Improvement by acetylcysteine of hemodynamics and oxygen transport in fulminant hepatic failure

Article Abstract:

When patients are critically ill the ability of tissues to extract oxygen from the blood is reduced, and may eventually lead to multiple organ failure. In fulminant hepatic failure (severe liver failure), survival depends on the number of failing organs, the ability of the body to deliver oxygen, and the ability of tissues to consume it. Hypoxia, or oxygen starvation in tissues, is associated with a poor prognosis. When liver failure is caused by an overdose of acetaminophen (an aspirin substitute, often sold under the trade names Tylenol and Datril), the chemical acetylcysteine is administered intravenously during the first 15 hours of treatment. However, recent studies have shown that survival improved even when acetylcysteine was administered after there was evidence of additional organ damage. The effects of acetylcysteine were assessed in 12 patients with liver failure due to acetaminophen poisoning and 8 others with liver failure from other causes. None of the patients with acetaminophen-induced disease had been treated with acetylcysteine because they were evaluated more than 15 hours after the overdose. The effects of acetylcysteine were also compared with those of epoprostenol, a drug that increases oxygen delivery and consumption in critically-ill patients. The results revealed that, like epoprostenol, acetylcysteine resulted in increased tissue oxygenation and improved end-organ function and survival. However, acetylcysteine actually enhanced the extraction of oxygen by the tissues. This is probably the result of stimulation of microcirculatory blood flow. If this is so, acetylcysteine may be effective in the treatment of patients with multiple-organ failure due to other causes. (Consumer Summary produced by Reliance Medical Information, Inc.)

Health aspects, Drug therapy, Liver failure, Hemodynamics, Acetaminophen, Acetylcysteine

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Plasma endothelin immunoreactivity in liver disease and the hepatorenal syndrome

Article Abstract:

Increased concentrations of endothelin-1 and endothelin-3 may play a role in the development of hepatorenal syndrome. Hepatorenal syndrome is a frequent complication of liver failure and is marked by renal vasoconstriction, or constriction of blood vessels in the kidneys, which in severe cases can lead to kidney failure. Endothelin-1 and endothelin -3 are small proteins produced in the body that can cause vasoconstriction. Endothelin levels in five groups of patients with liver or kidney disease were measured and compared with levels from healthy individuals. Endothelin-1 levels were significantly higher in all patient groups than in the healthy group and highest in the group with hepatorenal syndrome. Endothelin-3 levels among patients with hepatorenal syndrome, but not among patients from the other four groups, were significantly higher than in normal subjects.

Physiological aspects, Endothelin, Vasoconstrictors, Vasoconstrictor agents

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Treatment of hepatic encephalopathy

Article Abstract:

Hepatic encephalopathy occurs when liver disease causes a build-up of ammonia in the blood, which can damage the brain. This causes neurologic symptoms which are not necessarily unique to hepatic encephalopathy. When hepatic encephalopathy is caused by liver failure, the patient should be considered for a liver transplant. Milder cases of hepatic encephalopathy can be treated with a low-protein diet, lactulose and antibiotics to decrease the number of ammonia-producing bacteria in the gut, and ornithine aspartate to enhance the metabolism of ammonia in the tissues.

Care and treatment, Complications and side effects, Liver diseases, Liver cirrhosis, Hepatic encephalopathy, Liver encephalopathy

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