Hepatic Encephalopathy

[Guest guest]

HEPATIC ENCEPHALOPATHY - EFFECTIVE TREATMENTS AVAILABLE ONCE ACUTE PRECIPITANTS

HAVE BEEN ELIMINATED

The diagnosis is appropriate whenever a patient with liver disease has

neurological and psychological symptoms that cannot be attributed to

other pathologies.Hepatic encephalopathy is a clinical syndrome of unknown

pathogenesis. The diagnosis is appropriate whenever a patient with liver disease

has neurological and psychological symptoms that cannot be attributed to other

pathologies. The disease may arise from a variety of hepatic disorders, exhibit

a wide range of severities(ranging from minimal cerebral dysfunction to

coma),follows a fluctuating course, and is reversible. The first line of therapy

in hepatic encephalopathy should always be elimination of known precipitating

factors.Subsequent therapeutic options depend on the severity and duration of

disease.

Neurotoxins Possibly to Blame

Elevated blood ammonia levels may cause hepatic encephalopathy. In patients with

cirrhosis of the liver,increased portal vein pressure can lead to the formation

of collateral vessels which allow intestinal ammonia to bypass the liver. Liver

disease itself also reduces the capacity of the organ to metabolise ammonia. The

resultant elevation in blood ammonia levels may increase energy consumption in

the brain and lead to swelling of astroglial cells. Hyperammonaemia does not

fully explain hepatic encephalopathy, however, because 10%of affected patients

have normal blood ammonia levels.[1]Other possible endogenous neurotoxins

include mercaptans, phenols, and short- and medium-chain fatty acids.[1]

Faulty Blood-brain Barrier Suspected

Changes in the blood-brain barrier have been observed in patients with acute or

chronic liver disease.This can result in absorption of more neutral amino acids

and less glucose, ketone bodies and basic amino acids by the brain.[1]

Neurotransmitter Abnormalities Offer Clues

Disturbances in amino acid metabolism in patients with liver disease may result

in the formation of 'false neurotransmitters' which compete with normal

transmitters for receptors in the brain. Other changes in neurotransmitter

systems that may contribute to hepatic encephalopathy include elevated

É¡-aminobutyric acid(GABA) activity and increased cerebral formation of

serotonin.[1]

[Guest guest]

HEPATIC ENCEPHALOPATHY - EFFECTIVE TREATMENTS AVAILABLE ONCE ACUTE PRECIPITANTS

HAVE BEEN ELIMINATED

The diagnosis is appropriate whenever a patient with liver disease has

neurological and psychological symptoms that cannot be attributed to

other pathologies.Hepatic encephalopathy is a clinical syndrome of unknown

pathogenesis. The diagnosis is appropriate whenever a patient with liver disease

has neurological and psychological symptoms that cannot be attributed to other

pathologies. The disease may arise from a variety of hepatic disorders, exhibit

a wide range of severities(ranging from minimal cerebral dysfunction to

coma),follows a fluctuating course, and is reversible. The first line of therapy

in hepatic encephalopathy should always be elimination of known precipitating

factors.Subsequent therapeutic options depend on the severity and duration of

disease.

Neurotoxins Possibly to Blame

Elevated blood ammonia levels may cause hepatic encephalopathy. In patients with

cirrhosis of the liver,increased portal vein pressure can lead to the formation

of collateral vessels which allow intestinal ammonia to bypass the liver. Liver

disease itself also reduces the capacity of the organ to metabolise ammonia. The

resultant elevation in blood ammonia levels may increase energy consumption in

the brain and lead to swelling of astroglial cells. Hyperammonaemia does not

fully explain hepatic encephalopathy, however, because 10%of affected patients

have normal blood ammonia levels.[1]Other possible endogenous neurotoxins

include mercaptans, phenols, and short- and medium-chain fatty acids.[1]

Faulty Blood-brain Barrier Suspected

Changes in the blood-brain barrier have been observed in patients with acute or

chronic liver disease.This can result in absorption of more neutral amino acids

and less glucose, ketone bodies and basic amino acids by the brain.[1]

Neurotransmitter Abnormalities Offer Clues

Disturbances in amino acid metabolism in patients with liver disease may result

in the formation of 'false neurotransmitters' which compete with normal

transmitters for receptors in the brain. Other changes in neurotransmitter

systems that may contribute to hepatic encephalopathy include elevated

É¡-aminobutyric acid(GABA) activity and increased cerebral formation of

serotonin.[1]

[Guest guest]

Hi everyone,

I don't think I've posted here more than once before, but I read everything

you share. Recently someone posted a link about toxic encephalopathy and

when I went there I found another link to hepatic encephalopathy. This is what

I believe my daughter is suffering from, as she has had many of the symptoms,

including being unable to perform personal cares.

My question is, does anyone know if mold exposure can be the cause of

hepatic encephalopathy? I haven't ever seen any connection mentioned, but my

daughter was exposed to mold at a very young age and remains quite ill.

Thanks for anything you might have on this.....and thanks for being here

with all the support and great information.

Jean

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