Electrolyte abnormalities have been seen with AML. Severe hyponatremia associated with SIADH secretion has occurred at presentation. Hypokalemia is a more frequent finding at presentation and is related to kaliuresis. Hypercalcemia can occur. Severe lactic acidosis prior to treatment has been reported. Hypophosphatemia as a result of phosphate uptake by leukemic cells can occur. But hypernatremia secondary to a diabetes insipidus (DI) is rare but has been described.
Interestingly, this phenomenon( mostly central) has been seen with certain cytogenetics in AML.
It appears that when you have monosomy 7 variant of AML, it can also lead to in some cases a central DI. Sometimes CDI might be the primary event presenting the AML. Prior literature is not clear the association of this and doesn't appear its CNS involvement but perhaps a genetic association. Literature reveals many abstracts when you google and pubmed this entity.
Typically,one would think that the combination of DI and AML is associated with structural abnormalities of the neurohypophysis. But there are cases presenting without any abnormalities of the neurohypophysis on radiological scanning and with normal cerebrospinal fluid examination. AML may directly result in dysregulation of transcription factors resulting in development of DI in AML patients.
One study even compared monosomy 7 with DI and AML and without DI, the group with DI had a
poorer outcome.
This association is hard to understand and why this is the case?
Ref:
http://www.ncbi.nlm.nih.gov/pubmed/19380027
http://www.ncbi.nlm.nih.gov/pubmed/3319680
http://www.ncbi.nlm.nih.gov/pubmed/1398517
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