Isolated Cranial Diabetes Insipidus Unmasked After Hyperosmolar Hyperglycemic State in Type 2 Diabetes Mellitus
https://doi.org/10.15605/jafes.041.S1
- Author:
Suseelah Bala Subramaniam
1
;
Rabeah Md Zuki
2
;
Loh Hoong Heng
1
Author Information
1. Department of Internal Medicine, Hospital Kulim
2. Department of Endocrinology, Hospital Sultan Abdul Halim
- Publication Type:Journal Article
- MeSH:
Diabetes Mellitus, Type 2;
Hyperglycemic Hyperosmolar Nonketotic Coma;
Diabetes Insipidus
- From:
Journal of the ASEAN Federation of Endocrine Societies
2026;41(S1):94-95
- CountryPhilippines
- Language:English
-
Abstract:
Introduction:Central diabetes insipidus (CDI) is characterized by
impaired arginine vasopressin secretion, resulting in
hypotonic polyuria and hypernatremia. In patients with
coexisting diabetes mellitus, persistent polyuria may be
misattributed to hyperglycemia, delaying recognition
of a concurrent water balance disorder. CDI without
identifiable structural abnormalities may be overlooked,
leading to delayed diagnosis and complications.
Case:We report a 30-year-old Malay female with underlying type
2 diabetes mellitus and premorbid obesity who presented
with hyperosmolar hyperglycemic state, accompanied
by persistent polyuria, polydipsia, weight gain, and
amenorrhea. Despite resolution of hyperglycemia, she had
ongoing polyuria with hypernatremia, raising suspicion
of a concomitant water balance disorder.
Biochemical evaluation demonstrated a hyperosmolar state
with serum osmolality 334 mOsm/kg and inappropriately
dilute urine (urine osmolality 254 mOsm/kg), supporting
impaired vasopressin activity. A modified water deprivation
test showed a >50% rise in urine osmolality following
desmopressin, consistent with CDI. Diabetes autoantibody
screening was negative. Anterior pituitary function was
preserved, with normal thyroid and adrenal axes (thyroidstimulating hormone 3.30 mIU/L, cortisol 290.6 nmol/L),
and gonadotropins not suggestive of hypopituitarism
(luteinizing hormone 6.8 IU/L, follicle-stimulating hormone
24.6 IU/L).
Neuroimaging with computed tomography brain showed
no structural hypothalamic–pituitary lesion. Magnetic
resonance imaging of the pituitary demonstrated absence
of the posterior pituitary bright spot, with preserved gland
morphology and no focal lesion, supporting CDI without
an identifiable structural cause. Her clinical course was complicated by severe hospitalacquired infection leading to septic shock, requiring
intensive care support, mechanical ventilation, and renal
replacement therapy. She was commenced on desmopressin,
with subsequent clinical and biochemical improvement,
alongside multidisciplinary management.
Conclusion:In patients with type 2 diabetes mellitus, persistent polyuria
may obscure an underlying water balance disorder. This
case highlights the importance of considering alternative
causes of polyuria and a systematic endocrine approach to
ensure accurate diagnosis and appropriate management.
- Full text:2026080415501628765EP_A135.pdf