Endocrine Abstracts (2012) 28 P28

Tolvaptan for the treatment of hyponatraemia secondary to SIADH in cancer patients

Sami Kenz & G Brabant


Endocrinology, Christie Hospital, Manchester, United Kingdom.


Introduction: SIADH is frequently observed as a paraneoplastic secretion in many cancer types with the highest frequency described in small-cell lung cancer. The paraneoplastic secretion of ADH/vasopressin may induce hyponatraemia which is associated with increased morbidity and mortality. Conventional treatment of the condition consists of fluid restriction and demeclocycline. Tolvaptan, an oral V2-receptor antagonist, that directly targets the mechanism of SIADH, has been previously shown to improve hyponatraemia. However, currently only few data are published on the use of the drug in cancer patients with SIADH.

Cases: A series of twelve patients with paraneoplastic SIADH (4 males/8 females, age 46–87 yrs) developed SIADH. The diagnosis was based on severe hyponatraemia (110–126 mmol/L), decreased plasma osmolality (235–264 mmosmol/L) and raised urinary osmolality (297–834 mmosmol/L). Thyroid function and cortisol were normal. Conventional therapy did not alter the condition and all patients were hospitalized for the condition. Starting patients on a low dose of 7.5 mg tolvaptan/alternate days improved the condition with a maximum increase in sodium levels of 11 mmol/L within the first 2 days in all patients and they reached sodium levels of 135–139 mmol/L within the first 6 days. Plasma osmolality increased between 13 and 46 mosl/L despite stopping fluid restriction and demeclocycline. All patients could be discharged from the hospital. One patient was maintained on this dose of tolvaptan for 3-weeks with normalized sodium levels.

Conclusion: This case series of patients with paraneoplastic SIADH supports a high sensitivity of these patients to the effects of tolvaptan. The approach used allowed a slow and safe correction of the condition.

Declaration of interest: There is no conflict of interest that could be perceived as prejudicing the impartiality of the research reported.

Funding: No specific grant from any funding agency in the public, commercial or not-for-profit sector.

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