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A patient was recently seen on the consult
service for evaluation of hyponatremia. She had a history of multiple myeloma
and a previous bone marrow transplant and had significant cholestatic
liver dysfunction related to GVHD. Her serum sodium at the time of presentation
was 120 mmol/L. The initial thought was that she may have SIADH but her serum
osmolarity came back at 290 suggesting that we were in fact dealing with a case
of pseudohyponatremia.
The commonest causes of pseudohyponatremia are
severe hypergammaglobulinemia and hypertriglyceridemia. Neither was present in
this case. A previous case report in the NEJM in 2003 described
pseudohyponatremia in a patient with cholestatic jaundice that was felt to be
the result of accumulation of lipoprotein X. This is formed when there is
reflux of cholesterol and phospholipids into the circulation from blocked
biliary ducts. Because it is not soluble, it increases the solid portion of
plasma and leads to pseudohyponatremia. A plasma sample confirmed to presence of
lipoprotein X in this patient.
One point that was raised during the assessment
was that the diagnosis of pseudohyponatremia cannot be made by measuring the
serum osmolarity alone. It is important to confirm this by measuring the serum
sodium with a direct ion sensitive electrode as this will measure the sodium
concentration in the plasma water alone and therefore give a true result. This is because there
are occasional cases where a patient with true hyponatremia will present after
ingestion of a large quantity of alcohol. In this case, the serum sodium will
be low, there will be a significant osmolar gap (suggesting that the patient
has pseudohyponatremia) but the directly measured serum sodium will also be low
– confirming the presence of true hyponatremia.

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