ABSTRACT
No disponible
Subject(s)
Humans , Urea/therapeutic use , Inappropriate ADH Syndrome/drug therapy , Receptors, Vasopressin/antagonists & inhibitors , Isotonic Solutions , Hyponatremia/drug therapyABSTRACT
Objetivo: Analizar la efectividad del uso de tolvaptán y la adecuación de su prescripción en un hospital de tercer nivel. Método: Estudio observacional prospectivo de las prescripciones de tolvaptán desde octubre de 2010 hasta diciembre de 2011. Resultados: Se incluyeron 30 pacientes (60,0% varones), 50,0% diagnosticados de insuficiencia cardíaca y 30,0% de SIADH. Tolvaptán permitió alcanzar niveles de sodio superiores a 135 mEq/L en el 53,3% de los pacientes que partían con una media de 125,3±7,3 mEq/L. La mediana de días de tratamiento fue de 5,0 (rango intercuartílico = 3-45). Se observó un incremento significativo de los niveles de ácido úrico asociado al tratamiento con tolvaptán. La prescripción se adecuó a lo establecido en la GFT en el 63,3% de los casos. Conclusiones: Tolvaptán incrementa un 7,5 mEq/L los niveles de sodio tanto en hiponatremia secundaria al SIADH como en insuficiencia cardiaca (AU)
Purpose: To analyse the effectiveness of the use of Tolvaptan and the adequacy of Tolvaptan prescription at a tertiary level hospital. Methods: Prospective observational study of Tolvaptan prescription from October of 2010 to December of 2011. Results: 30 patients (60.0% males) were included, 50.0% of which were diagnosed with heart failure and 30.0% with SIADH. Tolvaptan allowed achieving sodium levels higher than 135 mEq/L in 53.3% of the patients with a mean baseline value of 125.3±7.3 mEq/L. The median treatment duration was 5.0 days (interquartile range = 3-45). A significant increase of uric acid associated to Tolvaptan treatment was observed. The prescription was in agreement to what has been established in GFT in 63.3% of the cases. Conclusions: Tolvaptan increases sodium levels by 7.5 mEq/L, both in SIADH-associated hyponatremia and in heart failure, with an appropriate safety profile (AU)
Subject(s)
Humans , Heart Failure/complications , Inappropriate ADH Syndrome/complications , Hyponatremia/drug therapy , Receptors, Vasopressin/antagonists & inhibitors , Prospective Studies , Drug Prescriptions/statistics & numerical data , Treatment OutcomeABSTRACT
OBJECTIVE: In the present study, the peripheral mechanism that mediates the pressor effect of angiotensin-(1-7) in the rostral ventrolateral medulla was investigated. METHOD: Angiotensin-(1-7) (25 pmol) was bilaterally microinjected in the rostral ventrolateral medulla near the ventral surface in urethane-anesthetized male Wistar rats that were untreated or treated (intravenously) with effective doses of selective autonomic receptor antagonists (atenolol, prazosin, methyl-atropine, and hexamethonium) or a vasopressin V1 receptor antagonist [d(CH2)5 -Tyr(Me)-AVP] given alone or in combination. RESULTS: Unexpectedly, the pressor response produced by angiotensin-(1-7) (16 ± 2 mmHg, n = 12), which was not associated with significant changes in heart rate, was not significantly altered by peripheral treatment with prazosin, the vasopressin V1 receptor antagonist, hexamethonium or methyl-atropine. Similar results were obtained in experiments that tested the association of prazosin and atenolol; methyl-atropine and the vasopressin V1 antagonist or methyl-atropine and prazosin. Peripheral treatment with the combination of prazosin, atenolol and the vasopressin V1 antagonist abolished the pressor effect of glutamate; however, this treatment produced only a small decrease in the pressor effect of angiotensin-(1-7) at the rostral ventrolateral medulla. The combination of hexamethonium with the vasopressin V1 receptor antagonist or the combination of prazosin, atenolol, the vasopressin V1 receptor antagonist and methyl-atropine was effective in blocking the effect of angiotensin-(1-7) at the rostral ventrolateral medulla. CONCLUSION: These results indicate that angiotensin-(1-7) triggers a complex pressor response at the rostral ventrolateral medulla that involves an increase in sympathetic tonus, release of vasopressin and possibly the inhibition of a vasodilatory mechanism.
Subject(s)
Animals , Male , Rats , Angiotensin I/pharmacology , Medulla Oblongata/drug effects , Peptide Fragments/pharmacology , Vasodilator Agents/pharmacology , Angiotensin I/administration & dosage , Arterial Pressure/drug effects , Heart Rate/drug effects , Hexamethonium/administration & dosage , Microinjections , Medulla Oblongata/physiopathology , Peptide Fragments/administration & dosage , Rats, Wistar , Receptors, Vasopressin/antagonists & inhibitors , Time Factors , Vasodilator Agents/administration & dosageABSTRACT
Ascites and dilutional hyponatremia are frequent conditions in cirrhotic patients and its occurrence has a worse prognosis. Thus, patients with ascites should generally be considered for referral for liver transplantation. The present article explores issues related with ascites classification and the treatment corresponding to each of the 3 degrees of ascites. Regarding refractory ascites, recommendations are included on the use of diuretics, large volume paracentesis with the administration of intravenous albumin and use of transjugular intrahepatic portosystemic shunt (TIPS). Finally, physiopathological aspects involved in the development of dilutional hyponatremia and vaptans treatment, are presented, which are aquaretics that selectively blockade vasopressin V2 receptors in the principal cells of the collecting ducts, being one of the most innovative pharmacological interventions for the management of hyponatremia in cirrhotic patients, in the recent years.
La ascitis e hiponatremia dilucional son complicaciones frecuentes en pacientes con cirrosis avanzada y su aparición implica un peor pronóstico. Por ello, los pacientes con ascitis deberían ser referidos para trasplante hepático. El presente artículo explora los aspectos relacionados con la clasificación de la ascitis y el tratamiento correspondiente a cada uno de los 3 grados de ascitis. En relación al manejo de la ascitis refractaria, se incluyen recomendaciones respecto a la eficacia del uso de diuréticos, paracentesis evacuadora radical con reposición de albúmina intravenosa y uso de cortocircuito porto-sistémico intrahepático (TIPS). Finalmente, se abordan los aspectos fisiopatológicos involucrados en el desarrollo de hiponatremia dilucional y el tratamiento con vaptanes, que son acuaréticos que bloquean selectivamente los receptores V2 de vasopresina en las células principales del túbulo colector, constituyendo una de las intervenciones farmacológicas más innovadoras en el manejo de la hiponatremia en cirrosis en los últimos años.
Subject(s)
Humans , Ascites/therapy , Liver Cirrhosis/complications , Hyponatremia/therapy , Ascites/classification , Ascites/diagnosis , Ascites/etiology , Liver Cirrhosis/therapy , Diuretics/therapeutic use , Hyponatremia/etiology , Hyponatremia/drug therapy , Paracentesis , Receptors, Vasopressin/antagonists & inhibitors , Severity of Illness IndexABSTRACT
No disponible
No disponible
Subject(s)
Animals , Humans , Polycystic Kidney, Autosomal Dominant/genetics , Receptors, Vasopressin/antagonists & inhibitors , Cell Division , Chromosomes, Human, Pair 14/genetics , Chromosomes, Human, Pair 16/genetics , Disease Models, Animal , Drug Design , Nephrons/embryology , Polycystic Kidney, Autosomal Dominant/diagnosis , Polycystic Kidney, Autosomal Dominant/drug therapy , Signal Transduction/genetics , Early DiagnosisABSTRACT
A hiponatremia é uma condição grave associada às lesões neurológicas, notadamente aos sangramentos no sistema nervoso central. Duas teorias têm sido apontadas como causadoras desta condição: a síndrome cerebral perdedora de sal e a síndrome da secreção inapropriada do hormônio antidiurético (HAD). Utilizou-se um bloqueador seletivo do receptor V2 renal do hormônio antidiurético em um modelo de sangramento intracerebroventricular...
