Central diabetes insipidus and panhypopituitarism in acute myeloid leukemia

Ali Dhouibi; Ghada Saad; Maissa Thabet; Salem Braham; Nesrine Bensayed; Hadj Slama Nassim Ben; Yahya Wissal Ben; Ahmed Guiga; Neirouz Ghannouchi

doi:10.1530/endoabs.110.P902

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Endocrine Abstracts (2025) 110 P902 | DOI: 10.1530/endoabs.110.P902

ECEESPE2025 Poster Presentations Pituitary, Neuroendocrinology and Puberty (162 abstracts)

Central diabetes insipidus and panhypopituitarism in acute myeloid leukemia

Ali Dhouibi ¹ , Ghada Saad ² , Maissa Thabet ¹ , Salem Braham ³ , Nesrine Bensayed ⁴ , Nassim Ben Hadj Slama ² , Wissal Ben Yahya ¹ , Ahmed Guiga ¹ & Neirouz Ghannouchi ¹

Author affiliations

¹Farhat Hached University Hospital, Faculty of Medecine of Sousse, Internal Medecine, Sousse, Tunisia; ²Farhat Hached University Hospital, Faculty of Medecine of Sousse, Endocrinology and Diabetology, Sousse, Tunisia; ³Farhat Hached University Hospital, Medical Imaging, Sousse, Tunisia; ⁴Farhat Hached University Hospital, Clinical Hematology, Sousse, Tunisia

JOINT3861

Introduction: Acute myeloid leukemia (AML) is characterized by the rapid and uncontrolled proliferation of blasts in the bone marrow. Central diabetes insipidus (CDI) is an uncommon manifestation of AML.

Case Report: We report the case of a 68-year-old Tunisian patient with no significant medical history, admitted for evaluation of persistent dry mouth and dry eyes, associated with a polyuria-polydipsia syndrome in the context of a two-month history of general deterioration. Clinical examination revealed marked weight loss, a polyuria-polydipsia syndrome (fluid intake = 6L/day, urine output = 4.5L/day), dehydration, hypotension (BP = 90/50 mmHg), xerophthalmia, and xerostomia (grade III sialadenitis). Laboratory investigations showed: Blood glucose = 0.3 g/l; Serum sodium = 155 mmol/l; Plasma osmolality = 321 mosmol/l; Urine osmolality = 240 mosmol/l; Hemoglobin = 8 g/dl; Mean corpuscular volume (MCV) = 86 fL; White blood cell count = 7,000/mm³; Platelet count = 100,000/mm³; Peripheral blood smear: 20% circulating blasts. The diagnosis of AML was confirmed based on indings on bone marrow aspiration. Given the presence of polyuria-polydipsia syndrome, hypotension, and hypoglycemia, a global pituitary dysfunction was suspected and confirmed by: The absence of the posterior pituitary bright spot on MRI and evidence of panhypopituitarism (cortisol = 46 ng/mL, FT4 = 4 pmol/l, FSH = 2,58 mUI/l, testosterone = 0,35 ng/ml) Pituitary MRI revealed infiltration of the pituitary stalk and oss of T1 hyperintensity of the posterior pituitary. Cytogenetic analysis revealed monosomy 7. The patient was treated with desmopressin, hydrocortisone hemisuccinate, and L-thyroxine, leading to clinical improvement. Chemotherapy was subsequently initiated.

Conclusion: The associations between DI and AML remain enigmatic and the underlying cause of DI in patients with AML is likely multifactorial. It has been associated with chromosomal abnormalities involving chromosomes 3 or 7. Diagnosis remains challenging, but clinical improvement following chemotherapy supports this etiology.