Current management of portal hypertension

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Natural History of portal hypertension and variceal bleeding

The management of portal hypertension should be based on an updated knowledge of its natural history. Portal hypertension is an almost unavoidable complication of cirrhosis, and it is responsible for the more lethal complications of this syndrome: gastro-esophageal varices and massive gastrointestinal bleeding, ascites, hepatorenal syndrome, and hepatic encephalopathy. Appearance of these complications represents the major cause of death and liver transplantation in patients with cirrhosis. The

Rationale for therapy

A very important concept which has been strongly substantiated in recent years is that the major factor determining the development of the complications and the clinical significance of portal hypertension is that portal pressure increases above a critical threshold value. HVPG [22], which accurately reflects portal pressure in the majority of liver diseases [23], [24], is the most commonly used method to assess portal pressure in clinical practice. Varices do not develop until the HVPG

Current recommended therapy

The treatment of portal hypertension includes the prevention of variceal hemorrhage in patients who have never bled, the treatment of the acute bleeding episode and the prevention of rebleeding in patients who have survived a bleeding episode from esophageal or gastric varices. An additional scenario may come into practice: the ā€˜pre-primaryā€™ prophylaxis, or treatment of compensated patients without varices in order to prevent the development of varices and ascites. The main difference among

Drug therapy: beta-adrenergic blockers, nitrates and their combination

Non-selective beta-adrenergic blockers are the most widely used drugs to treat portal hypertension. However, only 30ā€“40% of the patients under long-term therapy reduce their portal pressure ā‰„20% from baseline or to levels ā‰¤12Ā mmHg [12]. Lack of achievement of these hemodynamic targets constitutes the strongest independent predictor of variceal bleeding or rebleeding [12], [27], indicating that the available armamentarium to treat portal hypertension is far from optimal.

The first question is the

Drugs that decrease hepatic resistance

Theoretically, in portal hypertension an ideal drug should act by decreasing intrahepatic vascular resistance, therefore decreasing portal pressure, while maintaining or enhancing hepatic blood flow. The vasodilatory effect of such a drug should be limited to the hepatic microcirculation to prevent a worsening in splanchnic/systemic vasodilatation. Furthermore, if such a drug were also capable of decreasing hepatic fibrosis and improving liver function, then many hepatologists would become

Declaration

The authors received funding from National Research Agencies (FIS, CICYT, NIHā€“DDK, VA) which enabled them to carry out their research.

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    Copyright Ā© 2003 European Association for the Study of the Liver. Published by Elsevier Ireland Ltd. All rights reserved.