Abstract: FR-PO658
Tolvaptan in Portal Hypertension: Real-Life Experience
Session Information
- Fluid and Electrolytes: Clinical - Potassium, Sodium, Water
November 08, 2019 | Location: Exhibit Hall, Walter E. Washington Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Fluid and Electrolytes
- 902 Fluid and Electrolytes: Clinical
Authors
- Tejedor, Marta, Hospital Infanta Elena, Valdemoro, Madrid, Spain
- Delgado Vázquez, Agustín Alejandro, Hospital General Universitario "Gregorio Marañón", Madrid, Spain
- Melero, Maria Rosa, Hospital General Universitario "Gregorio Marañón", Madrid, Spain
- Rodriguez benitez, Patrocinio, Hospital General Universitario "Gregorio Marañón", Madrid, Spain
- Fernandez-Alonso, Victor, Hospital General Universitario "Gregorio Marañón", Madrid, Spain
- Salcedo plaza, Magdalena, Hospital General Universitario "Gregorio Marañón", Madrid, Spain
- Tejedor jorge, Alberto, Fundación para la Investigación Biomédica del Hospital General Universitario "Gregorio Marañón", Madrid, Spain
Background
Tolvaptan (TVP) is an antagonist of V2 ADH receptors, used for hyponatremia in SIADH, congestive heart failure (CHF) and cirrhosis.
Methods
Retrospective review of TVP use between 2012 and 2017 to study the use of TVP in real life in patients with portal hypertension (PHT) (past history of non-malignant ascites or variceal bleed).
Results
81 patients received TVP. Of them, 19 had PHT. CHF was more frequent in patients with PHT (53 vs 26%, p=0.03). There were no differences in natremia at the start of treatment (126±1.3 vs 128±0.6mEq/l). There was a delay in the correction of hyponatremia in the PHT subgroup over the first month, being the final serum sodium concentration 135±1.6 vs 139±0.8mEq/l (p=0.02). We found no difference in survival.
In the PHT subgroup, 8 had confirmed cirrhosis and 11 severe CHF. The cause of cirrhosis was hepatitis C (n=3), alcohol (n=4) and unknown (n=1). 4 had hepatocellular carcinoma. Mean MELD score at the time of receiving tolvaptan was 12±2.3. Only one patient received a liver transplant 4 months after treatment with TVP. Cirrhotics had significant comorbidities (13% CHF; 13% microcytic lung cancer; 75% squamous cell carcinoma; 25% SIADH) and polypharmacy (13% antidepressants; 38% diuretics; 13% antiepileptics; 38% benzodiazepines; 13% cytostatics; 13% antipsychotics). Cirrhotics had fewer episodes of hyponatremia (8.4±1.1 vs 10.6±2.8), although not statistically significant. There was a trend for TVP treatment to be longer in cirrhotics (23.2±7.4 vs7.3±2.6 days, p=0.07). We studied the delay in hyponatremia correction observed in patients with PHT: it was attributable to patients with CHF, in whom the mean increase in serum sodium concentration over the first month was 1.4±1.9 vs 7.2±1mEq/l in cirrhotic patients (p=0.03). Median survival time was 105 weeks (CI95% 0-239) in CHF vs 5 weeks (CI95% 3-7) in cirrhotics, but was not statisticallt significant.
Conclusion
Even though TVP is approved for its use in hyponatremia associated to advanced cirrhosis as a bridge to liver transplant, in our centre its use is reserved to patients with significant comorbidities that can contribute to the development of hyponatremia and worsen its prognosis. Presence of ascites in CHF as a surrogate for PHT complicates management, delaying the correction of hyponatremia.