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Hepatic encephalopathy

Hepatic encephalopathy is a complication of cirrhosis of the liver and its resultant portal hypertension, toxic substances accumulate in the blood and impair the function of brain cells. Signs can include impaired cognition, a flapping tremor (asterixis), and a decreased level of consciousness. more...

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Pathogenesis

Cirrhosis will obstruct the passage of blood through the liver causing portal hypertension. This means it is difficult for blood from the intestines to go through the liver, to get back to the heart. Portal-systemic anastamoses ("shunts") develop, and portal blood (from the intestinal veins), will bypass the liver, and return to the heart via another route without undergoing first-pass detoxification by the liver. Furthermore, the liver (damaged from the cirrhosis) will not be functioning as well as it should be, so blood that does travel through the liver, may not be as detoxified as it otherwise would be.

The toxic substances involved are not well understood, but have been felt to include ammonia (NH3) and mercaptans. Ammonia is normally converted to urea by the liver, and, as with mercaptans, is produced by the bacterial breakdown of protein in the intestines.

Ammonia can cross the blood-brain barrier, where it causes the support cells of the brain (astrocytes) to swell. The swelling of the brain tissue increases intracranial pressure, and can lead to coma or death via herniation of the brainstem.

Grading of symptoms

Grading of the symptoms of hepatic encephalopathy is as follows:

  • Grade 0 - Clinically normal mental status but minimal changes in memory, concentration, intellectual function, and coordination
  • Grade 1 - Mild confusion, euphoria, or depression; decreased attention; slowing of ability to perform mental tasks; irritability; and disordered sleep pattern, such as inverted sleep cycle
  • Grade 2 - Drowsiness, lethargy, gross deficits in ability to perform mental tasks, obvious personality changes, inappropriate behavior, and intermittent disorientation, usually regarding time
  • Grade 3 - Somnolent but can be aroused, unable to perform mental tasks, disorientation about time and place, marked confusion, amnesia, occasional fits of rage, present but incomprehensible speech
  • Grade 4 - Coma with or without response to painful stimuli

Treatment

It is important to remove excess protein from the lumen of the gut. If there is a gastrointestinal bleed (for instance, ruptured oesophageal varices) this should be stopped, as it serves as a protein supply for bacteria. Dietary intake of protein should be minimised. Special enteral feeding formulations with a high concentration of branched-chain amino acids are sometimes used in therapy, as is parenteral nutrition.

Lactulose is a compound that will cause osmotic diarrhoea, lessening the time bacteria have to metabolise proteins and produce toxic substances. As well as this, it acidifies the bowel, causing ammonia (NH3) to be converted to ammonium (NH4+) which is less readily absorbed. Recent evidence suggests it is not very effective (Als-Nielsen et al 2004).

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Natural sedatives linked to brain disorder - hepatic encephalopathy
From Science News, 7/21/90 by Kathy A. Fackelmann

Natural sedatives linked to brain disorder

Natural tranquilizers may play a key role in the development of a brain disorder that strikes people with liver disease, according to a preliminary study. If confirmed, the finding may lead to more effective treatment of this potentially fatal disease, called hepatic encephalopathy.

The prevailing theory holds that high blood levels of ammonia, caused by a malfunctioning liver, lead to the symptoms of hepatic encephalopathy, which include drowsiness, memory loss, stupor and in some cases coma. But a report in the July 14 LANCET implicates mysterious natural substances that behave like benzodiazepine drugs such as Valium.

"The report raises the suggestion that patients with advanced liver disease could be accumulating a substance in their blood that makes them confused by simulating the action of Valium," says study coauthor Kevin D. Mullen of Case Western Reserve University in Cleveland.

Mullen's previous research had revealed unidentified, benzodiazepine-like substances in the cerebrospinal fluid of rabbits with hepatic encephalopathy. Mullen knew the rabbits weren't popping Valium, and he knew high doses of benzo-diazepine drugs could cause stupor and loss of consciousness. He began to search for similar compounds in the body fluids of people with liver disease who showed signs of encephalopathy.

Now Mullen and his colleagues report that eight people hospitalized with liver failure and severe encephalopathy show evidence of benzodiazepine-like compounds in their cerebrospinal fluid at much higher levels than eight control patients hospitalized for other conditions. The researchers excluded study volunteers who said they had taken a synthetic benzodiazepine during the past three months. They also scrutinized medical records and talked with volunteers' physicians to make sure the participants hadn't taken such synthetic drugs.

The team then turned to people with varying stages of hepatic encephalopathy, taking blood samples from 23 patients and urine samples from 36. Indirect tests indicated that these samples contained significantly higher levels of benzodiazepine-like substances than samples from controls with healthy livers. People with the highest levels of the substances seemed to have the most severe symptoms of hepatic encephalopahty, Mullen adds.

The scientist don't know where the puzzling substances originate, but they hypothesize that people with liver failure may somehow accumulate high levels of the natural benzodiazepine compounds present in foods. Some foods, such as wheat and potatoes, contain minuscule amounts of natural benzodiazepines, but they do not cause sedative effects in healthy people, Mullen notes. He speculates that people with liver disease may store up dietary benzodiazepines until the compounds reach a level that causes drowsiness, stupor or even coma.

The new report bolsters previous research suggesting that drugs that block benzodiazepine receptors in the brain might reverse symptoms of hepatic encephalopathy. European researchers have reported that one such drug can rouse comatose liver-disease patients. U.S. scientists have yet to test the experimental drug, notes Anthony S. Basile of the National Institute of Diabetes and Digestive and Kidney Diseases. Basile's own unpublished research has identified two specific benzodiazepines in the brain tissue of people who died of hepatic encephalopathy.

Mullen and others say further research must prove the link between naturally occuring benzodiazepines and the symptoms of liver encephalopathy. Without such proof, many continue to back the ammonia theory. Leslie Zieve, a liver specialist at the University of Minnesota in Minneapolis, calls Mullen's findings intriguing and worthy of further attention, but says he still believes ammonia is the major culprit in this brain disorder.

COPYRIGHT 1990 Science Service, Inc.
COPYRIGHT 2004 Gale Group

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