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Abstract: PO1157

A Rare Case of Acute Myeloid Leukemia Presenting as Central Diabetes Insipidus

Session Information

Category: Fluid, Electrolyte, and Acid-Base Disorders

  • 902 Fluid, Electrolyte, and Acid-Base Disorders: Clinical


  • Shah, Dharika P., The Ohio State University Wexner Medical Center, Columbus, Ohio, United States
  • Tyagi, Alka A., The Ohio State University Wexner Medical Center, Columbus, Ohio, United States
  • Doraiswamy, Mohankumar, The Ohio State University Wexner Medical Center, Columbus, Ohio, United States
  • Madhavan, Sethu M., The Ohio State University Wexner Medical Center, Columbus, Ohio, United States

Central Diabetes Insipidus (CDI) is an uncommon condition, with an overall incidence of approximately 1:25,000 and is usually associated with neurosurgery, trauma, autoimmune and vascular disease, infiltrative disorders, hypoxic brain injury, and brain metastasis. Patients with acute myeloid leukemia (AML) mostly present with symptoms of pancytopenia, noted to have hematologic abnormalities and are subsequently diagnosed with AML after bone marrow biopsy. Here we describe a unique case of a patient who presented with symptoms of CDI and incidentally diagnosed with AML.

Case Description

A 64-year-old male with a history of coronary artery disease presented to his primary physician complaining of polyuria and polydipsia which affected his work as a truck driver. Labs were notable for mild anemia (Hgb 11 g/dL) with macrocytosis, thrombocytosis (platelet 667 K/uL), serum sodium was 146 mmol/L, Hgb A1c 5%, prostate-specific-antigen 1.4 ng/dL, normal lipid panel, and normal thyroid function. No definitive diagnosis was made and he underwent evaluation by hematology. Peripheral smear showed increased (44%) blasts/promyelocytes, consistent with acute leukemia. Cytogenetic analysis showed an abnormal clone of cells with an inverted chromosome 3 and monosomy for chromosome 7. He was admitted for induction therapy and presenting symptoms worsened (~10 L urine output per day) along with hypernatremia which peaked at 160 mmol/L, serum osmolality 319 mOsmo/kg and urine osmolality of 174 mOsmo/kg despite large oral and peripheral free water supplementation. MRI brain was negative for intracranial findings or abnormal enhancement. Given the degree of hypernatremia, and history concerning for CDI, empiric treatment with intra-nasal vasopressin (DDAVP) was given with significant improvement of symptoms, serum sodium, serum osmolality and urine osmolality.


The presentation of AML with concurrent CDI is associated with chromosome 3 or 7 abnormities, not brain lesions, as in this case; the management of CDI involves continued DDAVP administration. Unfortunately this translocation has been associated with poor clinical outcome. With this case, we suggest screening patients for CDI who have an unclear reason of developing of polydipsia and polyuria and if hematologic abnormalities are noted, should undergo prompt evaluation for AML.