Randomized comparison of long-term losartan versus propranolol in lowering portal pressure in cirrhosis.

BACKGROUND & AIMS: It has been suggested that losartan, an angiotensin II (A-II) type 1 receptor blocker, may have a pronounced portal pressure reducing effect, far greater than that of propranolol. This randomized controlled trial compared the hemodynamic and renal effects of continued 6-week administration of losartan (n = 25) vs. propranolol (n = 15) in portal hypertensive patients with cirrhosis treated endoscopically after a variceal bleeding episode. METHODS: Hepatic venous pressure gradient (HVPG), systemic hemodynamics, renal function, and vasoactive factors were measured before and at 6 weeks of treatment. RESULTS: Losartan did not reduce HVPG (-2% +/- 12%, NS) but significantly decreased mean arterial pressure (MAP, -8% +/- 10%, P = 0.001). On the contrary, propranolol significantly reduced HVPG (-10% +/- 11%, P = 0.003) and cardiac output (-16% +/- 12%, P = 0.001) but did not modify MAP (2.5% +/- 10%, NS). Losartan increased A-II levels, reduced aldosterone, and decreased glomerular filtration rate (GFR) in Child B patients. Propranolol did not modify renal function. Adverse events related to therapy were mild and similar in both groups. CONCLUSIONS: Unlike propranolol, long-term losartan administration does not significantly reduce HVPG in patients with cirrhosis treated after a variceal bleeding episode, and it caused hypotension and reduced GFR in patients with moderate liver failure. Therefore, losartan is not an alternative to propranolol in preventing variceal rebleeding.

Stenosis of the suprahepatic inferior vena cava as a complication of transjugular intrahepatic portosystemic shunt in Budd-Chiari patients.

We report 2 patients with Budd-Chiari (BC) syndrome secondary to thrombogenic conditions who underwent transjugular intrahepatic portosystemic shunt (TIPS) placement because of refractory ascites and impending liver failure. After TIPS placement, there was marked symptomatic relief and improvement in liver function, but the courses of both patients were complicated by the development of an inferior vena cava (IVC) syndrome caused by segmental stenosis of the suprahepatic IVC just at the outflow jet of the TIPS at 11 and 9 months later. One patient underwent liver transplantation, and the other patient, caval angioplasty and stenting. Stenosis of the IVC represents an unrecognized complication of TIPS in patients with BC syndrome.

[Hepatocellular carcinoma in a patient with hereditary hemochromatosis without cirrhosis]. / Carcinoma hepatocelular en una paciente afectada de hemocromatosis hereditaria sin cirrosis.

Hepatocellular carcinoma in patients with hereditary hemochromatosis in the cirrhotic phase is one of the complications causing greatest mortality and may present in spite of removal of excess iron by bloodletting. Hepatocellular carcinoma is usually considered to occur in cirrhotic livers and consequently measures for the early diagnosis of this complication are only recommended in this type of patient. We present the case of a 69-year-old female patient with non-cirrhotic hemochromatosis who, 6 years after undergoing successful treatment, developed hepatocellular carcinoma. This observation should be added to the 12 cases published in the literature. Criteria should be established for the early diagnosis of hepatocellular carcinoma in patients with hereditary hemochromatosis, irrespective of whether they have cirrhosis.

Pharmacological treatment of portal hypertension.

In liver cirrhosis, increased resistance to portal blood flow is the primary factor in the pathophysiology of portal hypertension. The recognition of a dynamic component in hepatic resistance due to the active-reversible contraction of different elements of the portohepatic bed, has led to the active development of hepatic vasodilators. On the other hand, a significant increase in portal blood flow caused by arteriolar splanchnic vasodilation and hyperkinetic circulation, aggravates portal hypertension and provides the rational for the use of splanchnic vasoconstrictors, such as beta-blockers, vasopressin derivatives and somatostatin and its analogs. This review covers current developments in the treatment of portal hypertension.

Persistent hypertransaminasemia as the presenting feature of celiac disease.

Asymptomatic persistent hypertransaminasemia unrelated to hepatitis viral infection is a common cause of referral to the hepatologist. Less frequent liver diseases should then be considered, as well as extrahepatic-origin hypertransaminasemia. Celiac disease, although it has repeatedly been reported as a cause of persistent hypertransaminasemia, is often not included in its differential diagnosis in the absence of the classic malabsorption syndrome. We present the cases of four patients sent to a liver unit for evaluation of persistent hypertransaminasemia in whom celiac disease was finally discovered. Our report highlights the importance of including celiac disease in list of conditions potentially responsible for chronic hypertransaminasemia of unknown cause.