneous basal-bolus insulin and was discharged on day 3. At three months, hemoglobin A1c was 7.0%. This case illustrates that HHS may be the first manifestation of autoimmune T1DM even in a lean adolescent and emphasizes the importance of interpreting glucose, sodium, and effective osmolality together while prioritizing controlled fluid replacement before insulin.
SN  - 2168-8184
ER  -