A 57- year old male patient was treated surgically for transitional cell carcinoma of the bladder. A symptomatic hyponatremia was observed when he was admitted for early recurrence of his cancer with systemic metastases. SIADH was considered as the cause of the hyponatremia after ruling out other possibilities. A normalization of the serum sodium level at the end of water restriction confirmed the diagnosis of SIADH. The SIADH of the patient was considered paraneoplastic, i.e. secondary to his tumor because it accompanied the progression of the disease.
SIADH was first described by Schwartz et al., in two patients with bronchogenic carcinoma of the lung. Since that time it has been realized as the etiology of most hyponatremic cases observed in cancer patients.
Essential diagnostic criteria for SIADH are reduced effective extracellular volume osmolality (Plasma osmolality <275 mOsm/kg H2O); inappropriate urine concentration (Urine osmolality >100 mOsm/kg H2O) in the presence of normal renal function; euvolemia; increased sodium excretion; exclusion of any other potential conditions which can cause euvolemic hypoosmolality such as hypothyroidism, hypocortisolism and diuretic use. Water restriction test is not essential for the diagnosis. However it can provide supporting information.
All the above mentioned criteria were met by the patient and the water restriction confirmed the diagnosis of SIADH. SIADH can be induced by various pulmonary and central nervous system diseases or it can be caused by ectopic secretion of ADH by tumors. Small cell lung cancer is the most frequent cause of paraneoplastic SIADH. SIADH was also reported with pancreatic carcinomas and rarely with other cancers such as neuroblastoma and lymphoma.
To our knowledge, only one case of SIADH related to the bladder cancer was reported in the literature. In this report, SIADH was diagnosed twenty months prior to the emergence of bladder cancer and as an early finding.
However, in our case, hyponatremia was not observed during the initial diagnosis and it appeared when the tumor recurred with systemic metastases. Our report has some similarities with the case of Andersen and Sorensen, who observed the appearance of SIADH during disease progression in a patient with breast cancer.
We can hypothesize that the SIADH in our patient is secondary to an ectopic ADH secretion and it reached significant levels with clinical consequences following an increase of the tumor mass. The systemic chemotherapy failed to decrease the tumor mass as well as to correct the SIADH. A simple measure such as chronic water restriction was able to maintain the serum sodium within normal levels.
The SIADH can be frequently observed in neoplasms such as bladder or other cancers, but missed often because of complicated clinical situations of patients with extensive metastatic diseases. Serum electrolytes should be evaluated carefully in such patients, because a simple hyponatremia can alert on the possibility of SIADH which can cause some neurologic damages in the absence of adequate treatment or with rapid correction of the hyponatremia.