The Liver.
The liver is the largest organ in the body, located immediately below the diaphragm and occupying the entire upper right quadrant of the abdomen. In the healthy adult, it weighs about three pounds and is wedge shaped, with the upper part being wider than the lower. The liver performs over 500 vital functions, most of which are important for metabolism or detoxification.

The liver processes all of the nutrients that the body requires, including proteins, glucose, vitamins, cholesterol, and fats. It also renders harmless potentially toxic substances, including alcohol, ammonia, nicotine, drugs, and harmful by-products of digestion. The liver synthesizes blood clotting factors and albumin, the major protein in the blood. The liver also affects bilirubin, a yellow-green pigment produced from the breakdown of hemoglobin, the oxygen-carrying component in red blood cells. The liver converts bilirubin into a water-soluble form, which is then is excreted into bile. Bile is a green-colored fluid that is formed in the liver and contains, in addition to bilirubin, bile salts, fatty acids, cholesterol and other substances. Bile travels from the liver to the gallbladder, where it is stored until after meals, when it is secreted in the intestines to help digest fat.

These vital processes rely on a well-organized liver architecture consisting of bile ducts, blood vessels, working liver tissue (called the parenchyma) and supportive connective tissue. The liver has two major lobes (with the right one much larger than the left), which are separated from each other by walls of tough, fibrous connective tissue. The lobes are composed of about 100,000 elegantly patterned lobules that form microscopic columns. At the center of each lobule is a central vein running down the column from which radiate paths of liver cells bordered by blood vessels. Bracing the corners of each lobule are three small important structures: an artery (whose source of blood is the hepatic artery); a vein (whose original source of blood is the portal vein); and a bile duct. The arteries bring oxygen-rich blood to nourish the liver cells themselves. The blood passing through the veins, however, is the source of the nutrients and toxins that the liver cells take up as the blood travels to the central veins of the lobules. The central vein is a tributary that eventually joins with other hepatic veins, in turn, lead into the inferior vena cava, which conducts the blood back to the heart. Bile drains from tiny canals around the liver cells into the corner ducts, which eventually join to form the large common bile duct that leads from the liver to the gallbladder.

Cirrhosis.
Cirrhosis is an irreversible sequel to a number of disorders that damage the liver cells and causes fibrosis (scarring). Often, this process is accompanied by random clusters of regenerated liver cells that develop throughout the liver, usually forming nodules around the fibrosis. Eventually, this damaging pattern becomes so extensive that the normal architecture of the liver is distorted. The small blood vessels and bile ducts narrow. Blood that normally passes from the intestine backs up through the portal vein and seeks other routes. If it backs up into the spleen, the blood platelet count falls, which causes abnormal bleeding. Twisted swollen veins called varices form in the stomach and lower part of the esophagus. Bile builds up in the blood stream, causing high levels of bilirubin, which causes the yellowish cast in the skin called jaundice. Fluid build-up in the abdomen (called ascites) an swelling in the arms and legs often occur. The liver becomes very enlarged. In advanced cases, the liver sometimes shrinks, a condition called postnecrotic cirrhosis.

Alcoholic Cirrhosis.
Alcoholic cirrhosis, also called portal, Laennec's, nutritional, and micronodular cirrhosis, is the primary cause of cirrhosis in the U.S., and is estimated to be responsible for 44% of deaths from cirrhosis in North America. (Some believe this a low estimate. One Canadian study found alcohol to be the major contributor to 80% of all cirrhosis deaths.) The liver is particularly endangered by alcohol. Over time, alcohol abuse leads to increased demands for oxygen by the liver, and at the same time fat accumulates and impairs the liver's ability to absorb oxygen. The immune system over-responds causing an inflammatory process that damages and finally kills liver cell, a condition called alcoholic hepatitis. Initially, the fat-laden liver becomes greatly enlarged but eventually shrinks as cirrhosis develops with we-like scars that surround small knots of abnormal regenerated liver cells.

Cirrhosis from Chronic Hepatitis.
The next leading cause of cirrhosis in the U.S. 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; many expert believe hepatitis C is becoming a major world wide health problem. Viruses or other mechanisms that cause hepatitis produce inflammation in liver cells, resulting in their injury or destruction. If damage to the liver is extensive and cell injury occurs beyond the portal tract, progressive cell damage builds a layer of scar tissue over the liver, resulting in cirrhosis. In advanced cases, the liver develops postnecrotic cirrhosis and shrivels in size.

Primary Biliary Cirrhosis.
Primary biliary cirrhosis is a much less common form of liver scarring, accounting for 0.6% to 2% of deaths from cirrhosis. It is most likely an inherited autoimmune disease; that is the body's immune system attacks its own liver cells mistaking them for foreign proteins (antigens.) In the case of primary biliary cirrhosis, the cells under attack are in the bile ducts. Liver cells are destroyed as the disease progresses. Primary biliary cirrhosis is associated with reduced bone growth, partly because of the liver's inability to process vitamin D and calcium and also from some of its treatments. As a result, osteoporosis occurs in 20% to 30% of patients. Other diseases, including scleroderma or Sjogren's syndrome, may also accompany this form of cirrhosis.

Uncommon Causes of Cirrhosis.
Hemochromatosis is an inherited disorder that causes large amounts of iron to build up in liver cells. Wilson's disease is another rare inherited condition, which results in the accumulation of copper. Other rare causes include the genetic disease alpha1-antitrypsin globulin deficiency, schistosomiasis-a parasite found in the Far East, Africa, and South American, and small intestine bypass surgery (this was formerly used for obesity but is no longer performed.) A number of very rare inherited childhood diseases can also cause cirrhosis. Long-term or high level exposure to certain chemicals and drugs, including arsenic, methotrexate, and toxic doses of vitamin A can also cause liver damage leading to cirrhosis. Cancers that have metastasized to the liver, blood clots in the hepatic or portal vein, or obstructions in the bile duct can also cause changes that resemble cirrhosis.

People with Alcoholism.
Between 1950 and 1975 the rate of alcoholic cirrhosis dramatically increased; since then, however, the incidence has declined. Cirrhosis is currently estimated to occur in about 10% of people with alcoholism. High steady intake of large amounts of alcohol is the primary risk factor, although other conditions often must be present to cause permanent liver damage. One study of two communities in Italy found that the risk for cirrhosis was increased when alcohol was drunk without food or if multiple kinds of alcoholic beverages were consumed. Contrary to other reports, the study did not find that women were more susceptible than men to the effects of alcohol on the liver. In excess, all alcoholic beverages are equally harmful, although one study did find that beer increased the chance of cirrhosis by 50% compared to other drinks. Binge drinkers are at somewhat lower risk.

People with Chronic Hepatitis.
About 3% to 5% of people infected with hepatitis B develop the chronic form and about half of these patients develop cirrhosis. An estimated 10% to 60% of people originally infected with hepatitis C patients develop the chronic form, which poses a risk for cirrhosis of about 30%. Because of blood screening the risk for transmission for both viruses through transfusions has dramatically decreased since 1990. Hepatitis C can exist for decades, however, without symptoms and nearly 300,000 people who had transfusions before 1990 may have contracted the virus. In one study or cirrhosis that had been caused by chronic hepatitis C, transfusions posed the highest known risk, accounting for about 23.4% of cirrhosis cases. About a third of the cases of hepatitis-related cirrhosis were caused by infections incurred in hospitals. In more than a quarter of these patients, the cause of the original hepatitis infection was not known. In the same study, sexual exposure to an infected partner, and industrial-chemical exposure accounted fairly equally for the remaining cirrhosis cases. A ratio of two enzymes, aminotransferase (AST), to alanine aminotransferase (ALT), can predict a higher risk if the ratio of AST/ALT is greater than 1.

Risk Factors for Primary Biliary Cirrhosis.
About 95% of primary biliary cirrhosis cases occur in women, mostly between the ages of 30 and 50. Genetic factors are involved but the inheritance pattern is unclear.

General Symptoms.
People may experience few symptoms at the onset of cirrhosis. Fatigue and loss of energy are common early symptoms, along with loss of appetite and nausea. Spider angiomas may develop on the skin; these are pinhead-sized red spots from which tiny blood vessels radiate. Patients in later stages develop jaundice, a yellowish cast to the skin and eyes, which is caused when the liver cannot process bilirubin for elimination from the body. The palms of the hands may be reddish and blotchy, a condition known as palmar erythema. Patients may lose body hair. In men with alcoholic cirrhosis, the testicles may atrophy and their breasts may become swollen, sometime painful.

Symptoms of Complications.
A swollen belly is a sign of ascites, a condition that occurs when fluid accumulates in the abdomen. Fever, abdominal pain, and tenderness when the belly is pressed indicates infection of the fluid. (Infection may occur, however, without any symptoms.) Forgetfulness, unresponsiveness, and trouble concentrating may be early symptoms of hepatic encephalopathy, which is damage to the brain caused by build-up of toxins. Sudden changes in the patient's mental state, including agitation or confusion, may indicate an acute condition. Other symptoms include bad fruity-smelling breath and tremors. Late stage symptoms of encephalopathy are stupor and, eventually, coma.

Symptoms Specific to Rate Cases of Cirrhosis.
People with primary biliary cirrhosis are subject to severe, general itching and often develop small fatty yellow lumps called xanthomas on the eyelids, hands, and elbows. They may have an unpleasant condition called steatorrhea, in which the feces contain excessive fat causing them to float and to be very foul-smelling. In the rare disorder hemochromatosis there is often a bronze cast to the skin, an indication of iron build-up. A thin bronze crescent bordering the cornea is called the Kayser-Fleisher ring and is a sign of copper build-up in people with Wilson's disease.

Cirrhosis is the seventh leading cause of death by disease in the U.S., killing over 25,000 people each year. The most serious complications of cirrhosis are bleeding, infections, and encephalopathy--damage to the brain. Nearly every bodily process is affected by a damaged liver, including those of the digestive, hormonal, and circulatory systems. Less protein is produced by the liver, for example, which causes fluid build-up, bleeding problems, and susceptibility to infection. Additionally, the liver cannot detoxify harmful substances, which accumulate and impair brain function. Cirrhosis is also a cause of liver cancer.

Cirrhosis is irreversible, but the rate of progression can be very slow in some patients depending on its cause. For instance, in patients with hepatitis B, the five-year survival rate after a diagnosis of cirrhosis is 71%. For alcoholics with cirrhosis, continued intake of alcohol severely limits the chance of survival. For those who abstain, a survival rate of five years or more can be as high as 85%; for those who continue drinking, the chance for living beyond five years is no higher than 60%. For cirrhosis that has developed slowly in people with chronic hepatitis, is difficult to determine prognosis at the time of diagnosis because the physician is usually unable to tell when cirrhosis first occurred. People with primary biliary cirrhosis and no symptoms can have a normal life span. Once symptoms of liver damage, such as jaundice occur, however, the average survival time is 12 years. New treatments, however, may improve this outlook.

Infections.
Abdominal infection occurs in up to 25% of patients with cirrhosis within a year of diagnosis. At high risk are patients whose tests results show very low protein levels and very high bilirubin levels.

Encephalopathy.
Encephalopathy (damage to the brain) causes mental confusion and in worst cases, coma and death. The development of encephalopathy is often precipitated by other problems including gastrointestinal bleeding, constipation, excessive dietary protein, infection, surgery or dehydration. No single toxin accounts for the mental effects of encephalopathy; a combination of conditions causes this serious complication. One such condition is the build-up in the blood of harmful intestinal toxins, such as ammonia. Another suspect is an imbalance of amino acids, which may result in excessive amounts of some amino acids that effect the central nervous system.

Ascites.
Ascites is fluid in the abdomen. It is usually caused by portal hypertension, which can also cause swelling in the arms and legs and an enlarged spleen. (Ascites can result from other conditions, and physicians should check for other possibly serious causes, including cancer and infections. Ascites itself is not fatal, but it is uncomfortable and can reduce breathing function and urination. It is also associated with a condition called hyperaldosteronism. Aldosterone is a steroid hormone produced in the adrenal gland that regulates sodium and potassium. High amounts (hyperaldosterone) can result in a fluid electrolyte imbalance called hypokalemic (low potassium) alkalosis (too alkaline,) which in turn can cause weakness, abnormal heart rhythms, a sense of paralysis, and in severe cases encephalopathy.

Other Complications.
Gallstones and peptic ulcers are more common in people with cirrhosis than in the general population. Respiratory problems are also a particular risk, especially since smoking is common in people with alcoholic cirrhosis. There is also an increased risk for liver cancer.

Physical Examination.
The cirrhotic liver is often enlarged. It is also firm and may even feel rock-hard. The left side can often be felt by the physician when pressing on the abdomen. In advanced stages, however, the liver may become small and shriveled. If significant ascites is present, the physician may also detect a dull shifting wave of fluid in the abdomen.

Biopsy.
A liver biopsy is the only definite method for diagnosing cirrhosis. It also helps determine its cause. The procedure uses a needle inserted through the abdomen to obtain a tissue sample from the liver. The biopsy may also be performed during peritoneoscopy, which uses a catheter and tiny camera to view the surface of the liver. Biopsies can be dangerous, so they cannot be performed in patients who have test results that indicate clotting problems, in those who have had previous liver biopsies or who have ascites.

Blood Tests.
A number of blood tests may be performed to measure liver function and to help determine the severity and cause of cirrhosis. High bilirubin levels are a strong indication of advanced liver disease, particularly when accompanied by other symptoms. Measurements of blood levels of alkaline phosphatase, aminotransferase, and other enzymes found in the liver may be useful for diagnosing cirrhosis. To help determine the outlook experts may use a calculation called a discriminant function (DF), which combines two important measurements: serum albumin concentration and prothrombin time (PT). Serum albumin measure protein in the blood with low levels indicating poor liver function. The PT test measure in seconds the time it takes for blood clots to form; the longer it takes the greater the risk for bleeding.

Caffeine Clearance Test.
A simple, inexpensive and harmless test that measures caffeine in saliva, may prove to be an accurate method for determining the severity of cirrhosis.

Imaging Tests.
A number of imaging test may be used to diagnose cirrhosis and its complications. Magnetic resonance imaging (MRI), computed tomography (CT), and ultrasound are all imaging techniques that are useful 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. Arteriography uses dye injected into the hepatic arteries that then shows up on x-ray. Spleenoportography uses dye injected into the spleen, which allows the physician to measure portal vein pressure; this procedure is risky.

Hepatic Vein Wedge Pressure.
Hepatic vein wedge pressure involves insertion of a catheter into the hepatic veins. The blood pressure in the veins of the liver is then measured which in turn is an indicator of portal vein pressure. If pressure is high, cirrhosis is likely. One study found that this measurement offers a useful predictor for outcome in that a low measurement indicates a better prognosis.

Paracentesis.
If ascites is present, paracentesis is performed. This procedure involves using a thin needle to withdraw fluid from the abdomen. The appearance of the fluid is helpful in determining a cause. For example, cloudy fluid may mean an infection, and bloody fluid, the presence of a tumor. The fluid is tested for difference factors including protein levels, bacteria cultures, and white blood cell counts. Low levels of protein in the fluid and a low white blood cell count suggest that cirrhosis is the cause of the ascites. A high white blood cell count may mean infection is present.

Treatment for Alcoholism.
The only treatment for alcoholic cirrhosis is to stop drinking. [For more information on how to stop, see Well Connected, Report #56, Alcoholism.] Individuals with alcoholic cirrhosis are almost always malnourished and therefore, require increased calories and rigorous nutritional support, which can improve survival rates. Corticosteroids may be useful for alcoholic hepatitis, and acute condition in which the liver is inflamed but they are not beneficial after cirrhosis has developed. Drugs under investigation include propylthiouracil and colchicine, which inhibit deposits of collagen, the critical protein building block in connective and scar tissue. Researchers are also investigating drugs that block factors in the immune system called thrombaxanes, which may play an important role in the inflammatory process that kills liver cells in alcoholic cirrhosis.

Treatment for Chronic Hepatitis B or C.
The standard drug currently used for chronic viral hepatitis B, D, and C is interferon alpha-2b (Roferon-A, Intron A). Other interferons are being tested, including recombinant type-I interferon (Infergen) and interferon beta, which is benefiting many children with hepatitis B who do not respond to interferon-alpha. In those who respond to interferon, studies are showing improved symptoms, a normal long-term survival rate, and in some no return of the disease. The percentage of patients who benefit over the long-term, however, is small. Not all patients are candidates; among others, the treatment is inappropriate for patients with advanced hepatitis, fluid in the abdomen or any serious medical or psychiatric problems. Even when the drug is effective the disease recurs half the time and requires additional treatment. Patients with hepatitis B should be given interferon if they show signs of liver damage; it is not recommended for those with normal aminotransferase levels. The drug has eliminated the virus and sustained significant remission in 25% to 40% of patients with chronic hepatitis B. In patients with hepatitis C taking interferon for six months there is an even lower average rate of sustained response--about 15%. (Although studies indicate this rate can be boosted to 24% with treatment of a year or longer.) Early eradication of the virus is the most important factor for success. In one study, over 75% of patients whose viral count was eliminated in the first week had a sustained response. However, only 35% of those whose count was down by week two and 12.5% of those whose count was down by the fourth week had a sustained response. In some cases, very short course of corticosteroids may be used initially to boost the effect of interferon. Reducing iron levels through a series of blood-drawings in certain patients may also enhance the effect of interferon. A recent study reported that interferon may prevent liver cancer in cirrhosis patients who have hepatitis B. Combinations with other drugs are being investigated. Common side effects are flu-like symptoms that usually occur within six hours and last for 12. More chronic effects include depression, irritability, weight loss, vomiting, and general weakness. Interferon often causes a drop in platelet and white blood cell counts, increasing susceptibility to bacterial infections. It may also trigger an autoimmune response, possibly causing anemia, diabetes, lupus-like symptoms, thyroid abnormalities or even autoimmune hepatitis. In patients with very advanced cirrhosis, standard doses of interferon may be dangerous causing bleeding and severe infection.

Among the drugs showing promise for patients who do respond to interferon are nucleoside analogues, which directly affect viral replication; they include ribavirin, lamivudine (Epivir), famciclovir (Famvir), and adefovir. Studies are showing that the drugs reduce virus levels of hepatitis B to nearly undetectable levels. Unfortunately, the virus recurs in almost all cases, although this recurring mutation may be weaker than the original strain. Administering the drug for longer periods may produce sustained remission in more patients while still being safe. For hepatitis C patients, the most promising treatment is a combination of ribavirin and interferon alpha (Rebetol), which has produced sustained improvement in 40% to 77% of patients. This treatment may not be effective, however, in people with severe or late-stage disease.

Immunomodulators are drugs that modify or regulate part of the immune system. One of these, thymosin a drug known as an immunomodulator because it regulates the immune system, is a promising therapy when used alone or in combination with interferon for hepatitis B or when used in combination with interferon for hepatitis C. Vaccines, including Hepagene are being investigated for treating and preventing hepatitis B. Amanthdine (Symmetrel) is a drug commonly used for Parkinson's disease, which in studies is showing promise for hepatitis C patients who have failed interferon. Ursodiol or ursodeoxycholic acid improves aminotransferase levels and may prove useful for hepatitis C in combination with interferon, although it has no anti-viral effects and is not useful alone.

Because cirrhosis is irreversible, therapies are aimed at treating causes, slowing progression and preventing and treating complications.

Dietary Factors.
A healthy lifestyle is important for everyone and particularly people with cirrhosis. Because important antioxidant vitamins are depleted in the cirrhotic liver, people should maintain a diet rich in fresh fruits, vegetables, and whole grains that contain not only vitamins A, E, and C but also other substances important for health. Vitamin supplements themselves are not recommended except with the advice of a physician. Patients whose condition is caused by hepatitis C sometimes have abnormally high iron levels. Such 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. Restricting salt consumption is particularly important for patients with ascites. High-quality dietary of protein may be helpful for patients with ascites and for repairing muscle mass, but encephalopathy may be triggered by excessive protein loads. 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. Water intake should be limited in patients with ascites.

Treating Ascites.
If body fluid is not reduced by drinking less then a diuretic, usually spironolactone (Aldactone), is given. This drug not only reduces fluid but also prevents hyperaldosteronism (low potassium levels with a high alkaline pH in the blood). Breast swelling in men is a common side effect. Other, more diuretics may be given if spironolactone is not effective. In such cases, patients should be monitored carefully for excessive and too rapid fluid loss, which can set off complications including hypokalemia (dangerously low potassium levels), kidney failure or encephalopathy. Weight loss from diuretics should not exceed one or two pounds a day. If spironolactone or other diuretics are not successful, some patients will require large-volume paracentesis. In this procedure, albumin (protein) is administered intravenously while large volumes of fluid are removed through a tube in the abdomen. Peritoneovenous (LeVeen) shunting an older more invasive procedure, involving insertion of a tube or shunt under the skin that routes the fluid from the abdomen into the jugular vein. This procedure does not improve survival, however, can have serious complications, including infection, blood clots, and rapture of blood vessels in the esophagus.

Preventing and Treating Encephalopathy.
The first step in managing encephalopathy is to treat any precipitating cause, if known, such as bleeding, high ammonia levels, low oxygen, infection, dehydration or use of sedatives. 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) and lactitol, known as disaccharides help lower blood ammonia levels. 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, including L. acidophilus and E. faecium, to the intestine is showing promise as a safe and effective treatment. In some studies, taking zinc supplements have produced good results for lowering ammonia levels in those who were zinc-deficient, a common problem in cirrhosis. Some studies indicate that manganese poisoning may be partially responsible for encephalopathy in cirrhosis; studies are needed to determine if drugs that remove manganese improve this complication.

Balloon tamponade uses a tube, which is inserted through the nose and down through the esophagus until it reaches the upper part of the stomach. A balloon at the tube's end is inflated and positioned tightly against the esophageal wall. It is usually deflated in about 24 hours. Serious complications can occur, the most dangerous being rupture of the esophagus. A recurrence of bleeding following this procedure is common.

Treatment for Gastrointestinal Bleeding.
Gastrointestinal (GI) bleeding is often first treated with medications to reduce stomach acid. Reduced clotting factors or platelets are common causes of GI bleeding in people with alcoholic cirrhosis. Some will respond to three days of injected vitamin K. People with alcoholism also often require folic acid. Transfusions of replacement clotting factors or platelets may be needed.

Infection.
Antibiotics are administered when ascites fluid examination and tests indicate the presence of infection. For a first episode, typically, the antibiotic cefotaxime is administered intravenously, requiring hospitalization. Some research indicates that the oral antibiotic ofoxacin may be as effective in patients without other complications allowing them to be treated at home. In patients at high risk for recurrence, long-term therapy generally with the drug norfloxacin is prescribed.

Treatment for Primary Biliary Cirrhosis.
The itching caused by primary biliary cirrhosis can be relieved by taking cholestyramine with meals. The drug naltrexone relieved itching in one study. (High doses of this drug are toxic to the liver, but the low doses used in the study were safe.) Therapy using light may also reduce itching. Because primary biliary cirrhosis results in decreased fat absorption. These patients are at risk for deficiencies in important fat-soluble vitamins including K, D, A and E. High doses or injections of some of these vitamins may be required. Zinc supplements may also be required. For steatorrhea, a preparation of agents called medium-chain triglycerides may be helpful. Colchicine, the drug that inhibits collagen. Has produced some improvement in liver function and survival and has only minor side effects. Ursodiol or ursodeoxycholic acid (Actigall), a drug generally used to treat gallstones, inhibits prostaglandin E2, a factor in the inflammatory process. It improves many aspects of the disease, including symptoms and has only minor side effects; unfortunately, it is very expensive and does not appear to prolong survival. Azathioprine, methotrexate and cyclosporine are drugs that suppress the immune system, in studies have shown modest benefits on survival, but they have severe side effects. One study reported that methotrexate caused remission in a group of patients.,but although encouraging, other studies have indicated that many patients do not respond to this drug. Corticosteroids which reduce inflammation have been helpful in improving liver function and symptoms, but can accelerate osteoporosis, an already existing risk in these patients.

Treatment for Other Forms of Cirrhosis.
Secondary biliary cirrhosis caused by blockage in the bile ducts can be relieved by surgery. For hemochromatosis, weekly bleedings (phlebotomies) may be performed until iron levels are normal, then repeated as needed. If treatment is given before cirrhosis develops life expectancy may be normal. D-penicillamine is the drug most used for Wilson's disease.

Liver Transplantation.
Liver transplantation may be an option for people with primary biliary cirrhosis. Primary sclerosing cholangitis or for some people with alcoholic cirrhosis who have completely abstained from alcohol, usually for more than six months. Some people with cirrhosis and small localized liver cancers may also be suitable candidates. Liver transplantation is also an option for people with chronic hepatitis, although hepatitis B patients have a success rate of only 50% to 60% because of recurrence. (The success rate is higher in those who have hepatitis D.) Patients should seek medical centers that have performed more than 50 results. Experiments using monthly infusions of hepatitis B immune globulin (HBIg) after transplantation show great promise in preventing recurrence in these patient. This treatment may need to be administered life-long. One study reported that lamivudine may be helpful in preventing recurrence of hepatitis B after liver transplantation. Hepatitis C also commonly returns in transplanted livers, progressing to cirrhosis within an average of 51 months in 8% of patients. In general, 70% of patients who have had liver transplantation lived five years or more and some have lived over 20 years. Unfortunately, there are only about half the number of available livers as there are transplant candidates. Regulations controlling liver transplantation may give priority to patients with the best chance of long-term survival--such as a young person with severe mushroom poisoning as opposed to an elderly person with alcoholic cirrhosis. Such regulations are being opposed.

National Institute of Diabetes and Digestive and Kidney Disease (NIDDK)
National Digestive Diseases Information Clearinghouse
2 Information Way
Bethesda, MD 20892-3570

Call (301) 654-3810 or on the Internet (http://www.niddk.nih.gov/)

Has excellent information on hepatitis.

Primary Biliary Cirrhosis Patient Support Network
Box 177
Tamworth, ON KOK 360
Canada
Call (613) 379-2534

Centers for Disease Control and Prevention
Hepatitis Branch
1600 Clifton Road NE.
Mail Stop G37
Atlanta, GA 30333
For a special number on hepatitis call (888) 4HEPCDC or (888) 443-7232
or on the Internet at (http://www.cdc.gov/ncidod/diseases/hepatitis/index.htm)

This is an important source on hepatitis. The CDC provides an excellent fax on-demand service.  Call (404) 332-4565. For hepatitis, after calling the fax number, request code #000004 for Directory. The directory will then provide the codes for numerous faxes, which will provide specialized information on specific topics on hepatitis. For example, code #361351 give information o Hepatitis B Vaccine, #361351 on Hepatitis C, and #361353 on Treatment information for hepatitis B and C.

American Association for the Study of Liver Diseases
1200 19th Street NW., Suite 300
Washington, DC 20036-2422
Call (202) 429-5179

Hepatitis Foundation International
30 Sunrise Terrace
Cedar Grove, NJ 07009
Call (800) 891-0707

This organization focuses just on viral hepatitis. It provides educational materials, offers support by phone and gives referral to other physicians.

American Liver Foundation
1425 Pompton Ave
Cedar Grove, NJ 07009
call (800-GO Liver) or (800-465-4837) or on the Internet (http://www.liverfoundation.org/)

American Gastrointestinal Association
7910 Woodmont Ave., Seventh Floor
Bethesda, MD 20814
Call (301) 654-2055 or on the Internet (http://www.gastro.org/)

This is an association for physicians and other professionals. They provide names of gastroenterologists in local areas.

Alcoholic Anonymous
P.O. Box 459
New York, NY 20814
Call (212) 870-3400) or on the Internet (http://www.alcoholicsanonymous.org/)

Meetings for this group can be found by calling AA in the phone book. If it is not located there, check with a physician, clergyman or a hospital.

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 hot line that requires a touch-tone phone. A recorded message will provide a local number for counseling, help and information after individual keys in their zip codes.