Update on Peripheral Arterial Vasodilation, Ascites and Hepatorenal Syndrome in Cirrhosis
In cirrhosis of the liver, according to the peripheral arterial vasodilation hypothesis, relative underfilling of the arterial tree triggers a neurohumoral response (activation of renin-angiotensinaldosterone system, sympathetic nervous system, nonosmotic release of vasopressin) aimed at restoring c...
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Main Authors: | , , |
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Format: | Article |
Language: | English |
Published: |
Wiley
2000-01-01
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Series: | Canadian Journal of Gastroenterology |
Online Access: | http://dx.doi.org/10.1155/2000/340128 |
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Summary: | In
cirrhosis of the liver, according to the peripheral arterial vasodilation
hypothesis, relative underfilling of the arterial tree triggers a
neurohumoral response (activation of renin-angiotensinaldosterone
system, sympathetic nervous system, nonosmotic release
of vasopressin) aimed at restoring circulatory integrity by
promoting renal sodium and water retention. Evidence has accumulated
for a major role of increased vascular production of nitric
oxide as the primary cause of arterial vasodilation in cirrhosis. Ascites
is a common complication in cirrhosis. Treatment of ascites
consists of a low salt diet with diuretics, and paracentesis together
with plasma volume expanders in diuretic-resistant patients. Progression
of cirrhosis may result in hepatorenal syndrome, a state of
functional renal failure that carries an ominous prognosis. Orthotopic
liver transplantation has remained the only curative treatment
for patients with advanced liver disease; other modalities
such as transjugular intrahepatic portosystemic shunt or vasopressin
analogues may serve as a bridge to transplantation. Another
complication of decompensated cirrhosis is spontaneous
bacterial peritonitis, the incidence of which can be reduced by primary
or secondary antibiotic prophylaxis by using orally active antibiotics. |
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ISSN: | 0835-7900 |