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Fiordoliva et al. J Cancer Metastasis Treat 2019;5:59 I http://dx.doi.org/10.20517/2394-4722.2019.23 Page 5 of 8

Table 1. Comparison between prostate and liver histology
Prostate Liver
Morphology Acinar adenocarcinoma with neuroendocrine Small cell neuroendocrine
differentiation (5%), Gleason score 5 + 4 = 9 carcinoma
(grade group 5)
PSMA Diffuse positivity Negative
Synaptophysin Focal Diffuse
Mib1 50% 90%
PSMA: prostate specific membrane antigen

After Endocrinological Consultant, we performed the following evaluations: glucose = 96 mg/dL, serum
creatinine = 0.35 mg/dL, blood urea nitrogen = 9.8 mg/dL, plasma osmolality = 259 mOsm/kg, urinary
osmolality = 322 mOsm/kg, urinary calcium = 2.4 mg/dL, urinary sodium = 115 mEq/L, urinary
potassium = 5.3 mEq/L, TSH = 1.1 mcU/mL, ACTH = 14 pg/mL, plasmatic cortisol = 9.9 mcg/dL, venous
bicarbonates = 25 mmol/L. Therefore, considering also euvolemic status and no concomitant use of

diuretics, we diagnosed SIAD and started treatment with Tolvaptan 15 mg/die in October 2nd 2015

carefully monitoring plasmatic sodium every six hours. Sodium increase was < 10 mmol/die up to Na =
+
133 mEq/L and the patient continued progressively to reduce Tolvaptan dosage till a maintenance dose of
3.75 mg/die, monitoring plasmatic sodium daily.

Considering last histological examination and the clinical benefit with vaptan, after evaluation, the patient
2
2
started a second-line chemotherapy with Cisplatin 80 mg/m i.v. day 1 and Etoposide 100 mg/m i.v. days
1-3 every three weeks. After three cycles of chemotherapy, the patient experienced grade 3 anemia,
grade 2 thrombocytopenia, grade 4 leucopenia and grade 4 neutropenia, requiring blood transfusion
and administration of granulocyte growth factor and antibiotics. No other toxicities were reported.
Patient underwent a fourth cycle with reduced doses. PSA value was stable, while NE tumor markers
increased.

In December 2015, patient experienced bone disease progression at CT scan. A month later, he died
due to liver failure.

DISCUSSION
Hyponatremia is defined as serum sodium concentration (Na ) lower than 135 mmol/L [8,9] and it is one
+
of the most common electrolyte disorders occurring in cancer patients with an estimated incidence
between 5% and 20% [10,11] . The most frequent causes include SIAD, due in most cases to ectopic
production of antidiuretic hormone, extracellular fluid depletion or renal toxicity of chemotherapy,
especially platinum-based .
[5]
The main diagnostic criteria for SIAD are: euvolemic status, reduced plasma osmolality < 275 mOsm/kg,
increased urine osmolality > 100 mOsm/kg, increased urinary sodium > 30 mEq/L, normal kidney,
thyroid and adrenal function. Additional diagnostic criteria are: no use of diuretics, reduced blood
uric acid < 4 mg/dL, reduced blood urea nitrogen (BUN) < 10 mg/dL, increased sodium renal excretion
fraction > 1% and increased urea excretion fraction > 55% .
[6]

Correct management of hyponatremia represents an important issue for cancer patients considering
its well-demonstrated role in increasing mortality, costs and length of hospitalization [12-14] . Treatment
depends on underlying causes of hyponatremia but also on severity and time of onset. In the context
[15]
of SIAD, vaptans represent a relevant therapeutic option for mild-moderate reduction .