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ObjectiveOnly 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.MethodsZolmitriptan, 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.ResultsIn 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.ConclusionZolmitriptan 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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Introduction Hepatocellular carcinoma (HCC) is considered the main primary neoplasm of the liver and its incidence is expected to increase in the next years. HCC is frequently associated with chronic liver disease secondary to hepatitis B or C infections, as well to alcohol abuse, fatty liver and metabolic syndrome. Multidisciplinary and individualized management has been shown to improve clinical outcome; nevertheless, in Panama and others Latin-American countries, there is no clear consensus for the management of this disease. Methodology Using Appraisal of Guidelines for REsearch and Evaluation II (AGREE II) methodology and the Institute of Medicine (IOM) criteria, we developed a multidisciplinary consensus for the management of hepatocarcinoma patients in Panama. Results This document synthesizes the current evidence on risk factors in conjunction with recommendations on the management of early, advanced and terminal disease. All healthcare personnel involved in the approach and treatment of hepatocarcinoma in Panama can find utility and applicability in their daily practice. Conclusion Here, we present the first National Consensus for the Screening, Diagnosis and Treatment of Hepatocellular Carcinoma in Panama

images in clinical medicineT h e ne w e ngl a nd jou r na l o f m e dic i ne n engl j med 362;5 nejm.org february 4, 2010 e13A 52-year-old man with cirrhosis associated with alcohol abuse presented to the emergency department with hematemesis and lightheadedness, which had developed 3 hours earlier, after binge drinking. He had no history of decompensated liver disease and took no medications. During the physical examination, he was alert and oriented, with a pulse rate of 140 beats per minute and a blood pressure of 90/60 mm Hg. Spider angiomata and ascites were present. Results of laboratory tests showed a hematocrit of 21%. The alanine aminotransferase level was 47 U per liter, the aspartate aminotransferase level was 102 U per liter, the albumin level was 2.6 g per deciliter, the total bilirubin level was 2.3 mg per deciliter (39 μmol per liter), the direct bilirubin level was 1.4 mg per deciliter (24 μmol per liter), and the prothrombin time was 15.4 seconds. The patient was hospitalized, and he underwent volume resuscitation and was given omeprazole and octreotide. Emergency upper endoscopy showed active bleeding from esophageal varices (video), which was controlled with band ligation. Hemorrhage from esophageal varices is a severe complication of cirrhosis with portal hypertension. After band ligation, the patient's condition stabilized, with no further bleeding.