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 Digestion and 
   Metabolism

 Protecting Liver Health
 Liver Disease

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 ตับ หน้าที่และการดูแลสุขภาพตับ Liver function and Disease      

It's Role in Digestion and Metabolism

The liver performs many functions that are fundamental to life. It is essential in the 
digestion of fats
and performs key functions in metabolism, the processing, storing,
and producing of substances that maintain life. Eighty-five to ninety percent of the 
blood that leaves the stomach and intestines passes through the liver first. Here, 
carbohydrates, proteins, fats, vitamins, and minerals are processed and 
converted into substances the body can use.

Carbohydrates
Dietary carbohydrates are the body's primary source of energy. Foods such as 
grains, cereals, fruit, and sugar are the main source of energy for the brain, cells, 
and muscles. The liver maintains this source of energy. During mealtimes, 
carbohydrates are broken down in the intestines to sugars. These sugars are 
absorbed and sent to the liver.

Absorbed sugars are used to replenish blood sugar (glucose), or excess sugar 
amounts can be stored in the liver in a form called glycogen. The liver can store a 
two day energy supply as glycogen. If this supply is depleted, the liver is able to 
help generate new glucose from other substances in the body. For example, 
during strenuous exercise, starvation, or even during sleep, various organs 
(especially the brain) require energy. The liver receives a hormonal message in 
the blood and creates glucose from its stores. This glucose is sent by the blood to 
the requesting organs.

Fats
The liver functions both in the digestion and metabolism of dietary fats. During 
digestion, bile produced by the liver and stored in the gallbladder is released into 
the intestine. Bile acts to emulsify fats, breaking them into smaller droplets so that 
they can be digested and absorbed.

The liver is also the hub for receiving dietary fat and cholesterol from the intestines.
Here fats can be used for energy if needed. Fats and cholesterol are processed 
and sent to different parts of the body. Fat is an energy source for the liver and is 
also the most efficient long-term storage form of energy. The liver plays a major 
role in the production and metabolism of fat. Glucose that exceeds the needs of 
the body can be converted by the liver into fat and stored.

The liver also has the capability of producing cholesterol. Cholesterol is a 
necessary component of every cell, used for production of bile and body 
hormones, and necessary for vitamin D production. Of course, too much 
cholesterol can be associated with serious cardiovascular disorders.

Proteins
The liver is also the site of protein metabolism. Here proteins that are broken 
down into amino acids and absorbed in the intestine may be rebuilt into proteins 
for use throughout the body. The liver may also break down body protein for use 
as energy when sugars are not available. Proteins produced by the liver perform 
a variety of vital functions including coagulating blood, maintaining fluid balance, 
iron storage, and delivery of iron, vitamin A, zinc, and copper within the body.

Vitamins and Minerals
The liver is involved in the storage, activation, transport, and excretion of many 
vitamins and minerals. Vitamins A, D, E, K, and B12, iron, zinc, copper, and 
magnesium are all stored in the liver. The liver is the major storage site for iron, 
storing 10 percent of the body's total iron stores. Carotene (a precursor to 
vitamin A), folate, and vitamin D all require the liver to be come active, usable 
forms for the body.

References:
Jones AL (1996). Anatomy of the Normal Liver. IN: Zakim D, and Boyer TD (eds.) 
Hepatology: A Textbook of Liver Disease.
Pennsylvania, WB Saunders Company, pp 3-31.

Sherlock S and Dooley J (1993). Anatomy and Function. Diseases of the Liver and Biliary System. 
Oxford, Blackwell Scientific Publications, pp 1-17.

Stolz, A (1998). Liver Physiology and Metabolic Function. IN: Feldman M, Scharschmidt BF, 
and Sleisenger MH (eds), Gastrointestinal and Liver Disease: Pathophysiology, Diagnosis, and 
Management.
Pennsylvania, W.B. Saunders Company, pp. 1061-1080.

Wanless, IR. (1998). Anatomy and Developmental Anomalies of the Liver. IN: Feldman M, 
Scharschmidt BF, and Sleisenger MH (eds), Gastrointestinal and Liver Disease: Pathophysiology, 
Diagnosis, and Management.
Pennsylvania, W.B. Saunders Company, pp. 1055-1058.

Zankim D (1996). Metabolism of Glucose and Fatty Acids by the Liver. IN: Zakim D, and Boyer TD 
(eds.) Hepatology: A Textbook of Liver Disease. Pennsylvania, WB Saunders Company, pp 58-91.

 

 

Protecting Liver Health

There are many risk factors associated with liver disease. Being knowledgeable of these factors and taking preventative measures to avoid these risks can reduce a person's chance of developing liver disease. Moreover, if you live with someone who has known liver disease, practicing healthy living together skills can help decrease chance of sharing liver disease.

Protecting Liver Health
Alcohol Excessive alcohol intake (beer, wine, hard liquor) can damage the liver and lead to cirrhosis. If you choose to drink alcohol at all, do so in moderation. If you already have liver disease, don’t use alcohol at all.
Sex

Hepatitis A and B can be transmitted through sexual contact. This is especially a risk when a person is suffering from other sexually transmitted diseases that produce sores or breaks in the skin. Practicing safe sex can avoid this risk.

Hepatitis C is rarely transmitted through sexual contact, however, use of a latex condom is recommended as hepatitis C can be transmitted through blood-to-blood contact.

Drugs

Intravenous drug use involving dirty needles is the most common mode of transport for viral hepatitis. Just sharing a needle once at any point in a person's life is a major risk factor for hepatitis. There is unacceptable danger here.

Also, mixing several drugs, or drugs and alcohol, can tax the liver and potentially cause damage. Avoid mixing drugs and alcohol and always consult your physician before adding a medication, prescription or over-the-counter drug, to your routine.

Tattoo Viral hepatitis can be transferred with dirty needles during tattooing.
Health Workers For those whose work increases risk of blood and body fluid exposure (dentists, doctors, nurses, lab technicians, etc.), follow precautionary measures of wearing protective apparel, using proper needle handling techniques, and get prophylactic vaccinations for hepatitis B when recommended.
Herbs and Supplements

It is unknown how the majority of herbal extracts are prepared and how they interact with the liver and other medications. Certain herbs have been known to induce liver injury alone or in combination with other drugs. The fact that herbs are ‘natural’ does not mean that they are free of toxic effects.

Avoid high doses of vitamins or minerals unless prescribed by your healthcare practitioner.

Over-the-Counter Medications

Be cautious about using prescription or over-the-counter medications. Follow instructions carefully. ((

NSAIDs (such as aspirin), ibuprofen, and acetominophen (Tylenol) are safe when taken as directed. However, high concentrations such as might occur with overdose can lead to liver damage. If you have liver disease, these medications may have to be avoided altogether. Usually, discontinuing medications that appear to be starting to causing liver injury will avert permanent damage.

Environmental Toxins

Use appropriate precautions when working around industrial chemicals.

Consult with your local health department about infectious disease risks when traveling to foreign countries. Get vaccinations as appropriate for protection from hepatitis A. Take appropriate food handling precautions when in areas where food and water safety is in question. For example, boil water prior to use. Thoroughly cook foods. Peel all fruits and vegetables.

Hygiene

Practice good personal hygiene and handwashing. Hepatitis A is most readily transmitted as a result of inadequate handwashing and hygiene.

Practice good food hygiene. Do not eat uncooked shellfish. Avoid shellfish from water whose cleanliness is questionable. Shellfish, that smells and tastes fine, may be infected by bacteria and viruses carried in sewage runoff. Vibrio vulnificus is a bacterial organism that is found in contaminated oysters and other seafood. In healthy people, it rarely causes serious infection, but in individuals with cirrhosis it can quickly cause death. Hepatitis A virus can be contracted from uncooked clams and oysters.

Other Blood-to-Blood Contact

Protect all cuts, open sores, your eyes and mouth from contact with blood. Use latex gloves when handling blood of anyone who has known hepatitis infection or whose hepatitis status is unknown to you.

Don't share toothbrushes or razors. If you are pregnant, get tested for hepatitis B and C and ask for guidance from your physician.




  Liver Disease
  1. ABC's of Hepatitis
  2. Alcoholic Liver Disease
  3. Cirrhosis
  4. Liver Cancer
  5.Other Liver Diseases

1. ABC's of Hepatitis

Viral hepatitis encompasses a variety of viruses that infect and attack liver tissue. 
Eight to 10 viruses have been identified, of which hepatitis A, B, C, D, E, and G are 
the most well known. They can be transmitted through various routes although 
intravenous drug use is the most common. Viral infection can be either acute 
(rapid onset and of short duration) or chronic (long duration and slow progression). 
Once a diagnosis is made and doctors are aware that a person has viral hepatitis,
they can determine through more specialized blood tests whether a person has 
acute or chronic viral hepatitis and the exact type of infection present.

Sometimes the virus may be cleared, making the person immune to it. This means,
unless the next exposure to the virus is different (like a different cold virus), the 
person will not be infected again. If a person has chronic disease, the doctor may 
recommend a liver biopsy to determine the progression of disease. A liver biopsy 
is helpful to direct the doctor in treatment and to provide a prognosis.

Hepatitis A Virus (HAV)
People are exposed to HAV from a fecal oral route or person-to-person contact. 
People who are at the greatest risk are daycare workers (changing diapers), 
injection drug use, recent travel, or from a food or waterborne outbreak. Forty-two 
percent of cases of HAV have no known source of infection. HAV infection is 
always of short duration; it is not a long-term disease. Sixty percent of people with
HAV recover in two months and 100 percent recover in six months.
Incidence: Occurs in 9.1 persons per 100,000 in the U.S.
Symptoms: Fatigue, weakness, anorexia, nausea, vomiting, and abdominal pain. Jaundice occurs in 90 percent of people with HAV and lasts less than two weeks. Once jaundice occurs, symptoms tend to decrease.
Medications: None
Vaccine: A vaccine is available for HAV.

Hepatitis B Virus (HBV)
Transmission of HBV occurs through needle exposure, transfusions, sexual contact and exposure while giving birth. HBV infection can be either short-term (acute) or long-term (chronic). Chronic infection develops in 90 percent of infants infected at birth and 25 to 50 percent of children infected between 1 and 5 years of age. Ninety-five percent of people with acute HBV will spontaneously clear the virus, however, in 2 to 5 percent of adults, the virus will become chronic. Persons who develop chronic HBV may develop liver failure, cirrhosis, and 22 percent of people with chronic disease will
develop liver cancer. There are no medications for acute HBV and the virus will ordinarily spontaneously clear. Interferon and lamivudine are approved medications in the U.S. for chronic infection. The way interferon works is not clearly understood but it appears to interfere with the body's ability to replicate the virus. About 30 to 40 percent of people on interferon respond to treatment and clear the virus. Lamivudine, an antiviral that also inhibits viral replication, may be given with interferon to help clear hepatitis B virus. Transplantation may not be a very good option for people who have HBV due to the high rate of re-infection with HBV after transplant.
Incidence: There are 350 million carriers of HBV worldwide. About 1 to 1.25 million persons in the U.S. are infected.
Symptoms: People with HBV commonly have no symptoms.
Medications: None for acute infection; Interferon and lamivudine available for chronic infection in the U.S..
Vaccine: A vaccine is available and highly effective. It is recommended that healthcare workers, adolescents and all newborns receive the vaccine.

Hepatitis C Virus (HCV)
Exposure to HCV occurs predominantly through intravenous drug use. Transfusion and any other blood-to-blood contact are other modes of transmission. Of the people who are exposed to HCV, 15 percent will clear the virus. Meanwhile, 85 percent will have chronic (long-term) infection; 20 to 50 percent will eventually be diagnosed with cirrhosis, 20 percent will have liver failure, and 20 percent will
have liver cancer. HCV is most commonly diagnosed during routine testing at the doctor's office or during a blood test prior to donating blood. This is because disease progression is silent, taking 20 to 30 years to develop into cirrhosis, although it is much quicker in the elderly and in persons with alcoholic liver disease. Combination therapy with interferon and ribavirin is often suggested for treatment of HCV. Interferon is injected three times a week for 12 months and ribavirin is taken daily by mouth for 12 months. The goal of treatment is to reduce replication of the virus and eventually clear the virus from the body. Close to 40 percent of people who undergo treatment clear HCV. The response rate is lower in those co-infected with HIV. Research on alternative HCV treatment is quite active. Incidence: Among intravenous drug users, 48 to 90 percent have HCV. In the U.S., 4 million people are infected.
Symptoms: People with HCV report the following symptoms, fatigue, depression, nausea, abdominal discomfort, and difficulty concentrating. Jaundice occurs more in people who have acute disease, and is rare in 
chronic disease.
Medications: Interferon and ribavirin are approved for use in the U.S. for chronic HCV.
Vaccine: None are available.

Hepatitis D Virus (HDV, Delta agent/virus)
HDV is a viral infection that only occurs in persons with preexisting HBV infection. The most common mode of transmission is of HDV is through intravenous drug use. It can either be acute or chronic. Co-infection of acute HBV and HDV has a short course. However, there is a risk that co-infected people
can have a severe and progressive course known as 'superinfection.' Fifteen percent of superinfected people have spontaneous recovery while 70 percent have a slow, progressive course leading to cirrhosis. People who use intravenous drugs usually have a more aggressive course of disease. For people who have chronic disease, interferon may be recommended.
Incidence: A total of 15 million people are infected worldwide.
Symptoms: Commonly there are no symptoms.
Medications: None for acute infection; interferon may be recommended for chronic infection.
Vaccine: There is no vaccine for HDV.

Hepatitis E Virus (HEV)
HEV is an acute disease with no chronic state that is most commonly transmitted
via water contaminated with feces. Pregnant women and travelers are most at 
risk for this disease. HEV causes inflammation of the liver with most people 
having a complete recovery. Pregnant women, however, have a high risk of liver 
disease and death to the mother and fetus.
Incidence: HEV is rare in the U.S.
Symptoms:
Fever, jaundice, dark urine, clay colored stools, lack of appetite, nausea, vomiting and abdominal pain.
Medications: None available.
Vaccine: There is no vaccine for HEV.

Hepatitis G Virus (HGV)
Transmission of HGV is common in blood and organ recipients, as well as intravenous drug users. HGV has just recently been identified and the symptoms, treatment, and recovery rate are yet unknown. It can be acute and chronic.
Incidence: Unknown.
Symptoms: Unknown.
Medications: None available.
Vaccine: None available.

References:

Poynard T, Marcellin P, Lee SS, et al (1998). Randomized trial of inteferon a2b plus ribavirin for 48 
weeks or for 24 weeks versus interferon a2b plus placebo for 48 weeks for treatment of chronic 
infection with hepatitis C virus.
Lancet;352:1426-1432.

Reichard O, Narkrans G, Fryden A, et al (1998). Randomized, double-blind, placebo-controlled trial of 
interferon a -2b with and without ribavirin for chronic hepatitis C.
Lancet;351:83-87.

Terrault NA, Wright TL (1998). Viral Hepatitis A Through G. IN: Feldman M, Scharschmidt BF, 
and Sleisenger MH (eds), Gastrointestinal and Liver Disease: Pathophysiology, Diagnosis, and 
Management.
Pennsylvania, W.B. Saunders Company, pp. 1123-1164.

2. Alcoholic Liver Disease

Alcoholic liver disease impacts two million people in the United States. The liver is the 'Poison Control Center' of the body, detoxifying toxic chemicals introduced into the blood. The development of alcoholic liver disease can often be compounded by the simultaneous intake of medications and other poisons, as the liver is then charged with detoxifying all substances at once. Although the exact cause of liver disease in those that drink alcohol is unclear, alcohol appears to cause liver damage by blocking the normal metabolism of proteins, carbohydrates, and fats. Substances called cytokines, chemicals involved in the immune system and inflammation, also seem to be involved.

   

Also, women appear to be more likely to suffer liver damage from alcohol than men. Women, as well as older adults, have less enzyme activity required to detoxify the alcohol. There is some data to suggest that part of the problem for women is the relative lack of an enzyme in the lining of the stomach that is need to metabolize alcohol. Moreover, a woman have relatively more body fat and less body water than a man, and this can result in a higher concentration of alcohol, even if she is the same weight and drinks the same amount as a man. For women, alcohol is truly more potent.

Researchers are currently studied other factors that make individuals who drink more susceptible to alcoholic liver disease. These may include ethnicity, nutritional status, drug use, or simultaneous hepatitis B or C infection.

Alcoholic liver disease, if left unchecked, can eventually result in cirrhosis of the liver. Cirrhosis refers to a process of liver scarring that is usually thought to be permanent. Of the 26,000 people who die from cirrhosis each year, 40 to 90 percent have a history of alcohol abuse. However, if detected and treated early, cirrhosis can be prevented.

How Much Alcohol is Too Much?

Liver disease most commonly develops only after a 'threshold' of alcohol has been consumed, although the amount of alcohol that can cause injury varies widely.

Generally, if a person drinks the equivalents of eight 12 ounce cans of beer, 1 1/3 bottles of wine, or 1/2 pint of distilled spirits daily for about 20 years, it is likely that liver disease will occur. Such liver damage may be anywhere on a spectrum ranging from relatively mild to extremely serious.

On the other hand, there are certainly some individuals who can consume these amounts of alcohol and never develop any identifiable liver abnormality.

Many alcohol users do not experience symptoms of liver disease until damage becomes extensive and complications such as cirrhosis, jaundice (buildup of bilirubin in the blood such that skin and eyes become yellow), ascites (abdominal fluid retention), and altered mental status arise. However, flu-like symptoms of fatigue and fever, as well as an enlarged liver may occur earlier in the disease process. If alcoholic liver disease is suspected, a liver biopsy is commonly performed. This test will determine the severity of disease and predict a prognosis.

Treatment
The primary treatments for alcoholic liver disease is cessation of alcohol use and improvement of nutritional state if necessary. The physician may assist in the process of alcohol withdrawal by providing counseling, referrals to supportive programs, and prescribing medication to minimize withdrawal symptoms.

Nutritionally, the person with alcoholic liver disease is encouraged to consume a diet high in calories, protein, and fruit and vegetables. Vitamin and mineral supplementation may also be recommended. People who have alcoholic liver disease are frequently malnourished. Alcohol, which has seven calories per gram, typically replaces more nutritious foods in the diet. The alcohol calories are 'empty' calories, totally devoid of nutrition. Malnutrition may weaken a person's ability to fight disease and repair tissue. If liver disease patients are experiencing an altered mental state , protein restriction may be necessary. In ascites, sodium and fluid intake may need to be restricted. A health care team can best evaluate liver function and complications and give recommendations for optimal nutrition care.

Further medications and procedures may be necessary to help reduce liver disease complications and maximize liver function. Some authorities believe that steroids can help in the management of some forms of alcoholic liver disease (although this is controversial). It is thought that these medications may help reduce inflammation, thus minimizing liver damage. Steroid use is associated with a great many serious complications, and the addition of steroids to any treatment program should only be considered after a careful review of possible benefits as compared to the wide range of steroid complications.

References:

Maher, JJ (1998). Alcoholic Liver Disease. IN: Feldman M, Scharschmidt BF, and Sleisenger MH (eds), Gastrointestinal and Liver Disease: Pathophysiology, Diagnosis, and Management. Pennsylvania, W.B. Saunders Company, pp. 1199-1210.

Sherlock S and Dooley J (1993). Alcohol and the Liver. Diseases of the Liver and Biliary System. Oxford, Blackwell Scientific Publications, pp 370-389.


 

3. Cirrhosis

Cirrhosis is the irreversible damage of the liver that can be caused by a variety 
of diseases including viral hepatitis, alcoholic liver disease, cancer, and others
Cirrhosis occurs when there is damage of liver tissue resulting an accumulation 
of scar tissue, decreased functioning liver tissue, and a distortion of normal liver 
structure that will ultimately further interfere with normal liver function. There are 
many debilitating complications associated with cirrhosis including 
encephalopathy
, ascites, portal hypertension, gastrointestinal bleeding
hepatorenal syndrome
, osteoporosis, and malnutrition. Liver transplantation is the 
only cure for people with cirrhosis.

Encephalopathy
Encephalopathy occurs when the liver is no longer able to clear waste products (especially protein byproducts) and toxins from the blood usually processed by the liver. Symptoms of encephalopathy include loss of consciousness, drowsiness, confusion, and coma. A person with encephalopathy has difficulty explaining simple statements or even stating the day, month, and year.

The initial treatment for encephalopathy is the medication lactulose that may be administered in combination with a low protein diet. About 75 to 80 percent of people who take lactulose respond to therapy with an improved mental state.

Increased protein in the diet has been shown to be the culprit in only 7 to 9 percent of the cases of encephalopathy. Adequate protein intake in liver disease is essential to maintaining health and improving healing and immune response. Protein requirements should be discussed with the health care team and determined individually by considering nutritional status, disease state, and

Common Symptoms of Cirrhosis
  • Anorexia
  • Indigestion
  • Nausea and vomiting
  • Constipation or diarrhea
  • Dull aching abdominal pain
  • Gastrointestinal bleeding
  • 'Mousy' breath
  • Itching
  • Extreme skin dryness
  • Changes in skin elasticity
  • Appearance of blood vessels under the skin
  • Jaundice
prior protein intake. Of course, preventing or stopping any bleeding in the gastrointestinal tract is also of extreme importance as digestion and absorption of digested blood will increase protein byproducts in the blood.

Ascites
Ascites is an accumulation of abdominal fluid caused by changes in portal blood
pressure
and the reduction of liver proteins responsible for maintaining fluid 
balance. Ascites may appear suddenly or without much notice. Symptoms 
associated with ascites include dehydration, muscle wasting (thin limbs and a 
large belly), and lack of sweating. When the conditions associated with ascites 
are present, normal blood flow throughout the body is reduced. The kidneys 
recognize this reduction and typically react by conserving sodium and water, often 
worsening the ascites and sometimes leading to kidney failure as well.

The treatment for ascites is a low sodium diet and medications called diuretics. A 
low sodium diet (less than 2000 milligrams/day) when followed on a daily basis 
can be extremely effective. Eating low sodium one day and a regular sodium diet 
the next day does not help reduce the accumulation of fluid. Follow-up visits are 
necessary to monitor weight, blood pressure, and adjust the dosage of the 
diuretic as necessary.

Portal Hypertension/Gastrointestinal Bleeding
As scar tissue accumulates and disrupts normal liver structure, blood flow through 
the liver can become difficult. The usual pathways for blood flow are often blocked 
or become inefficient. This difficulty of flow increase blood pressure in portal vein 
leading to the liver.

The most common consequence of portal hypertension is esophageal varices, 
or enlarged veins. As portal blood pressure rises, blood flow is diverted to other 
close blood vessels such as those feeding the digestive tract. These dilated 
blood vessels unused to the high flow and pressure of blood often break and 
bleed. Fifty to sixty percent of people with cirrhosis will develop varices. 
Symptoms include vomiting of blood and dark stools. Upon examination, the 
doctor will feel the liver and spleen. An enlarged spleen is one of the most useful 
diagnostic signs of portal hypertension, and a firm liver suggests that the scarring 
of cirrhosis may be present.

To diagnose varices, the doctor can visualize the esophagus using using an 
endoscope (a small flexible tube that is swallowed). Varices can often be seen 
bulging in the lining of the esophagus. Endoscopy allows the doctor to grade the 
severity of the varices and to treat varices that are bleeding. The greater the size 
of the varices, the greater the chance they will bleed.

If bleeding occurs, the chance of having a second bleed is high, 60 to 70 percent 
chance over a two-year period. Factors that can increase the risk of bleeding 
include alcohol intake, aspirin, and non-steroidal anti-inflammatory drugs (NSAID) 
use such as Advil, Motrin, ibuprofen, Naprosyn. There are endoscopy-related 
procedures
a doctor can use to treat and prevent bleeding such as sclerotherapy 
or variceal banding.

Hepatorenal Syndrome
This syndrome usually but not always affects patients with end stage alcoholic 
cirrhosis. The cause of this hepatorenal syndrome is unclear but likely results from 
changes in blood flow to the kidney associated with portal hypertension and 
some medications such as diuretics. Symptoms include poor appetite, weakness, 
and fatigue initially and then nausea, vomiting, and thirst. Management of 
hepatorenal syndrome typically involves admission to the hospital for careful 
monitoring and treatment to restore normal kidney function.

Osteoporosis
Nutrient deficiencies are common in people with cirrhosis due to their symptoms 
of poor appetite, nausea, vomiting, and diarrhea that make getting adequate 
nutrients difficult. Osteoporosis (reduced bone mass) caused by limited calcium 
intake can be common. Also, alcohol, one cause of liver disease, can interfere 
with bone formation as well as adequate nutrient intake. If osteoporosis is present, 
a calcium supplement may be used to help prevent any further bone loss.

Malnutrition
Malnutrition, literally meaning bad nutrition, is a term used to describe a person 
is not getting the essential nutrients necessary for proper body function. Many 
people with cirrhosis are malnourished due to their symptoms and the body's 
additional energy requirements due to disease. Worsening this situation, the 
decreased production of bile by the damaged liver may impair the body's ability 
to absorb nutrients. Diet restrictions such as low sodium and low protein can also 
impact food choices and food taste and decreasing intake of food. Malnutrition 
can result in decreased immune function and decreased ability to heal. People 
who find themselves eating less, losing more than 10 pounds in one month, or 
having difficulty finding enough food to eat because of a restrictive diet should 
consult their physician and a dietitian to discuss meal planning to optimize 
nutrition without compromising liver health.

References:
Bass NM and Somberg KA (1998). Portal Hypertension and Gastrointestinal Bleeding. IN: Feldman M, 
Scharschmidt BF, and Sleisenger MH (eds), Gastrointestinal and Liver Disease: Pathophysiology, 
Diagnosis, and Management.
Pennsylvania, W.B. Saunders Company, pp. 1284-1295.

Hasse J, Weseman B, Fuerman MP, Loeffler M et al (1997). Nutrition Therapy for End-Stage Liver 
Disease: A Practical Approach.
Support Line; 19(4), 8-15.

Runyon BA (1997). Treatment of Patients with Cirrhosis and Ascites. Seminars in Liver Disease;17(3), 
249-260.

Sherlock S and Dooley J (1993). Hepatic Encephalopathy. Diseases of the Liver and Biliary System.  
Oxford, Blackwell Scientific Publications, 1993, pp 86-101.

Sherlock S and Dooley J (1993). Ascites. Diseases of the Liver and Biliary System. Oxford, Blackwell 
Scientific Publications, pp 114-131.

Sherlock S and Dooley J (1993). The Portal Venous System and Portal Hypertension. Diseases of the 
Liver and Biliary System.
Oxford, Blackwell Scientific Publications, pp 132-178.

Sherlock S and Dooley J (1993). Hepatic Cirrhosis. Diseases of the Liver and Biliary System. Oxford, 
Blackwell Scientific Publications, pp 357-369.

 

4. Liver Cancer

Liver cancer is the 7th most common cause of cancer in men and the 9th in women 
worldwide. About 310,000 to one million cases occur each year with risk for liver 
cancer increasing as a person ages. Tumors in the liver can either originate in the 
liver or spread to the liver from remote or adjacent organs. Major risk factors for 
liver cancer are chronic, active hepatitis B (HBV) and C (HCV) and cirrhosis.

In simple terms, cancer is the uncontrolled overgrowth of cells. Under normal 
circumstances, cell growth is organized. It takes place at a natural pace for each 
organ or tissue type and is controlled by each cell's genetic material. 
Occasionally this genetic material is corrupted, and more often than not, this 
'mutation' is corrected. But, at times, it is not and the pace and control of cell 
growth goes array. In the case of chronic, active liver diseases, experts speculate 
that an increased incidence of cancer occurs because of the accelerated 
regeneration of liver tissue in response to constant injury.

The liver is a difficult organ to examine and often the growth of cancer can progress with minimal symptoms. When a liver tumor is big enough to be felt by hand, the tumor has already reached an appreciable size. Because of the ability of the liver to accommodate itself to changes, the tumor must reach a large size before the liver has difficulty functioning. Unfortunately, the tumor is typically advanced at the time of the first doctor visit.
Common Symptoms of Liver Cancer
  • Abdominal pain
  • Weight loss
  • Weakness
  • Abdominal swelling
  • Gastrointestinal symptoms
  • Jaundice
Ascites may be present at the initial visit, however most people with ascites 
already have cirrhosis which can cause abdominal fluid rentention also. Weight 
loss and decreased lean muscle mass may be present initially or it can occur as 
the disease progresses. Jaundice does not usually happen initially, but can occur 
as the disease progresses.

Small liver cancers are a common complication of cirrhosis. The presence of the 
cancer can be masked by other symptoms. However, if symptoms of cirrhosis 
worsen, it may be a signal that disease process has changed or worsened.

Common blood tests of liver function do not distinguish liver cancer from other 
masses or from cirrhosis. The blood test of choice to detect liver cancer is 
alpha-fetoprotein (a protein that is produced by cancer cells), and an elevated 
test can indicate potential tumors. Elevations in cholesterol can occur in 10 to 40 
percent of people with liver cancer, however, this is not diagnostic of cancer. 
Computed tomography
(CT) detects the majority of liver cancer and can define 
the extent of the tumor within the liver and in other parts of the body. Magnetic 
resonance imaging (MRI) is useful in detecting small tumors.

Treatment for liver cancer depends on the size of the cancer, the number of 
cancers, and if they have spread into other organs. Surgery can provide the best 
chance of a cure only when the tumor is in a confined space and the remaining 
non-cancer tissue is not already damaged (cirrhotic). There is a high recurrence 
rate after surgery, usually making the person with liver cancer in eligible for 
transplant
. Chemotherapy, attempting to erradicate the cancer with toxic 
medications, has a success rate of 20 percent. Discussions with an oncologist will 
determine if a person is eligible for this type of therapy. For more information on 
cancer visit Mediconsult's About Cancer program listed in the resources section.

 

References:
Kew MC (1998). Hepatic Tumors and Cysts. IN: Feldman M, Scharschmidt BF, and Sleisenger MH 
(eds), Gastrointestinal and Liver Disease: Pathophysiology, Diagnosis, and Management. 
Pennsylvania, W.B. Saunders Company, pp. 1404-1415

 


5.Other Liver Diseases

There are a variety of diseases other than viral hepatitis, alcohol, and cancer that 
can cause liver disease. The most common are discussed here.

Primary Biliary Cirrhosis (PBC)
PBC is an uncommon, chronic, progressive disease. There are only 40 to 150 
cases per one million people in the U.S. and the majority of cases (90 percent) 
are women. PBC is usually diagnosed around 50 years of age. Symptoms of this 
disease commonly include itching and fatigue. Other signs include jaundice, 
cholesterol deposits in the skin, and ascites (swollen abdomen). About 25 percent 
of people who are diagnosed with PBC have no symptoms and normal liver 
function tests. This liver disease destroys the bile ducts of the liver and causes 
portal hypertension. Fibrosis is initially seen with the disease progressing to 
cirrhosis
. The only completely effective treatment available for liver disease is 
transplantation.

Complications that can occur with PBC include osteoporosis, itching, deficiency of 
fat-soluble vitamins (ADEK), elevated cholesterol and lipids, and fatty diarrhea. 
Most of these complications are due to the inability of the liver to process bile 
acids correctly that leads to poor fat absorption in the intestinal tract.

Primary Sclerosing Cholangitis (PSC)
PSC is a liver disease of unknown cause. In PSC, the bile ducts become 
narrowed due to inflammation and scarring. This progressive narrowing can 
cause blocked bile flow that can result in liver damage. About 75 percent of the 
cases diagnosed with the disease are men who are about 40 years of age. There 
is an association between PBC and irritable bowel disease (IBD). In fact 70 
percent of people who have PBC have IBD; of those people, 87 percent have 
ulcerative colitis and 13 percent have Crohn's disease.

Most people do not have symptoms at the time of diagnosis and the disease 
usually progress slowly over 10 to 15 years. As the disease becomes more 
advanced, a person may complain of fatigue, itching, and fatty diarrhea. Upon 
further evaluation, vitamin A, D, and E deficiencies can be found along with 
elevated cholesterol and osteoporosis. Liver biopsy is helpful in staging the 
severity of disease. Currently there is no dependable treatment although studies 
continue with several medications. Liver transplantation is the treatment of choice 
and PSC is the fourth leading cause of transplantation.

Wilson's Disease
Wilson's Disease is a hereditary disorder of the liver that causes the liver to store 
excess copper. It effects 1 in 30,000 people and is detected between ages 3 and 
40. If diagnosed promptly and treated consistently, the prognosis is good.

Copper is an essential mineral required by the body and most people consume 
1.5 to 4 milligrams (mg) a day. Copper is absorbed in the upper intestine and 
excess copper is excreted in the bile (about 1 to 4 mg). In people with Wilson's 
disease, the excess copper is not used properly by the liver to make essential 
proteins and is not excreted efficiently in the bile, resulting in copper overload.

The symptoms of Wilson's disease include malaise, anorexia, and nausea. 
Some people may develop severe chronic liver disease and develop symptoms 
of enlarged liver and spleen, ascites, low albumin, and an abnormal ability to 
coagulate blood. Wilson's disease rarely progresses into liver cancer.

Unique symptoms experienced by those with liver disease include:

  • Neurological Involvement
    A person may have poor coordination, loss of fine motor control, changes in gait, drooling, and swallowing difficulties. Intellectual ability is not impaired.
  • Psychiatric Changes
    This impacts only 20 percent of people with Wilson's Disease. People may have neurotic and/or compulsive behaviors and fears.
  • Eyes Changes
    While vision changes are not noticed, a classic symptom of Wilson's Disease is Kayser-Fleischer rings, a characteristic brown pigment that can be seen on slit-lamp exam by an ophthalmologist. These develop when excess copper is distributed throughout the cornea.

The treatment for people with Wilson's disease includes reducing the amount of 
copper rich foods they eat and medication. Copper rich foods include organ 
meats, shellfish, nuts, chocolate, and mushrooms. Medications used for the 
treatment of Wilson's disease work by increasing the excretion of excess copper 
in the urine or the feces.

Hereditary Hemochromatosis (HHC)
HHC is a disorder causing iron overload due to an increase in intestinal 
absorption of iron. In a normal diet, 1 to 2 mg of iron is absorbed each day. In 
people with HHC, about 3 to 6 grams (gm) is absorbed daily resulting in iron 
overload and liver damage. If it is diagnosed and treated early, a person can 
have a normal lifespan. Detection is most likely to occur during a routine blood 
screening.

Detection typically occurs between 4 and 50 years of age with more men than 
women found to have HHC. Some people are identified because of other 
relatives and will present with no symptoms. Others may complain of weakness, 
fatigue, abdominal pain, loss of libido, and joint pain. Diabetes and bronzed skin 
may be present. People may also present with symptoms of liver damage 
including an enlarged liver and spleen, ascites, swelling, and jaundice.

If a HHC is diagnosed and effective treatment undertaken before cirrhosis 
develops, the person will not develop any long-term liver complications. If 
detected after cirrhosis develops, the risk of liver cancer rises. Treatment of HHC 
involves weekly removal of 1 to 2 pint of blood until the blood levels of iron drop to 
within the normal range. Once iron levels are normal, blood draws of one pint may 
only be required every 2 to 3 months.

Drug-Induced Liver Disease
Liver injury caused by drugs or other chemicals accounts for less than 5 percent of 
jaundice or acute hepatitis and very few cases of chronic liver disease. The 
mechanism of injury is often poorly understood. Factors that put a person at risk 
for drug-induced liver disease include age, sex, dose of drug taken, history of 
other drug use, alcohol, nutrition status (obesity or fasting), preexisting liver 
disease, and the presence of other diseases such as diabetes, HIV/AIDS, kidney 
failure, and prior organ transplant. The diagnosis of drug induced liver disease is 
confirmed by a liver biopsy.

Symptoms and treatment of drug-induced liver disease vary widely and depend 
on the extent of liver damage. They also include removal of the offending agent.

Acetominophen Induced Injury
Acetominophen (Tylenol) is safe when taken at its recommended dosage (1 to 4 
gm a day). However, when taken in excess, it is the leading cause of liver injury 
and has been recognized as such since the 1960's. Moderate doses of 15 to 20 
gm over a three day time period in people who are fasting or taking drugs that can 
interact with Acetominophen can cause liver injury. The combination of 
acetominophen and alcohol leads to further risk of liver injury.

Most commonly, people present with symptoms such as nausea, vomiting, 
malaise and liver pain. In severe cases, jaundice, low blood sugars, and features 
of liver failure may be present. Liver function tests (the transaminase enzymes) 
can be extremely high, often a clue to the diagnosis. If a person presents within 
four hours of ingestion of acetominophen, the stomach should be emptied by 
placing a tube in the stomach and suctioning out the contents. Blood levels of 
acetominophen should be determined to determine the extent of the exposure, 
options for treatment, and outcome. As with other drug-induced liver injuries, 
symptoms and treatment will be determined by extent of damage.

References:

Bacon, BR (1997). Diagnosis and Management of Hemochromatosis. Gastroenterology; 113:995-999.

Bacon BR, Britton, RS (1998). Hereditary Hemochromatosis. IN: Feldman M, Scharschmidt BF, and 
Sleisenger MH (eds), Gastrointestinal and Liver Disease: Pathophysiology, Diagnosis, and 
Management
. Pennsylvania, W.B. Saunders Company, pp. 1097-1102.

Cox DW, Roberts EA (1998). Wilson's Disease. IN: Feldman M, Scharschmidt BF, and Sleisenger MH 
(eds), Gastrointestinal and Liver Disease: Pathophysiology, Diagnosis, and Management. 
Pennsylvania, W.B. Saunders Company, pp. 1104-1111.

Farrell GC (1998). Liver Disease Caused by Drugs, Anesthetics and Toxins. IN: Feldman M, 
Scharschmidt BF, and Sleisenger MH (eds), Gastrointestinal and Liver Disease: Pathophysiology, 
Diagnosis, and Management.
Pennsylvania, W.B. Saunders Company, pp. 1221-1247.

Harnois DM, Lindor KD (1997). Primary Sclerosing Cholangitis: Evolving Concepts in Diagnosis and 
Treatment.
Digestive Diseases;15:23-41.

Lindor KD (1998). Primary Biliary Cirrhosis. IN: Feldman M, Scharschmidt BF, and Sleisenger MH (eds),  
Gastrointestinal and Liver Disease: Pathophysiology, Diagnosis, and Management.
Pennsylvania, 
|W.B. Saunders Company, pp. 1275-1281.

Neuberger J (1997). Primary Biliary Cirrhosis. Lancet;350:875-79.

Schilsky, ML (1996). Wilson Disease: Genetic Basis of Copper Toxicity and Natural History. Seminars i
n Liver Disease; 16(1), 83-93.

Sherlock S and Dooley J (1993). Primary Biliary Cirrhosis. Diseases of the Liver and Biliary System. 
Oxford, Blackwell Scientific Publications, pp 236-248.

Sherlock S and Dooley J (1993). Sclerosing Cholangitis. Diseases of the Liver and Biliary System. 
Oxford, Blackwell Scientific Publications, pp 249-259.

Sherlock S and Dooley J (1993). Wilson's Disease. Diseases of the Liver and Biliary System. Oxford, 
Blackwell Scientific Publications, pp 400-407.