Carreño, N. (N.)

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    Zolmitriptan: a novel portal hypotensive agent which synergizes with propranolol in lowering portal pressure
    (Public Library of Science, 2013) Banales, J.M. (Jesús M.); Alegre, F. (Félix); Chang, H.C.Y. (Haisul C. Y.); Rodriguez-Ortigosa, C.M. (Carlos M.); Garcia, M. (Mónica); Sangro, B. (Bruno); Roboredo, M. (Mercedes); Prieto, J. (Jesús); Herrero, J.I. (José Ignacio); Moran, M.A. (María Asunción); Perez-Vizcaino, F. (Francisco); Barbero, R. (Roberto); Quiroga, J. (Jorge); Carreño, N. (N.)
    OBJECTIVE: Only a limited proportion of patients needing pharmacological control of portal hypertension are hemodynamic responders to propranolol. Here we analyzed the effects of zolmitriptan on portal pressure and its potential interaction with propranolol. METHODS: ZOLMITRIPTAN, PROPRANOLOL OR BOTH WERE TESTED IN TWO RAT MODELS OF PORTAL HYPERTENSION: common bile duct ligation (CBDL) and CCl4-induced cirrhosis. In these animals we measured different hemodynamic parameters including portal venous pressure, arterial renal flow, portal blood flow and cardiac output. We also studied the changes in superior mesenteric artery perfusion pressure and in arterial wall cAMP levels induced by zolmitriptan, propranolol or both. Moreover, we determined the effect of splanchnic sympathectomy on the response of PVP to zolmitriptan. RESULTS: In both models of portal hypertension zolmitriptan induced a dose-dependent transient descent of portal pressure accompanied by reduction of portal flow with only slight decrease in renal flow. In cirrhotic rats, splanchnic sympathectomy intensified and prolonged zolmitriptan-induced portal pressure descent. Also, propranolol caused more intense and durable portal pressure fall when combined with zolmitriptan. Mesenteric artery perfusion pressure peaked for about 1 min upon zolmitriptan administration but showed no change with propranolol. However propranolol enhanced and prolonged the elevation in mesenteric artery perfusion pressure induced by zolmitriptan. In vitro studies showed that propranolol prevented the inhibitory effects of β2-agonists on zolmitriptan-induced vasoconstriction and the combination of propranolol and zolmitriptan significantly reduced the elevation of cAMP caused by β2-agonists. CONCLUSION: Zolmitriptan reduces portal hypertension and non-selective beta-blockers can improve this effect. Combination therapy deserves consideration for patients with portal hypertension failing to respond to non-selective beta-blockers.
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    Tratamiento de la infección crónica por el VHB
    (Gobierno de Navarra. Departamento de Salud, 2004) Sangro, B. (Bruno); Moreno, D. (D.); Carreño, N. (N.)
    The treatment of the patient with chronic hepatitis B virus infection (HBV) must be carried out with the knowledge that the percentage of patients infected with the B virus that develop chronic hepatitis remains between 5-10%. Of these, 10-30% will present chronic infection with active viral replication, necroinflammatory hepatic lesion, evolution to hepatic cirrhosis and the risk of developing hepatocarcinoma. For this reason, the aim of treatment is to achieve negativisation of the HBeAg, seroconversion to anti-HBe and a reduction of viral replication to undetectable values (estimated by level of DNA-HBV), for protracted periods of time. When a sustained loss of HBeAg and a reduction of viral replication are obtained, a biochemical, clinical and histological remission is achieved. Up until now the therapeutic alternatives in chronic infection by the B virus have been immunomodulation with Interferon alpha and the blocking of viral replication with lamivudine or adefovir dipivoxil. A difference must be drawn between the biochemical response, defined as a fall in the transaminases to normal values, and the virological response, which refers to a fall in the levels of DNA-HBV below 10(5) copies/ml. Finally, the complete response is defined as the virological and biochemical response with negativisation of the HBsAg. If a sustained response is obtained for several months, a histological response can be predicted with reduction in the intensity of the hepatic lesion and an absence or stabilisation in the process of fibrosis. The sustained response should last for no less than 6 to 12 months following the end of treatment