Professional Documents
Culture Documents
Cirrhosis
March 2001
WHAT IS CIRRHOSIS?
Cirrhosis
Cirrhosis is an irreversible result of various disorders that damage liver cells over time. Eventually, damage becomes so extensive that the
normal structure of the liver is distorted and its function is impaired. [For a description of the liver, see Box The Liver.]
The disease process often takes the following path:
Scarring. The main damage in cirrhosis is triggered by scarring ( fibrosis ) that occurs from injuries due to alcohol, viruses, or other
assaults.
In response to the scarring, liver cells regenerate in abnormal clumps and form nodules around the scarred areas.
The scar tissue and regenerated nodules act like small dams and alter the flow of blood and bile in and out of the liver.
Altered Blood and Bile Flow. The changes in blood and bile flow have significant consequences, with both the liver and other organs
responding to the altered flow:
The spleen overproduces nitric oxide, which relaxes and opens the blood vessels.
On the other hand, blood vessels in other organs, including the kidney, narrow.
The small blood vessels and bile ducts in the liver itself constrict.
Blood flow coming into the liver from the intestine, then, backs up through the portal vein and seeks other routes. One result is the
development of new, abnormally twisted and swollen veins called varices that form in the stomach and lower part of the
esophagus.
Bile also builds up in the blood stream, resulting in high levels of bilirubin, which causes a yellowish cast in the skin called
jaundice.
Fluid build-up in the abdomen (called ascites) and swelling in the arms and legs is common.
Changes in Liver Size. The liver enlarges in the first phases of the disease. In advanced stages, the liver sometimes shrinks, a condition
called postnecrotic cirrhosis.
THE LIVER
The liver is the largest organ in the body. In the healthy adult, it weighs about three
pounds. The liver is wedge shaped, with the top part wider than the bottom. It is located
immediately below the diaphragm and occupies the entire upper right quadrant of the
abdomen.
Vital Functions
The liver performs over 500 vital functions. Damage to the liver can impair these and
many other processes. Among them are the following:
Processing Healthful Nutrients. It processes all of the nutrients the body requires,
including proteins, glucose, vitamins, and fats.
Bile Production. The liver produces bile , a green-colored fluid that is formed in the liver
and helps the body absorb fats and fat-soluble vitamin. It is produced from bilirubin, a
yellow-green pigment produced from the breakdown of hemoglobin, the
oxygen-carrying component in red blood cells. Bile contains bile salts, fatty acids,
cholesterol and other substances. Bile travels from the liver to the gall bladder, where it
is stored until after a meal. It is then secreted into the intestines where it helps digest fat.
Eliminating Toxins. One of the liver's major contributions to life is to render harmless
potentially toxic substances, including alcohol, ammonia, nicotine, drugs, and harmful
by-products of digestion.
Recycling Blood. Old red blood cells are removed from the blood by the liver and
spleen, and the iron contained in them is recycled to the bone marrow to make new red
blood cells.
The Liver's Architecture
The vital processes the liver performs rely on well-organized liver architecture.
The Building Blocks. The basic building blocks of the liver are the following structures:
Bile ducts.
Blood vessels.
Working liver tissue (called the parenchyma ).
Supportive ( connective ) tissue.
The Architecture. The liver is a hierarchy of lobes:
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Cirrhosis
The lobes. The liver is divided into two major lobes, a right and a smaller left,
that are separated by tough, fibrous connective tissue and formed from an
intricate system of ducts and vessels.
The lobules. The livers two major lobes contain about 100,000 smaller lobes,
called lobules. Each lobule contains microscopic columns of liver cells and blood
vessels. Bracing the corners of each lobule column are an artery and a vein that
carry blood and a bile duct that drains bile.
The arteries and veins. The arteries bring oxygen-rich blood to nourish the liver
cells. The veins supply the liver cells with blood containing the nutrients and
toxins that the liver cells process. A central vein runs through each column and
collects the processed blood from both sources. These veins join to form the
hepatic vein. [See The Liver's Blood Supply, below.]
The bile ducts. The bile ducts in the column corners collect bile draining from
tiny canals around the liver cells. These ducts eventually join to form the large
common bile duct that leads from the liver to the gall bladder.
The Liver's Blood Supply
The liver is rich in blood. It holds about a pint, or 13% of the bodys supply. It is furnished
with blood from two large vessels, the hepatic artery and the portal vein , and is drained
of blood by the hepatic vein . (The word hepatic derives from the Latin word for liver.)
The hepatic artery. This artery supplies blood to the liver directly from the heart,
and it is this blood that nourishes the liver.
The portal vein. The portal vein carries blood into the liver that has been
circulating through the stomach, spleen, and intestine. This is the blood that the
liver processes. The liver extracts nutrients and toxins from this blood.
The hepatic vein. This vein carries blood from the liver. It connects to the inferior
vena cava , a large vein that conducts blood back to the heart.
Chronic Hepatitis
The second leading cause of cirrhosis in the US is chronic hepatitis, either hepatitis B or C. Chronic hepatitis C is the more dangerous
form and accounts for one-third of all cirrhosis cases. Viruses or other mechanisms that cause hepatitis produce inflammation in liver
cells, resulting in their injury or destruction. If the condition is severe enough, the cell damage becomes progressive, building a layer of
scar tissue over the liver. In advanced cases, as with alcoholic cirrhosis, the liver shrivels in size, a condition called postnecrotic or
posthepatic cirrhosis.
Cirrhosis
Hemochromatosis is a disorder of iron metabolism that is characterized by excess iron deposits throughout the body, including the liver,
where they can cause cirrhosis. Once believed to be rare, hereditary hemochromatosis is now considered among the most common
genetic diseases among Caucasians. Between 2% and 4% of people of European ancestry are believed to carry the gene, and the
disease itself is estimated to occur in between 1.5 and 3 Caucasians per 1,000. Early symptoms of hemochromatosis include:
Fatigue.
Joint pain (arthralgia).
Impotence.
Arthritis.
(It should be noted that elevated iron levels, even in the absence of this disease, have been associated with liver scarring caused by other
disorders, including hepatitis, NASH, and alcoholism.)
Cirrhosis
Portal Hypertension
In cirrhosis, liver cell damage slows down blood flow and blood pressure therefore increases. This pressure causes a back-up of blood
through the portal vein, a condition called portal hypertension. The effects of portal hypertension can be widespread and serious.
Ascites and Fluid-Build-Up. Ascites is fluid build-up in the abdomen. It is uncomfortable and can reduce breathing function and urination.
Ascites is usually caused by portal hypertension, but it can result from other conditions. Swelling can also occur in the arms and legs and
in the spleen. Although ascites itself is not fatal, it is a marker for severe progression. Once ascites occurs, only half of patients survive
after two years. In fact, some experts refer to the phases of cirrhosis as preascitic and ascitic . Some physicians even believe that ascites
signals the need for liver transplantation, particularly in alcoholic cirrhosis.
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Cirrhosis
Variceal Bleeding. One of the most serious repercussions of portal hypertension is the development of varices , blood vessels that
enlarge to provide an alternative pathway for blood diverted from the liver. Varices often form in the stomach and esophagus (the tube
connecting the mouth and stomach). They pose a high risk for rupture and bleeding because of the following characteristics:
They are thin-walled.
They are often twisted.
They are subject to high pressure.
Internal bleeding from these varices (variceal bleeding) occurs in 20% to 30% of cirrhosis patients. The risk of death from a single
episode can reach 70%.
Bleeding commonly recurs within two weeks of the first episode, but after six weeks, the risk for recurrence is the same as for patients
who have not had a bleeding event.
Factors that predict variceal bleeding in general include the following:
Ascites.
Encephalopathy.
Large veins.
Factors that can increase the danger for a bleeding episode in high-risk individuals include the following:
Moderate to intense exercise.
Bacterial infection.
Certain times of the day: The greater risk in the evening. A lesser but still significant risk in the early morning.
Gastrointestinal Bleeding
Gastrointestinal (GI) bleeding can occur from abnormal blood clotting, often caused by deficiencies in vitamin K, low levels of clotting
proteins, and low counts of platelets (the blood cells that normally initiate the clotting process).
Infections
Bacterial infections are very common in advanced cirrhosis, and may even increase the risk for bleeding. Most bacterial infections,
including those in the urinary, respiratory, or gastrointestinal tracts, develop when patients are in the hospital. Abdominal infections are a
particular problem in cirrhosis and occur in up to 25% of patients with cirrhosis within a year of diagnosis.
Hepatorenal Syndrome
Hepatorenal syndrome is a life-threatening complication of late-stage liver disease. In general, the kidneys fail in trying to compensate for
altered blood flow in the liver by narrowing their own blood vessels.
Liver Cancer
Cirrhosis greatly increases the risk for liver cancer, regardless of the cause of cirrhosis. Although few studies have been conducted on the
risk for liver cancer in patients with primary biliary cirrhosis, one study reported an incidence of 2.3%. About 4% of patients with cirrhosis
caused by hepatitis C develop liver cancer. In Asia about 15% of people who have chronic hepatitis B develop liver cancer, but this high
rate is not seen in other parts of the world. (One Italian study that followed a group of hepatitis B patients for 11 years found no liver cancer
over that period of time.)
Osteoporosis
Primary biliary cirrhosis is associated with reduced bone growth, partly because of the livers inability to process vitamin D and calcium
and also from some of its treatments. As a result, osteoporosis occurs in 20% to 30% of these patients. Bone loss may also be a
complication of liver disease in alcoholics and patients with hepatitis. Treating osteoporosis in patients with cirrhosis can be complicated.
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Cirrhosis
One study found that calcitriol (a form of vitamin D) is especially helpful in preventing bone loss in patients with cirrhosis.
Insulin Resistance
Nearly all patients with cirrhosis are insulin resistant. Insulin resistance is a primary feature in type 2 diabetes and occurs when the body
is unable to use insulin, a hormone that is important for delivering blood sugar and amino acids into cells and helps determine whether
these nutrients will be burned for energy or stored for future use.
Other Complications
One study reported that nearly a quarter of patients with cirrhosis had gallstones. They may also face a higher than average risk for certain
abnormal heart rhythms. Peptic ulcers, sleep disorders, and respiratory problems are also more common in people with cirrhosis than in
the general population.
Biopsy
A liver biopsy is the only definite method for diagnosing cirrhosis. It also helps determine its cause, treatment possibilities, the extent of
damage, and the long-term outlook. For example, hepatitis C patients who show no significant liver scarring when biopsied appear to
have a low risk for cirrhosis.
The biopsy procedure may employ different methods:
One approach uses a needle inserted through the abdomen to obtain a tissue sample from the liver.
Another uses peritoneoscopy, a procedure that uses small incision through which the physician inserts a thin tube that contains
small surgical instruments and a tiny camera to view the surface of the liver.
Biopsies can be dangerous, so they cannot be performed on patients who have test results that indicate clotting problems, on those who
have had previous liver biopsies, or who have ascites [ see above ].
Blood Tests
A number of blood tests can measure liver function and help determine the severity and cause of cirrhosis.
Bilirubin. One of the most important factors indicative of liver damage is bilirubin, a red-yellow pigment that is normally metabolized in the
liver and then excreted in the urine. In patients with hepatitis, the liver cannot process bilirubin, and blood levels of this substance rise,
sometimes causing jaundice.
Discriminant Function (DF). To help determine outlook, experts may use a calculation called a discriminant function (DF), which uses two
important measurements:
Serum albumin concentration. Serum albumin measures protein in the blood (low levels indicate poor liver function).
Prothrombin time (PT). The PT test measures in seconds the time it takes for blood clots to form (the longer it takes the greater the
risk for bleeding).
Liver Enzymes. Enzymes known as aminotransferases , particularly aspartate (AST) and alanine (ALT) are released when the liver is
damaged. Measurements of these enzymes are important for determining the severity of liver damage and monitoring treatment
effectiveness in some cases.
Specific Blood Tests for Primary Biliary Cirrhosis. Very high levels of serum alkaline phosphatase, an enzyme produced in the liver, and
high levels of immune factors called mitochondrial antibodies are usually present in blood tests of patients with primary biliary blood
cirrhosis. Bilirubin measurements appear to be important factors in determining its severity.
Imaging Tests
A number of imaging tests can be used to diagnose cirrhosis and its complications.
Imaging Techniques. Magnetic resonance imaging (MRI), computed tomography (CT), and ultrasound are all imaging techniques that are
useful in detecting and defining the extent of cirrhosis. Such tests can reveal ascites, enlarged spleen, irregular liver surface, reversed
portal vein blood flow, and liver cancer. Sometimes they can even detect abnormally large blood vessels in the liver.
Liver Scans. Sometimes liver scans are performed using a small radioactive tracer and a special camera that records information
provided by the tracer as it passes through the liver:
Arteriography uses dye injected into the hepatic arteries that show up on x-ray.
Splenoportography uses dye injected into the spleen, which allows the physician to measure portal vein pressure; this procedure
is risky.
Cirrhosis
Paracentesis
If ascites is present, paracentesis is performed to determine its cause. This procedure involves using a thin needle to withdraw fluid from
the abdomen. The fluid is tested for different factors to determine the cause of ascites:
Bacteria cultures and white blood cell counts. (These are used to determine the presence of infection.)
Protein levels. Low levels of protein in the fluid plus a low white blood cell count suggest that cirrhosis is the cause of the ascites.
The appearance of the fluid is helpful in determining problems:
For example, a cloudy fluid plus a high white blood cell count means an infection is present.
Bloody fluid suggests the presence of a tumor.
Cirrhosis
bleeding, or protein levels. Larger, controlled studies are needed. One study suggested that the doses used in most large trials are too
low and that higher doses may have significant benefits. It may also be effective in combination with other agents, such as colchicine [
see below ]. Tauroursodeoxycholate, an agent similar to ursodeoxycholic acid, may prove to be more effective.
Colchicine . Colchicine, a drug that inhibits collagen (a protein in the body the makes up scar tissue) has produced some improvement in
liver function and survival, but it does not appear to be as effective as methotrexate. Like methotrexate, colchicine can have severe side
effects.
Corticosteroids (Budesonide) . Corticosteroids, such as budesonide, reduce inflammation and have been helpful in improving liver
function and symptoms. Long-term use can produce bone loss and other severe side effects. One study of budesonide reported that it
offered little additional benefits for patients who had failed ursodeoxycholic treatment, particularly in light of the risk for osteoporosis.
Another study indicated that a combination of budesonide and ursodeoxycholic acid may be much more effective than either one and have
minimal adverse effects.
Agents for Itching and Fatigue . Itching and fatigue are major problems with this disease and a number of agents have been used or
investigated for these symptoms:
In one study an antioxidant compound (Bio-Antax) plus coenzyme Q10, another antioxidant, relieved itching and fatigue.
Itching can be relieved by taking cholestyramine with meals.
Low doses of the drug naltrexone relieved itching in one study; high doses of this drug are toxic to the liver.
Phototherapy, which uses light, may also reduce itching.
Methotrexate, an anti-inflammatory drug that suppresses elements of the immune system, has been shown to reduce itching. It
was hoped that the drug might improve liver disease. A small 2000 study reported, however, that it improved liver tissue health in
only 18% of patients and, in fact, the disease accelerated in 50% of the patients.
Fat Absorption . Because primary biliary cirrhosis affects fat absorption, patients may need high doses or injections of important
fat-soluble vitamins, including K, D, A, and E. For steatorrhea, agents called medium-chain triglycerides may be helpful.
Dietary Factors
Healthy Foods. Because important antioxidant vitamins are depleted in the cirrhotic liver, cirrhosis patients should maintain a diet rich in
fresh fruits, vegetables, and whole grains.
Antioxidant Supplements. There is some preliminary laboratory evidence that various antioxidant supplements including vitamin E,
selenium, and S-adenosylmethionine (SAMe) may help protect against liver damage and cirrhosis. Supplements, however, are not
recommended for people with liver disease except with the advice of a physician. Some vitamins, such as vitamins D and A, are
metabolized in the liver and can be toxic.
Iron Restrictions. Elevated iron levels have been associated with cirrhosis from many causes. Patients should avoid iron-rich foods, such
as red meats, liver, and iron-fortified cereals and should avoid cooking with iron-coated cookware and utensils.
Supplemental Nutritional Products. Supplemental nutritional beverages may be helpful, particularly for patients with both alcoholism and
cirrhosis. In one study, patients with both alcoholism and cirrhosis drank Ensure every day as a supplement to their regular diet. After six
months they showed significant improvement in many signs of overall health compared to those who didnt consume the beverage.
Omega-3 Fatty Acids. Some research suggests that supplements of omega-3 fatty acids (found in fish oil and evening primrose oil) may
help protect the diseased liver.
Protein and Soy. High-quality dietary protein may be especially helpful for patients with ascites and for repairing muscle mass, but
excessive protein loads may trigger encephalopathy. Protein solutions have been devised that provide beneficial amino acids without
including those that increase this risk. There is no limit on vegetable proteins, such as those from soy.
Salt Restriction. Restricting salt consumption to less than 2,000 mg a day is particularly important for patients with ascites. The less salt
the better.
Zinc. In some studies, taking zinc supplements have lowered ammonia levels in some patients who were zinc-deficient, a common
problem in cirrhosis. Zinc replacement may reduce frequency and severity of muscle cramps and may even help protect against
encephalopathy.
Limiting Fluids
Fluid restriction is not usually necessary, but patients with severe ascites should discuss limiting fluid with their physicians.
Exercise
Exercise increases the risk for portal pressure and variceal bleeding. One study reported that taking a beta-blocker may reduce this risk,
although patients should discuss this with their physician.
Cirrhosis
advise annual flu shots for people with cirrhosis. Furthermore, they advise that patients who get the flu be treated immediately with
rimantadine, but not a similar treatment called amantadine.
Eliminating Ammonia
Ammonia is the leading toxin in causing encephalopathy related to cirrhosis. Eliminate ammonia in the intestine. Mild encephalopathy is
managed by directing therapy toward eliminating ammonia in the intestine:
The first step is to restrict animal protein, substituting meats and dairy products with vegetable protein, such as soy, and amino
acid supplements.
Enemas, which clean out the intestine, may be effective.
Lactulose (Cephulac, Chronulac, Constulose, Duphalac, Enulose) and lactitol, known as disaccharides, help lower blood
ammonia levels and may be beneficial in mild encephalopathy.
Antibiotics, such as metronidazole, rifamycin, or neomycin, are effective in reducing levels of ammonia-producing bacteria in the
intestine, although long-term use of these drugs can cause toxic side effects.
Adding non-ammonia producing bacteria to the intestine, including L. acidophilus and E. faecium, is showing promise as a safe
and effective treatment.
Investigative Agents. Certain drugs, such as flumazenil (Mazicon, Romazicon), are under investigation for treating encephalopathy.
Flumazenil is typically administered to counteract the effects of sedatives.
Cirrhosis
Investigative Agents
Researchers are testing certain drugs that may redress the imbalances in circulation that lead to portal hypertension and ascites. Of
particular interest are agents called nonpeptide vasopressin antagonists, also referred to as aquaretics. They may reverse the dilation in
blood vessels that lead to salt and fluid retention.
Liver Transplantation
The prognosis for patients with ascites is poor, even with intensive procedures. Liver transplantation should be considered for patients
when ascites does not respond to treatments and when poor liver function or other complications, such as peritonitis or kidney failure, are
present [ see Box Liver Transplantation].
Cirrhosis
Somatostatin, the natural hormone, controlled variceal bleeding in 87% of patients in one 2000 study, but it is short acting.
Octreotide (Sandostatin) is a derivative of somatostatin and is longer-acting. It has largely replaced the older agent. It is very safe,
even for heart patients, and has few serious side effects.
Vapreotide (Octastatin) also resembles somatostatin. A 2001 study concluded that a combination of vapreotide and endoscopic
treatment is more effective than endoscopic treatment alone for controlling bleeding, but the combination therapy did not improve
mortality rates at 42 days. The study suggested that these drugs should be taken for five days.
Vasoconstrictors. Vasoconstrictors narrow the blood vessels and reduce flow in the spleen. They are particularly effective when used with
nitroglycerin.
Vasopressin (Pitressin) is the most commonly used vasoconstrictor. It poses a risk to the heart, however, and it is not clear
whether it is actually helpful.
Terlipressin is a synthetic version of vasopressin that is proving to be as effective as sclerotherapy in controlling bleeding. It also
lacks vasopressin's side effects. In one study terlipressin helped reverse a syndrome known as hepatorenal syndrome, a
life-threatening condition in which kidneys fail in trying to compensate for altered blood flow in the liver. More research is warranted
to determine if the drug has any effect on mortality.
Shunt Procedures Used for Bleeding that Is Not Responsive to Other Treatments
Shunts are used for patients who are still bleeding in the esophagus after endoscopic sclerotherapy or who are bleeding in the stomach.
Choices include the following:
Transjugular intrahepatic portosystemic shunt (TIPS).
A surgical shunt.
Shunt operations usually eliminate variceal bleeding, but encephalopathy and shunt failure are frequent complications. Experts do not
recommend shunts as elective surgery for high-risk patients who are candidates for liver transplantation, since shunts makes this
operation more difficult.
Transjugular Intrahepatic Portosystemic Shunt (TIPS). A transjugular intrahepatic portosystemic (or portal-systemic) shunt (TIPS) involves
the following:
The patient only requires a local anesthetic and a sedative.
A long needle is inserted into the jugular vein in the neck and passed down through the vena cave, a large vein that conducts blood
back to the heart. This serves to widen the vein.
The needle then punctures the hepatic vein in the liver and a connection is then made to the portal vein.
A cylindrical wire-mesh stent is inserted into this vein to keep it open.
The shunt forces blood vessels to reroute around the scarred liver.
Blockage or closure of the shunt can develop over time.
TIPS is a good choice for bleeding that is not controlled by endoscopy, particularly when it is performed shortly after a bleeding episode. It
also reduces ascites. It is not useful for an initial bleeding episode, however, since it poses a much higher risk for encephalopathy than
with endoscopic sclerotherapy and there is no survival advantage.
TIPS is generally recommended only for the following patients:
Cannot tolerate sclerotherapy.
Are unlikely or unable to comply with the repeated procedures necessary for sclerotherapy.
Have poor blood circulation.
Surgical Shunts. There are two types of surgical shunts:
A portal shunt, or portal systemic shunt. It was introduced in 1945 and was the first significant treatment for bleeding varices. It
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Cirrhosis
relieves pressure in the portal vein by surgically joining it to the inferior vena cava, a large vein that conducts blood back to the
heart. It poses a high risk for encephalopathy and does not appear to improve survival, so is not used often.
A distal splenorenal shunt (DSRS) preserves blood flow through the portal vein while relieving pressure on the varices by joining
the left kidney vein to the splenic vein , also called the lienal vein. (The splenic vein returns blood from the spleen. It is one of two
veins that form the portal vein.) Studies show that DSRS has similar mortality rates compared to the portal shunt but lower rates of
encephalopathy afterwards. Patients with alcoholic cirrhosis fare worse with DSRS than nonalcoholic patients. It is probably best
used as an elective operation in patients with good liver function who continue to bleed in spite of endoscopy.
Liver Transplantation
Liver transplantation is indicated in patients who have developed life-threatening cirrhosis and who have a life expectancy of more than 12
years. Patients with liver cancer that has not spread beyond the liver may also be candidates. Current five-year survival rates after liver
transplantation are between 60% and 80%. Patients also report improved quality of life and mental functioning after liver transplantation.
Patients should seek medical centers that have performed more than 50 transplants per year and produced better-than-average results.
Unfortunately, as of November 2000 there were more than 16,000 people waiting for a liver donation, with only about 4,500 donated livers
available each year. The number of people waiting in 2000 is well over 10 times that of ten years ago. Given the large number of people
with hepatitis C, this situation will almost certainly worsen in future years.
Liver Transplantation in Patients with Hepatitis . One of the primary problems with many hepatitis patients is recurrence of the virus after
transplantation. It is a particular problem in hepatitis C. One study reported viral recurrence of 80% and cirrhosis of 10% within five years of
the procedure. Recurrence in hepatits B has been significantly reduced using monthly infusions of hepatitis B immune globulin (HBIg),
with or without lamivudine. Autoimmune hepatitis may also recur after liver transplantation, but only after several years.
Liver Transplantation in Primary Biliary Cirrhosis . Patients who require transplantation are those who develop major complications of
portal hypertension and liver failure or who have poor quality of life and short survival without the procedure. Patients with primary biliary
cirrhosis may be at higher risk for early rejection of the transplanted organ than patients with other forms of cirrhosis.
Liver Transplantation in Alcoholism. There is considerable controversy over whether liver transplantation should be performed in
alcoholics with cirrhosis who are unlikely to abstain. One French study reported no differences in survival, transplant rejection, and other
indicators of success and failure after transplantation between alcoholics and non-alcoholics and between alcoholics who abstained and
those who relapsed after the procedure.
Information on Alcoholism
National Institute on Alcohol Abuse and Alcoholism
6000 Executive Boulevard - Willco Building, Bethesda, Maryland 20892-7003.
On the Internet (http://www.niaaa.nih.gov/)
National Council on Alcoholism
12 West 21 Street, New York, NY 10010.
Call (800-NCA-CALL) or on the Internet (http://www.ncadd.org/).
Their 800 number is a hotline that requires a touch-tone phone. A recorded message provides local numbers for counseling, help, and
information after the caller keys in their zip code.
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Cirrhosis
Information on Transplantation
United Network for Organ Sharing (http://www.unos.org/)
UNOS is the official US contractor for administering the national Organ Procurement and Transplantation Network (OPTN) and the US
Scientific Registry on Organ Transplantation.
National Transplant Society
3340 Dundee Road, Unit 2C-3, Northbrook, IL 60062-2331.
Call 312-701-0700 or on the Internet (www.organdonor.org)
Nonprofit organization whose goal is to lobby and support people requiring transplants.
US government organ donor site (http://www.organdonor.gov/)
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