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Abstract: FR-PO591

Central Diabetes Insipidus in a Patient with Newly Diagnosed AML

Session Information

  • Trainee Case Reports - III
    October 26, 2018 | Location: Exhibit Hall, San Diego Convention Center
    Abstract Time: 10:00 AM - 12:00 PM

Category: Trainee Case Reports

  • 902 Fluid and Electrolytes: Clinical

Authors

  • El Shamy, Osama, Mount Sinai Hospital, Hasbrouck Heights, New Jersey, United States
  • Kattamanchi, Siddhartha, Mount Sinai Medical Center, New Rochelle, New York, United States
  • Coca, Steven G., Icahn School of Medicine at Mount Sinai, New York, New York, United States
Introduction

Central diabetes insipidus (CDI) has been reported as both a rare complication of AML that may precede its diagnosis, and a may be a manifestation of its relapse. The exact mechanism by which diabetes insipidus and AML are connected remains elusive. The prevalence of cytogenic abnormalities in AML has been implicated as a possible cause. Here we describe a case of AML-induced CDI with monosomy 7 and without evidence on imaging of pituitary infiltration

Case Description

A 28 y/o woman was transferred from an outside hospital with significant leukocytosis (WBC 163,000) in the setting of a non-healing dental extraction and worsening odynophagia. She was found to have a new diagnosis of AML (diagnosed by peripheral blood smear and a deletion of D7S522 (7q31) locus via FISH) and a left neck soft tissue infection. The patient was started on the 7+2 chemotherapy protocol (Cytarabine and Idarubicin) on 4/17/18. The renal service was consulted for AKI in the setting of polyuria (approximately 2.5 to 3 liters per day). Labs were notable for a serum creatinine of 2.1 mg/dL, serum sodium of 152 meq/L, and urine osm of 190 mosm/L. She was started on ddAVP, and was continued for several days, over which time her urine output decreased, urine osmolality increased, with concomitant improvements in serum sodium and serum creatinine. Re-induction chemotherapy for persistent blasts was started 2 weeks later with clinical response over the next 10 days as evidenced by only 0.3% blasts. ddAVP was able to be discontinued as well at this point, as the resolution of the CDI coincided with the re-induction chemotherapy and subsequently confirmed low blast count and undetectable B cells

Discussion

A review of the literature reveals that CDI is a rare complication of AML, which can occur anytime during the course of AML. Although the exact mechanism connecting AML and CDI is unknown, some proposed theories include infiltration of hypothalamic pituitary stalk and abnormal expression of GP130 on neutrophils and platelets in patients with deletions on chromosome 7 or monosomy 7. The deficient GP 130 leads to abnormalities in glycosylation of neutrophils and platelets which can lead to CDI via two mechanisms: 1) decreased pre-pro-vasopressin which results in less active ADH production and 2) the dysfuctional platelets may affect ADH function and transport. Successful treatment of AML can rapidly reverse CDI.