Liver facts

The liver is the largest solid organ in the body, weighing on average about 3.5 pounds.
The liver carries out a large number of critical functions, including manufacture of essential proteins, and
metabolism of fats and carbohydrates.
The liver also serves to eliminate harmful biochemical waste products and detoxify alcohol, certain drugs,
and environmental toxins.
The liver forms and secretes bile that contains bile acids to aid in the digestion and intestinal absorption
(taking in) of fats and the fat-soluble vitamins A, D, E, and K.
Diseases that may affect the liver include hepatitis (inflammation of the liver), cirrhosis (scarring), fatty
liver, and liver cancer (hepatocellular carcinoma).
Symptoms of liver disease may include bleeding or easy bruising, swelling, fatigue, and jaundice (yellow
coloring to the skin and whites of the eyes).
Liver overview
The liver is the largest solid organ in the body. People may not know that the liver is also the largest gland in
the body. The liver is actually two different types of gland. It is a secretory gland because it has a specialized
structure that is designed to allow it to make and secrete bile into the bile ducts. It also is an endocrine
gland since it makes and secretes chemicals directly into the blood that have effects on other organs in the
body. Bile is a fluid that both aids in digestion and absorption of fats as well as carries waste products into the
intestine.
There are all sorts of glands in the body that make and secrete substances, including the pancreas (digestive
enzymes), thyroid and other endocrine glands (hormones), gastric glands in the stomach (acid), and lymph
glands or nodes (lymph).
Reviewed by William C. Shiel Jr., MD, FACP, FACR on 10/7/2011










How large is the liver?
The liver weighs about three and a half pounds (1.6 kilograms). It measures about 8 inches (20 cm) horizontally
(across), and 6.5 inches (17 cm) vertically (down), and is 4.5 inches (12 cm) thick.
Where is the liver located (liver anatomy)?
The liver is located just below the diaphragm (the muscular membrane separating the chest from the
abdomen), primarily in the upper right part of the abdomen, mostly under the ribs. However, it also extends
across the middle of the upper abdomen and part way into the left upper abdomen. An irregularly shaped,
dome-like solid structure, the liver consists of two main parts (a larger right lobe and a smaller left lobe) and two
minor lobes. As you can see in the diagram below, the upper border of the right lobe is at the level of the top of
the 5th rib (a little less than 1/2 inch below the nipple), and the upper border of the left lobe is just below the 5th
rib (about 3/4 inch below the nipple). During inspiration (breathing in), the liver is pushed down by the
diaphragm and the lower edge of the liver descends below the margin of the lowest rib (costal margin).

What is the function of the liver?
The liver has a multitude of important and complex functions. Some of these functions are to:
Manufacture (synthesize) proteins, including albumin (to help maintain the volume of blood) and blood
clotting factors
Synthesize, store, and process (metabolize) fats, including fatty acids (used for energy) and cholesterol
Metabolize and store carbohydrates, which are used as the source for the sugar (glucose) in blood that
red blood cells and the brain use
Form and secrete bile that contains bile acids to aid in the intestinal absorption (taking in) of fats and the
fat-soluble vitamins A, D, E, and K.
Eliminate, by metabolizing and/or secreting, the potentially harmful biochemical products produced by the
body, such as bilirubin from the breakdown of old red blood cells, and ammonia from the breakdown of
proteins
Detoxify, by metabolizing and/or secreting, drugs, alcohol, and environmental toxins
Reviewed by William C. Shiel Jr., MD, FACP, FACR on 10/7/2011



What special features enable the liver to do so much?
The liver has many special features. For example, in order to carry out its secretory functions, ducts (tubes)
closely connect it to the gallbladder and intestines. Thus, bile made by the liver travels through these tubes to
the gallbladder. The bile is stored in the gallbladder between meals, and then is discharged into the intestines
at mealtime to aid in digestion.
For another example, the liver is appropriately situated in the body to directly receive the blood that comes from
the intestines (portal blood). With this arrangement, the liver can readily process (metabolize) nutrients
absorbed from food as well as other contents of the portal blood. Indeed, because of its numerous biochemical
functions, the liver is considered the biochemical factory of the body.
What's more, the liver is organized strategically to coordinate its structure, including its blood circulation, with
its functions. Four key features of this organization of the liver are as follows.
1. The basic unit of the liver is called an acinus (pronounced as' i-nus: plural acini). (There are numerous
acini in the liver.) In each acinus, the liver cells (hepatocytes) are grouped into three zones that are
anatomically related to the liver's blood supply and drainage. Thus, the blood enters zone one first, and
then travels through the second and third zones before leaving the liver. Each zone has its own special
functions to perform. (Moreover, because of these different functions, as well as the different relationships
to the flow of blood, the zones have different susceptibilities to injury.)
2. Specialized areas of the walls of adjacent liver cells (hepatocytes) join to form bile canaliculi (pronounced
kan" ah-lik' u-li). The canaliculi are microscopic tubes that transport bile that is produced by the liver cells
(hepatocytes). Then, meeting with other canaliculi, they ultimately empty into tiny bile ducts. These bile
ducts join with other bile ducts to form larger bile ducts that ultimately leave the liver.
3. The liver has a unique, dual blood supply. One comes from the portal vein, as already mentioned, and the
other from the hepatic artery. The hepatic artery brings to the liver oxygenated blood that comes from the
lungs, heart, and branches of the aortic artery. So, finally, tiny branches of the portal vein and hepatic
artery travel in the liver together with the tiny bile ducts in tracts called portal tracts (triads).
4. The hepatic artery supplies blood to nourish the bile ducts and the liver cells (hepatocytes). This blood
joins with the portal vein blood in tiny blood vessels called sinusoids. Now, these sinusoids are situated on
each side of single-cell-thick plates of liver cells (hepatocytes), and they have an exceptionally porous
(hole-filled) lining (epithelium). This unique arrangement enables passage of even large molecules (for
example, lipoproteins) through the sinusoidal lining to and from the liver cells (hepatocytes). The blood
travels in the sinusoids through the three acinar zones. Finally, the blood is drained from the liver by the
hepatic veins and then heads back to the heart and lungs.
Reviewed by William C. Shiel Jr., MD, FACP, FACR on 10/7/2011



What diseases affect the liver?
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The most common liver diseases are various types of acute (sudden) hepatitis (inflammation), chronic (long
duration) hepatitis, fatty liver, cirrhosis(scarring), and cancer. Cancers that affect the liver are most commonly
metastatic cancers that have spread via the bloodstream to the liver from other sites in the body. However,
primary cancers (cancers that arise in the liver) can also occur. The most common type of primary liver cancers
are known as hepatocellular carcinomas. Viruses, drugs, and alcohol, as well as metabolic, immune (defense)
system, and genetic (hereditary) abnormalities are the common causes of many liver diseases. But note that,
contrary to a popular misconception, alcohol is only one of the many causes of liver disease. Moreover,
sometimes the cause of the liver disease is not known.
How do liver diseases cause symptoms?
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Acute and chronic liver diseases can interfere with the functions of the liver and thereby cause symptoms.
However, the liver has a hefty reserve capacity. In other words, it usually takes substantial damage to the liver
before a disease interferes with the functions of the liver and causes symptoms. Examples of such symptoms
are:
Jaundice (yellow skin) that can occur when the liver is unable to properly metabolize or secrete the yellow
pigment bilirubin in bile
Bleeding or easy bruising that can occur when the liver is unable to make enough of the normal blood
clotting proteins
Swelling of the legs with fluid (edema) that can occur when the liver is unable to make enough albumin
and the serum albumin gets too low
Fatigue that is of unknown cause, but may be related to some impaired metabolic function of the liver
Reviewed by William C. Shiel Jr., MD, FACP, FACR on 10/7/2011



What about blood tests for the diagnosis of liver disease?
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Damage to the liver often gives rise to telltale abnormalities in certain blood tests (suggesting liver disease), the
so-called liver blood tests (for example, ALT, AST, and alkaline phosphatase enzymes). As a matter of
convenience, the liver blood tests often are collectively referred to as liver function tests. But, abnormalities in
only some of them (i.e., elevated bilirubin, low albumin, and prolonged prothrombin time) actually reflect, at
least in part, abnormal function of the liver. And, it turns out that abnormalities of the other liver blood tests may
reflect the actual injury to the liver. For example, viral hepatitis can cause the ALT or AST enzymes in injured
liver cells to spill into the blood stream and increase their level in the blood.
Sometimes, the pattern of liver blood test abnormalities provides a clue as to the type of liver disease. For
example, an AST to ALT ratio greater than two (as long as both are less than nine times normal) suggests
alcoholic hepatitis or cirrhosis of any type.
Other blood tests are more specific for the diagnosis of particular liver diseases. For example, there are
serological tests for most of the different types of viral hepatitis and immunological tests for primary biliary
cirrhosis(antimitochondrial antibodies) or chronic autoimmune hepatitis (smooth muscle antibody). Additionally,
there are special tests for hemochromatosis(iron-related tests), Wilson's disease (copper-related tests), and
liver cancer (tumor markers).
Reviewed by William C. Shiel Jr., MD, FACP, FACR on 10/7/2011



Why does the doctor examine the liver?
The doctor examines the liver as part of the abdominal physical examination to try to gain helpful diagnostic
information about a patient's liver condition. For example, the liver can be tender (painful to touch) with acute
hepatitis or feel hard and irregular (bumpy) with cancer of the liver. Also, some conditions can cause the liver to
enlarge (fatty liver or certain types of chronic hepatitis or cirrhosis), while others can make the liver smaller
(advanced cirrhosis).
What is a liver biopsy?
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The most accurate way to diagnose the type of liver disease is by doing a liver biopsy, although a biopsy is not
necessary in most cases. This procedure involves removing, with a thin hollow needle, a small piece of liver
tissue for microscopic study. What's interesting about a liver biopsy is that the tiny sample is usually
representative of the disease (pathology) in the rest of this large organ. Put another way, most liver disease
involves the entire liver. When the disease is localized to only a small part of the liver, as for example, cancer
usually is, the biopsy can be done with ultrasonic visual guidance to be certain that the small, involved area is
biopsied.
What else is important about the liver?
There's one other interesting point about this remarkable organ. The liver has an extraordinary capacity to
regenerate (reproduce itself). For example, damage the liver, and it will soon regenerate in an attempt to
restore its functions. Cut out a part of the liver, and it likewise will grow back (regenerate) rapidly. In fact, when
a person donates a part of her or his liver for transplantation, much of the part that is removed will soon grow
back.
There's a famous story in Greek and Roman mythology that testifies to the liver's great capacity to regenerate.
Witness Prometheus chained to a rock on a mountain. This confinement was his punishment because he had
displeased the ruler Zeus (Jupiter, if you prefer Latin to Greek) by providing fire (and other benefits) to
humankind. Picture a vulture pecking away at the liver of the helpless Prometheus. He survived, however,
according to the legend, because his liver renewed itself as fast as the vulture devoured it.
REFERENCE: Fauci, Anthony S., et al. Harrison's Principles of Internal Medicine. 17th ed. United States: McGraw-Hill
Professional, 2008.

Previous contributing author: Leslie J. Schoenfield, MD, PhD


Patient Comments: Liver - Diseases

1. Take the Liver Disease Quiz
2. Hepatitis Slideshow: A Visual Guide to Hepatitis
3. Take the Alcohol Quiz
What type of liver disease do you have? Please discuss the
treatments and lifestyles changes you've made.
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Back to Liver

Comment from: Anne, 55-64 Female (Patient)Published: June 05
I was just advised by my doctor that I have a cyst on my liver. I'm not sure what that means. She is sending me for a CT
scan within the next few weeks.

I had pains under my left breast.

I had a liver biopsy today. It was not as bad as I had thought it would be. After the happy juice, I felt a small pinch while
numbing the liver area for puncture and the site where the sample would be taken. Then, poof, it was over. So don't worry,
and don't let others' experiences scare you.
























What is cirrhosis?
Cirrhosis is a complication of many liver diseases that is characterized by abnormal structure and function of
the liver. The diseases that lead to cirrhosis do so because they injure and kill liver cells, and the inflammation
and repair that is associated with the dying liver cells causes scar tissue to form. The liver cells that do not die
multiply in an attempt to replace the cells that have died. This results in clusters of newly-formed liver cells
(regenerative nodules) within the scar tissue. There are many causes of cirrhosis; they include chemicals (such
as alcohol, fat, and certain medications), viruses, toxic metals (such as iron and copper that accumulate in the
liver as a result ofgenetic diseases), and autoimmuneliver disease in which the body'simmune system attacks
the liver.
Why does cirrhosis cause problems?
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The liver is an important organ in the body. It performs many critical functions, two of which are producing
substances required by the body, for example, clotting proteins that are necessary in order for blood to clot,
and removing toxic substances that can be harmful to the body, for example, drugs. The liver also has an
important role in regulating the supply to the body of glucose (sugar) and lipids (fat) that the body uses as fuel.
In order to perform these critical functions, the liver cells must be working normally, and they must have an
intimate relationship with the blood since the substances that are added or removed by the liver are transported
to and from the liver by the blood.
The relationship of the liver to the blood is unique. Unlike most organs in the body, only a small amount of
blood is supplied to the liver by arteries. Most of the liver's supply of blood comes from the intestinal veins as
the blood returns to the heart. The main vein that returns blood from the intestines is called the portal vein. As
the portal vein passes through the liver, it breaks up into increasingly smaller and smaller veins. The tiniest
veins (called sinusoids because of their unique structure) are in close contact with the liver cells. In fact, the
liver cells line up along the length of the sinusoids. This close relationship between the liver cells and blood
from the portal vein allows the liver cells to remove and add substances to the blood. Once the blood has
passed through the sinusoids, it is collected in increasingly larger and larger veins that ultimately form a single
vein, the hepatic vein that returns the blood to the heart.
In cirrhosis, the relationship between blood and liver cells is destroyed. Even though the liver cells that survive
or are newly-formed may be able to produce and remove substances from the blood, they do not have the
normal, intimate relationship with the blood, and this interferes with the liver cells' ability to add or remove
substances from the blood. In addition, the scarring within the cirrhotic liver obstructs the flow of blood through
the liver and to the liver cells. As a result of the obstruction to the flow of blood through the liver, blood "backs-
up" in the portal vein, and the pressure in the portal vein increases, a condition called portal hypertension.
Because of the obstruction to flow and high pressures in the portal vein, blood in the portal vein seeks other
veins in which to return to the heart, veins with lower pressures that bypass the liver. Unfortunately, the liver is
unable to add or remove substances from blood that bypasses it. It is a combination of reduced numbers of
liver cells, loss of the normal contact between blood passing through the liver and the liver cells, and blood
bypassing the liver that leads to many of the manifestations of cirrhosis.
A second reason for the problems caused by cirrhosis is the disturbed relationship between the liver cells and
the channels through which bileflows. Bile is a fluid produced by liver cells that has two important functions: to
aid in digestion and to remove and eliminate toxic substances from the body. The bile that is produced by liver
cells is secreted into very tiny channels that run between the liver cells that line the sinusoids, called canaliculi.
The canaliculi empty into small ducts which then join together to form larger and larger ducts. Ultimately, all of
the ducts combine into one duct that enters the small intestine. In this way, bile gets to the intestine where it
can help with the digestion of food. At the same time, toxic substances contained in the bile enter the intestine
and then are eliminated in the stool. In cirrhosis, the canaliculi are abnormal and the relationship between liver
cells and canaliculi is destroyed, just like the relationship between the liver cells and blood in the sinusoids. As
a result, the liver is not able to eliminate toxic substances normally, and they can accumulate in the body. To a
minor extent, digestion in the intestine also is reduced.

What are the symptoms and signs of cirrhosis?
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Patients with cirrhosis may have few or no symptoms and signs of liver disease. Some of the symptoms may
be nonspecific, that is, they don't suggest that the liver is their cause. Some of the more common symptoms
and signs of cirrhosis include:
Yellowing of the skin (jaundice) due to the accumulation of bilirubin in the blood
Fatigue
Weakness
Loss of appetite
Itching
Easy bruising from decreased production of blood clotting factors by the diseased liver.
Patients with cirrhosis also develop symptoms and signs from the complications of cirrhosis that are discussed
next.
What are the complications of cirrhosis?
Edema and ascites
As cirrhosis of the liver becomes severe, signals are sent to the kidneys to retain salt and water in the body.
The excess salt and water first accumulates in the tissue beneath the skin of the ankles and legs because of
the effect of gravity when standing or sitting. This accumulation of fluid is called edema or pitting edema.
(Pitting edema refers to the fact that pressing a fingertip firmly against an ankle or leg with edema causes an
indentation in the skin that persists for some time after release of the pressure. Actually, any type of pressure,
such as from the elastic band of a sock, may be enough to cause pitting.) The swelling often is worse at the
end of a day after standing or sitting and may lessen overnight as a result of the loss of the effects of gravity
when lying down. As cirrhosis worsens and more salt and water are retained, fluid also may accumulate in
theabdominal cavity between the abdominal wall and the abdominal organs. This accumulation of fluid
(called ascites ) causes swelling of the abdomen, abdominal discomfort, and increased weight.
Spontaneous bacterial peritonitis (SBP)
Fluid in the abdominal cavity (ascites) is the perfect place for bacteria to grow. Normally, the abdominal cavity
contains a very small amount of fluid that is able to resist infection well, and bacteria that enter the abdomen
(usually from the intestine) are killed or find their way into the portal vein and to the liver where they are killed.
In cirrhosis, the fluid that collects in the abdomen is unable to resist infection normally. In addition, more
bacteria find their way from the intestine into the ascites. Therefore, infection within the abdomen and the
ascites, referred to as spontaneous bacterial peritonitis or SBP, is likely to occur. SBP is a life- threatening
complication. Some patients with SBP have no symptoms, while others have fever, chills,abdominal pain and
tenderness, diarrhea, and worsening ascites.
Bleeding from esophageal varices
In the cirrhotic liver, the scar tissue blocks the flow of blood returning to the heart from the intestines and raises
the pressure in the portal vein (portal hypertension). When pressure in the portal vein becomes high enough, it
causes blood to flow around the liver through veins with lower pressure to reach the heart. The most common
veins through which blood bypasses the liver are the veins lining the lower part of the esophagus and the upper
part of the stomach.
As a result of the increased flow of blood and the resulting increase in pressure, the veins in the lower
esophagus and upper stomach expand and then are referred to as esophageal and gastric varices; the higher
the portal pressure, the larger the varices and the more likely a patient is to bleed from the varices into the
esophagus or stomach.
Bleeding from varices usually is severe and, without immediate treatment, can be fatal. Symptoms of bleeding
from varices include vomiting blood (thevomitus can be red blood mixed with clots or "coffee grounds" in
appearance, the latter due to the effect of acid on the blood), passing stool that is black and tarry due to
changes in the blood as it passes through the intestine (melena), and orthostatic dizziness or fainting (caused
by a drop inblood pressure especially when standing up from a lying position).
Bleeding also may occur from varices that form elsewhere in the intestines, for example, the colon, but this is
rare. For reasons yet unknown, patients hospitalized because of actively bleeding esophageal varices have a
high risk of developing spontaneous bacterial peritonitis.
Hepatic encephalopathy
Some of the protein in food that escapes digestion and absorption is used by bacteria that are normally present
in the intestine. While using the protein for their own purposes, the bacteria make substances that they release
into the intestine. These substances then can be absorbed into the body. Some of these substances, for
example, ammonia, can have toxic effects on the brain. Ordinarily, these toxic substances are carried from the
intestine in the portal vein to the liver where they are removed from the blood and detoxified.
As previously discussed, when cirrhosis is present, liver cells cannot function normally either because they are
damaged or because they have lost their normal relationship with the blood. In addition, some of the blood in
the portal vein bypasses the liver through other veins. The result of these abnormalities is that toxic substances
cannot be removed by the liver cells, and, instead, the toxic substances accumulate in the blood.
When the toxic substances accumulate sufficiently in the blood, the function of the brain is impaired, a condition
called hepatic encephalopathy. Sleeping during the day rather than at night (reversal of the
normal sleep pattern) is among the earliest symptoms of hepatic encephalopathy. Other symptoms include
irritability, inability to concentrate or perform calculations, loss of memory, confusion, or depressed levels of
consciousness. Ultimately, severe hepatic encephalopathy causes coma and death.
The toxic substances also make the brains of patients with cirrhosis very sensitive to drugs that are normally
filtered and detoxified by the liver. Doses of many drugs that normally are detoxified by the liver have to be
reduced to avoid a toxic buildup in cirrhosis, particularly sedatives and drugs that are used to promote sleep.
Alternatively, drugs may be used that do not need to be detoxified or eliminated from the body by the liver, for
example, drugs that are eliminated by the kidneys.
Hepatorenal syndrome
Patients with worsening cirrhosis can develop the hepatorenal syndrome. This syndrome is a serious
complication in which the function of the kidneys is reduced. It is a functional problem in the kidneys, that is,
there is no physical damage to the kidneys. Instead, the reduced function is due to changes in the way the
blood flows through the kidneys themselves. The hepatorenal syndrome is defined as progressive failure of the
kidneys to clear substances from the blood and produce adequate amounts of urineeven though some other
important functions of the kidney, such as retention of salt, are maintained. If liver function improves or a
healthy liver is transplanted into a patient with hepatorenal syndrome, the kidneys usually begin to work
normally. This suggests that the reduced function of the kidneys is the result of the accumulation of toxic
substances in the blood when the liver fails. There are two types of hepatorenal syndrome. One type occurs
gradually over months. The other occurs rapidly over a week or two.
Hepatopulmonary syndrome
Rarely, some patients with advanced cirrhosis can develop the hepatopulmonary syndrome. These patients
can experience difficulty breathing because certain hormones released in advanced cirrhosis cause the lungs
to function abnormally. The basic problem in the lung is that not enough blood flows through the small blood
vessels in the lungs that are in contact with the alveoli (air sacs) of the lungs. Blood flowing through the lungs is
shunted around the alveoli and cannot pick up enough oxygen from the air in the alveoli. As a result the patient
experiences shortness of breath, particularly with exertion.
Hypersplenism
The spleen normally acts as a filter to remove older red blood cells, white blood cells, and platelets (small
particles that are important for the clotting of blood.). The blood that drains from the spleen joins the blood in
the portal vein from the intestines. As the pressure in the portal vein rises in cirrhosis, it increasingly blocks the
flow of blood from the spleen. The blood "backs-up" and accumulates in the spleen, and the spleen swells in
size, a condition referred to as splenomegaly. Sometimes, the spleen is so swollen that it causes abdominal
pain.
As the spleen enlarges, it filters out more and more of the blood cells and platelets until their numbers in the
blood are reduced. Hypersplenism is the term used to describe this condition, and it is associated with a low
red blood cell count (anemia), low white blood cell count (leucopenia), and/or a low platelet count
(thrombocytopenia). The anemia can cause weakness, the leucopenia can lead to infections, and the
thrombocytopenia can impair the clotting of blood and result in prolonged bleeding.
Liver cancer (hepatocellular carcinoma)
Cirrhosis due to any cause increases the risk of primary liver cancer(hepatocellular carcinoma). Primary refers
to the fact that the tumor originates in the liver. A secondary liver cancer is one that originates elsewhere in the
body and spreads (metastasizes) to the liver.
The most common symptoms and signs of primary liver cancer are abdominal pain and swelling, an enlarged
liver, weight loss, and fever. In addition, liver cancers can produce and release a number of substances,
including ones that cause an increased in red blood cell count (erythrocytosis), low blood sugar
(hypoglycemia), and high blood calcium (hypercalcemia ).


What are the common causes of cirrhosis?
Alcohol is a very common cause of cirrhosis, particularly in the Western world. The development of
cirrhosis depends upon the amount and regularity of alcohol intake. Chronic, high levels of alcohol
consumption injure liver cells. Thirty percent of individuals who drink daily at least eight to sixteen ounces
of hard liquor or the equivalent for fifteen or more years will develop cirrhosis. Alcohol causes a range of
liver diseases; from simple and uncomplicated fatty liver(steatosis), to the more serious fatty liver with
inflammation (steatohepatitisor alcoholic hepatitis), to cirrhosis.
Nonalcoholic fatty liver disease (NAFLD) refers to a wide spectrum of liver diseases that, like alcoholic
liver disease, ranges from simple steatosis, to nonalcoholic steatohepatitis (NASH), to cirrhosis. All stages
of NAFLD have in common the accumulation of fat in liver cells. The term nonalcoholic is used because
NAFLD occurs in individuals who do not consume excessive amounts of alcohol, yet, in many respects,
the microscopic picture of NAFLD is similar to what can be seen in liver disease that is due to excessive
alcohol. NAFLD is associated with a condition called insulin resistance, which, in turn, is associated with
the metabolic syndromeand diabetes mellitus type 2. Obesity is the most important cause of insulin
resistance, metabolic syndrome, and type 2 diabetes. NAFLD is the most common liver disease in the
United States and is responsible for 24% of all liver disease. In fact, the number of livers that are
transplanted for NAFLD-related cirrhosis is on the rise. Public healthofficials are worried that the
current epidemic of obesity will dramatically increase the development of NAFLD and cirrhosis in the
population.
Cryptogenic cirrhosis (cirrhosis due to unidentified causes) is a common reason for liver
transplantation. It is termed cryptogenic cirrhosis because for many years doctors have been unable to
explain why a proportion of patients developed cirrhosis. Doctors now believe that cryptogenic cirrhosis is
due to NASH (nonalcoholic steatohepatitis) caused by long standing obesity, type 2 diabetes,
and insulinresistance. The fat in the liver of patients with NASH is believed to disappear with the onset of
cirrhosis, and this has made it difficult for doctors to make the connection between NASH and cryptogenic
cirrhosis for a long time. One important clue that NASH leads to cryptogenic cirrhosis is the finding of a
high occurrence of NASH in the new livers of patients undergoing liver transplant for cryptogenic cirrhosis.
Finally, a study from France suggests that patients with NASH have a similar risk of developing cirrhosis
as patients with long standing infection with hepatitis C virus. (See discussion that follows.) However, the
progression to cirrhosis from NASH is thought to be slow and the diagnosis of cirrhosis typically is made in
patients in their sixties.
Chronic viral hepatitis is a condition where hepatitis B or hepatitis Cvirus infects the liver for years. Most
patients with viral hepatitis will not develop chronic hepatitis and cirrhosis. For example, the majority of
patients infected with hepatitis A recover completely within weeks, without developing chronic infection. In
contrast, some patients infected with hepatitis B virus and most patients infected with hepatitis C virus
develop chronic hepatitis, which, in turn, causes progressive liver damage and leads to cirrhosis, and,
sometimes, liver cancers.
Inherited (genetic) disorders result in the accumulation of toxic substances in the liver which lead to
tissue damage and cirrhosis. Examples include the abnormal accumulation of iron (hemochromatosis) or
copper (Wilson's disease). In hemochromatosis, patients inherit a tendency to absorb an excessive
amount of iron from food. Over time, iron accumulation in different organs throughout the body causes
cirrhosis, arthritis, heart muscle damage leading to heart failure, and testicular dysfunction causing loss of
sexual drive. Treatment is aimed at preventing damage to organs by removing iron from the body through
bloodletting (removing blood). In Wilson disease, there is an inherited abnormality in one of the proteins
that controls copper in the body. Over time, copper accumulates in the liver, eyes, and brain.
Cirrhosis, tremor, psychiatric disturbances and otherneurological difficulties occur if the condition is not
treated early. Treatment is with oral medication that increases the amount of copper that is eliminated from
the body in the urine.
Primary biliary cirrhosis (PBC) is a liver disease caused by an abnormality of the immune system that is
found predominantly in women. The abnormal immunity in PBC causes chronic inflammation and
destruction of the small bile ducts within the liver. The bile ducts are passages within the liver through
which bile travels to the intestine. Bile is a fluid produced by the liver that contains substances required for
digestion and absorption of fat in the intestine, as well as other compounds that are waste products, such
as the pigment bilirubin. (Bilirubin is produced by the breakdown of hemoglobin from old red blood cells.).
Along with the gallbladder, the bile ducts make up thebiliary tract. In PBC, the destruction of the small bile
ducts blocks the normal flow of bile into the intestine. As the inflammation continues to destroy more of the
bile ducts, it also spreads to destroy nearby liver cells. As the destruction of the hepatocytes proceeds,
scar tissue (fibrosis) forms and spreads throughout the areas of destruction. The combined effects of
progressive inflammation, scarring, and the toxic effects of accumulating waste products culminates in
cirrhosis.
Primary sclerosing cholangitis (PSC) is an uncommon disease found frequently in patients
with ulcerative colitis . In PSC, the large bile ducts outside of the liver become inflamed, narrowed, and
obstructed. Obstruction to the flow of bile leads to infections of the bile ducts and jaundice and eventually
causes cirrhosis. In some patients, injury to the bile ducts (usually as a result of surgery) also can cause
obstruction and cirrhosis of the liver.
Autoimmune hepatitis is a liver disease caused by an abnormality of the immune system that is found
more commonly in women. The abnormal immune activity in autoimmune hepatitis causes progressive
inflammation and destruction of liver cells (hepatocytes), leading ultimately to cirrhosis.
Infants can be born without bile ducts (biliary atresia) and ultimately develop cirrhosis. Other infants
are born lacking vital enzymes for controlling sugars that leads to the accumulation of sugars and
cirrhosis. On rare occasions, the absence of a specific enzyme can cause cirrhosis and scarring of the
lung (alpha 1 antitrypsin deficiency).
Less common causes of cirrhosis include unusual reactions to some drugs and prolonged
exposure to toxins, as well as chronic heart failure (cardiac cirrhosis). In certain parts of the world
(particularly Northern Africa), infection of the liver with a parasite (schistosomiasis) is the most common
cause of liver disease and cirrhosis.




How is cirrhosis diagnosed and evaluated?
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The single best test for diagnosing cirrhosis is biopsy of the liver. Liver biopsies, however, carry a small risk for
serious complications, and, therefore, biopsy often is reserved for those patients in whom the diagnosis of the
type of liver disease or the presence of cirrhosis is not clear. The possibility of cirrhosis may be suggested by
the history, physical examination, or routine testing. If cirrhosis is present, other tests can be used to determine
the severity of the cirrhosis and the presence of complications. Tests also may be used to diagnose the
underlying disease that is causing the cirrhosis. The following are some examples of how doctors discover,
diagnose and evaluate cirrhosis:
In taking a patient's history, the physician may uncover a history of excessive and prolonged intake of
alcohol, a history of intravenous drug abuse, or a history of hepatitis. These pieces of information suggest
the possibility of liver disease and cirrhosis.
Patients who are known to have chronic viral hepatitis B or C have a higher probability of having cirrhosis.
Some patients with cirrhosis have enlarged livers and/or spleens. A doctor can often feel (palpate) the
lower edge of an enlarged liver below the right rib cage and feel the tip of the enlarged spleen below the
left rib cage. A cirrhotic liver also feels firmer and more irregular than a normal liver.
Some patients with cirrhosis, particularly alcoholic cirrhosis, have small red spider-like markings
(telangiectasias) on the skin, particularly on the chest, that are made up of enlarged, radiating blood
vessels. These spider telangiectasias also can be seen in individuals without liver disease, however.
Jaundice (yellowness of the skin and of the whites of the eyes due to elevated bilirubin in the blood) is
common among patients with cirrhosis, but jaundice can occur in patients with liver diseases without
cirrhosis and other conditions such as hemolysis (excessive break down of red blood cells).
Swelling of the abdomen (ascites) and/or the lower extremities (edema) due to retention of fluid is
common among patients with cirrhosis though other diseases can cause them commonly, e.g., congestive
heart failure.
Patients with abnormal copper deposits in their eyes or certain types of neurologic disease may have
Wilson's disease, a genetic disease in which there is abnormal handling and accumulation of copper
throughout the body, including the liver, that can lead to cirrhosis.
Esophageal varices may be found unexpectedly during upper endoscopy (EGD), and they strongly
suggesting cirrhosis.
Computerized tomography (CT or CAT) or magnetic resonance imaging(MRI) scans
and ultrasound examinations of the abdomen done for reasons other than evaluating the possibility of liver
disease may unexpectedly detect enlarged livers, abnormally nodular livers, enlarged spleens, and fluid in
the abdomen that suggest cirrhosis.
Advanced cirrhosis leads to a reduced level of albumin in the blood and reduced blood clotting factors due
to the loss of the liver's ability to produce these proteins. Thus, reduced levels of albumin in the blood or
abnormal bleeding suggest cirrhosis.
Abnormal elevation of liver enzymes in the blood (such as ALT andAST) that are obtained routinely as
part of yearly health examinations suggests inflammation or injury to the liver from many causes as well as
cirrhosis.
Patients with elevated levels of iron in their blood may have hemochromatosis, a genetic disease of the
liver in which iron is handled abnormally and which leads to cirrhosis.
Auto-antibodies (antinuclear antibody, anti-smooth muscle antibody and anti-mitochondrial antibody)
sometimes are detected in the blood and may be a clue to the presence of autoimmune hepatitis
or primary biliary cirrhosis, both of which can lead to cirrhosis.
Liver cancer (hepatocellular carcinoma) may be detected by CT and MRI scans or ultrasound of the
abdomen. Liver cancer most commonly develops in individuals with underlying cirrhosis.
If there is an accumulation of fluid in the abdomen, a sample of the fluid can be removed using a long
needle. The fluid then can be examined and tested. The results of testing may suggest the presence of
cirrhosis as the cause of the fluid.



How is cirrhosis treated?
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Treatment of cirrhosis includes 1) preventing further damage to the liver, 2) treating the complications of
cirrhosis, 3) preventing liver cancer or detecting it early, and 4) liver transplantation.
Preventing further damage to the liver
Consume a balanced diet and one multivitamin daily. Patients with PBC with impaired absorption of fat
soluble vitamins may need additional vitamins D and K.
Avoid drugs (including alcohol) that cause liver damage. All patients with cirrhosis should avoid alcohol.
Most patients with alcohol induced cirrhosis experience an improvement in liver function with abstinence
from alcohol. Even patients with chronic hepatitis B and C can substantially reduce liver damage and slow
the progression towards cirrhosis with abstinence from alcohol.
Avoid nonsteroidal anti-inflammatory drugs (NSAIDs, e.g., ibuprofen). Patients with cirrhosis can
experience worsening of liver and kidney function with NSAIDs.
Eradicate hepatitis B and hepatitis C virus by using anti-viral medications. Not all patients with cirrhosis
due to chronic viral hepatitis are candidates for drug treatment. Some patients may experience serious
deterioration in liver function and/or intolerable side effectsduring treatment. Thus, decisions to treat viral
hepatitis have to be individualized, after consulting with doctors experienced in treating liver diseases
(hepatologists).
Remove blood from patients with hemochromatosis to reduce the levels of iron and prevent further
damage to the liver. In Wilson's disease, medications can be used to increase the excretion of copper in
the urine to reduce the levels of copper in the body and prevent further damage to the liver.
Suppress the immune system with drugs such as prednisone andazathioprine (Imuran) to decrease
inflammation of the liver in autoimmune hepatitis.
Treat patients with PBC with a bile acid preparation, ursodeoxycholic acid (UDCA), also
called ursodiol (Actigall). Results of an analysis that combined the results from several clinical trials
showed that UDCA increased survival among PBC patients during 4 years of therapy. The development
of portal hypertension also was reduced by the UDCA. It is important to note that despite producing clear
benefits, UDCA treatment primarily retards progression and does not cure PBC. Other medications such
as colchicine and methotrexate also may have benefit in subsets of patients with PBC.
Immunize patients with cirrhosis against infection with hepatitis A and B to prevent a serious deterioration
in liver function. There are currently no vaccines available for immunizing against hepatitis C.
Treating the complications of cirrhosis
Edema and ascites. Retention of salt and water can lead to swelling of the ankles and legs (edema) or
abdomen (ascites) in patients with cirrhosis. Doctors often advise patients with cirrhosis to restrict dietary salt
(sodium) and fluid to decrease edema and ascites. The amount of salt in the diet usually is restricted to 2
grams per day and fluid to 1.2 liters per day. In most patients with cirrhosis, however, salt and fluid restriction is
not enough, and diuretics have to be added.
Diuretics are medications that work in the kidneys to promote the elimination of salt and water into the urine. A
combination of the diureticsspironolactone (Aldactone) and furosemide can reduce or eliminate the edema and
ascites in most patients. During treatment with diuretics, it is important to monitor the function of the kidneys by
measuring blood levels ofblood urea nitrogen (BUN) and cretonne to determine if too much diuretic is being
used. Too much diuretic can lead to kidney dysfunction that is reflected in elevations of the BUN and creatinine
levels in the blood.
Sometimes, when the diuretics do not work (in which case the ascites is said to be refractory), a long needle or
catheter is used to draw out the ascitic fluid directly from the abdomen, a procedure called abdominal
paracentesis. It is common to withdraw large amounts (liters) of fluid from the abdomen when the ascites is
causing painful abdominal distension and/or difficulty breathing because it limits the movements of the
diaphragms.
Another treatment for refractory ascites is a procedure called transjugular intravenous portosystemic shunting
(TIPS, see below).
Bleeding from varices. If large varices develop in the esophagus or upper stomach, patients with cirrhosis are
at risk for serious bleeding due to rupture of these varices. Once varices have bled, they tend to rebleed and
the probability that a patient will die from each bleeding episode is high (30%-35%). Therefore, treatment is
necessary to prevent the first (initial) bleeding episode as well as rebleeding. Treatments include medications
and procedures to decrease the pressure in the portal vein and procedures to destroy the varices.
Propranolol (Inderal), a beta blocker, is effective in lowering pressure in the portal vein and is used to
prevent initial bleeding and rebleeding from varices in patients with cirrhosis. Another class of oral
medications that lowers portal pressure is the nitrates, for example, isosorbide dinitrate ( Isordil). Nitrates
often are added to propranolol if propranolol alone does not adequately lower portal pressure or prevent
bleeding.
Octreotide (Sandostatin) also decreases portal vein pressure and has been used to treat variceal
bleeding.
During upper endoscopy (EGD), either sclerotherapy or band ligation can be performed to obliterate
varices and stop active bleeding and prevent rebleeding. Sclerotherapy involves infusing small doses of
sclerosing solutions into the varices. The sclerosing solutions cause inflammation and then scarring of the
varices, obliterating them in the process. Band ligation involves applying rubber bands around the varices
to obliterate them. (Band ligation of the varices is analogous to rubber banding of hemorrhoids.)
Complications of sclerotherapy include esophageal ulcers, bleeding from the esophageal ulcers,
esophageal perforation, esophageal stricture (narrowing due to scarring that can cause dysphagia),
mediastinitis (inflammation in the chest that can cause chest pain), pericarditis (inflammation around the
heart that can cause chest pain), and peritonitis (infection in the abdominal cavity). Studies have shown
that band ligation may be slightly more effective with fewer complications than sclerotherapy.
Transjugular intrahepatic portosystemic shunt (TIPS) is a non-surgical procedure to decrease the
pressure in the portal vein. TIPS is performed by a radiologist who inserts a stent (tube) through a neck
vein, down the inferior vena cava and into the hepatic vein within the liver. The stent then is placed so that
one end is in the high pressure portal vein and the other end is in the low pressure hepatic vein. This tube
shunts blood around the liver and by so doing lowers the pressure in the portal vein and varices and
prevents bleeding from the varices. TIPS is particularly useful in patients who fail to respond to beta
blockers, variceal sclerotherapy, or banding. (TIPS also is useful in treating patients with ascites that do
not respond to salt and fluid restriction and diuretics.) TIPS can be used in patients with cirrhosis to
prevent variceal bleeding while the patients are waiting for liver transplantation. The most common side
effect of TIPS is hepatic encephalopathy. Another major problem with TIPS is the development of
narrowing and occlusion of the stent, causing recurrence of portal hypertension and variceal bleeding and
ascites. The estimated frequency of stent occlusion ranges from 30%-50% in 12 months. Fortunately,
there are methods to open occluded stents. Other complications of TIPS include bleeding due to
inadvertent puncture of the liver capsule or a bile duct, infection, heart failure, and liver failure.
A surgical operation to create a shunt (passage) from the high-pressure portal vein to veins with lower
pressure can lower blood flow and pressure in the portal vein and prevent varices from bleeding. One
such surgical procedure is called distal splenorenal shunt (DSRS). It is appropriate to consider such a
surgical shunt for patients with portal hypertension who have early cirrhosis. (The risks of major shunt
surgery in these patients is less than in patients with advanced cirrhosis.) During DSRS, the surgeon
detaches the splenic vein from the portal vein, and attaches it to the renal vein. Blood then is shunted from
the spleen around the liver, lowering the pressure in the portal vein and varices and preventing bleeding
from the varices.
Hepatic encephalopathy. Patients with an abnormal sleep cycle, impaired thinking, odd behavior, or other
signs of hepatic encephalopathy usually should be treated with a low protein diet and oral lactulose. Dietary
protein is restricted because it is a source of the toxic compounds that cause hepatic encephalopathy.
Lactulose, which is a liquid, traps the toxic compounds in the colon. Consequently, they cannot be absorbed
into the blood stream and cause encephalopathy. To be sure that adequate lactulose is present in the colon at
all times, the patient should adjust the dose to produce 2-3 semiformed bowel movements a day. (Lactulose is
alaxative, and the adequacy of treatment can be judged by loosening or increasing frequency of stools.) If
symptoms of encephalopathy persist, oral antibiotics such as neomycin or metronidazole (Flagyl), can be
added to the treatment regimen. Antibiotics work by blocking the production of the toxic compounds by the
bacteria in the colon.
Hypersplenism. The filtration of blood by an enlarged spleen usually results in only mild reductions of red
blood cells (anemia), white blood cells (leukopenia) and platelets (thrombocytopenia) that do not require
treatment. Severe anemia, however, may require blood transfusions or treatment witherythropoietin or epoetin
alfa (Epogen, Procrit), hormones that stimulate the production of red blood cells. If the numbers of white blood
cells are severely reduced, another hormone called granulocyte-colony stimulating factor is available to
increase the numbers of white blood cells. An example of one such factor is filgrastim (Neupogen).
No approved medication is available yet to increase the number of platelets. As a necessary precaution,
patients with low platelets should not use aspirin or other nonsteroidal antiinflammatory drugs (NSAIDS) since
these drugs can hinder the function of platelets. If a low number of platelets is associated with significant
bleeding, transfusions of platelets usually should be given. Surgical removal of the spleen (called splenectomy)
should be avoided, if possible, because of the risk of excessive bleeding during the operation and the risk
of anesthesia in advanced liver disease.
Spontaneous bacterial peritonitis (SBP). Patients suspected of having spontaneous bacterial peritonitis
usually will undergo paracentesis. Fluid that is removed is examined for white blood cells and cultured for
bacteria. Culturing involves inoculating a sample of the ascites into a bottle of nutrient-rich fluid that encourages
the growth of bacteria, thus facilitating the identification of even small numbers of bacteria. Blood and urine
samples often are obtained as well for culturing because many patients with spontaneous bacterial peritonitis
also will have infection in their blood and urine. In fact, many doctors believe that infection may have begun in
the blood and the urine and spread to the ascitic fluid to cause spontaneous bacterial peritonitis. Most patients
with spontaneous bacterial peritonitis are hospitalized and treated with intravenous antibiotics such
as ampicillin, gentamycin, and one of the newer generation cephalosporin. Patients usually treated with
antibiotics include:
Patients with blood, urine, and/or ascites fluid cultures that contain bacteria.
Patients without bacteria in their blood, urine, and ascitic fluid but who have elevated numbers of white
blood cells (neutrophils) in the asciticfluid(>250 neutrophils/cc). Elevated neutrophil numbers in ascitic fluid
often means that there is bacterial infection. Doctors believe that the lack of bacteria with culturing in some
patients with increased neutrophils is due either to a very small number of bacteria or ineffective culturing
techniques.
Spontaneous bacterial peritonitis is a serious infection. It often occurs in patients with advanced cirrhosis
whose immune systems are weak, but with modern antibiotics and early detection and treatment, the prognosis
of recovering from an episode of spontaneous bacterial peritonitis is good.
In some patients oral antibiotics (such as Cipro or Septra) can be prescribed to prevent spontaneous bacterial
peritonitis. Not all patients with cirrhosis and ascites should be treated with antibiotics to prevent spontaneous
bacterial peritonitis, but some patients are at high risk for developing spontaneous bacterial peritonitis and
warrant preventive treatment:
Patients with cirrhosis who are hospitalized for bleeding varices have a high risk of developing
spontaneous bacterial peritonitis and should be started on antibiotics early during the hospitalization to
prevent spontaneous bacterial peritonitis
Patients with recurring episodes of spontaneous bacterial peritonitis
Patients with low protein levels in the ascitic fluid (Ascitic fluid with low levels of protein is more likely to
become infected.)
Prevention and early detection of liver cancer
Several types of liver disease that cause cirrhosis are associated with a particularly high incidence of liver
cancer, for example, hepatitis B and C, and it would be useful to screen for liver cancer since early surgical
treatment or transplantation of the liver can cure the patient of cancer. The difficulty is that the methods
available for screening are only partially effective, identifying at best only 50% of patients at a curable stage of
their cancer. Despite the partial effectiveness of screening, most patients with cirrhosis, particularly hepatitis B
and C, are screened yearly or every six months with ultrasound examination of the liver and measurements of
cancer-produced proteins in the blood, e.g. alpha fetoprotein.
Liver transplantation
Cirrhosis is irreversible. Many patients' liver function will gradually worsen despite treatment and complications
of cirrhosis will increase and become difficult to treat. Therefore, when cirrhosis is far advanced, liver
transplantation often is the only option for treatment. Recent advances in surgical transplantation and
medications to prevent infection and rejection of the transplanted liver have greatly improved survival after
transplantation. On average, more than 80% of patients who receive transplants are alive after five years. Not
everyone with cirrhosis is a candidate for transplantation. Furthermore, there is a shortage of livers to
transplant, and there usually is a long (months to years) wait before a liver for transplanting becomes available.
Therefore, measures to retard the progression of liver disease and treat and prevent complications of cirrhosis
are vitally important.


What is new and in the future for cirrhosis?
Progress in the management and prevention of cirrhosis continues. Research is ongoing to determine the
mechanism of scar formation in the liver and how this process of scarring can be interrupted or even reversed.
Newer and better treatments for viral liver disease are being developed to prevent the progression to cirrhosis.
Prevention of viral hepatitis by vaccination, which is available for hepatitis B, is being developed for hepatitis C.
Treatments for the complications of cirrhosis are being developed or revised and tested continually. Finally,
research is being directed at identifying new proteins in the blood that can detect liver cancer early or predict
which patients will develop liver cancer.
Cirrhosis At A Glance
Cirrhosis is a complication of liver disease which involves loss of liver cells and irreversible scarring of the
liver.
Alcohol and viral hepatitis B and C are common causes of cirrhosis, although there are many other
causes.
Cirrhosis can cause weakness, loss of appetite, easy bruising, yellowing of the skin (jaundice), itching,
and fatigue.
Diagnosis of cirrhosis can be suggested by the history, physical examination and blood tests, and can be
confirmed by liver biopsy.
Complications of cirrhosis include edema and ascites, spontaneous bacterial peritonitis, bleeding from
varices, hepatic encephalopathy, hepatorenal syndrome, hepatopulmonary syndrome, hypersplenism, and
liver cancer.
Treatment of cirrhosis is designed to prevent further damage to the liver, treat complications of cirrhosis,
and preventing or detecting liver cancer early.
Transplantation of the liver is becoming an important option for treating patients with advanced cirrhosis.

Last Editorial Review: 12/1/2005


Patient Comments: Cirrhosis Of The Liver - Diagnosis

1. Take the Liver Disease Quiz
2. Hepatitis Slideshow: A Visual Guide to Hepatitis
3. Take the Alcohol Quiz
How was your cirrhosis diagnosed?
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Comment from: janet, 55-64 Female (Patient)Published: May 10
I was diagnosed last month with cirrhosis. I had a distended abdomen, and because I had been learning the signs to look
for, because of my drinking habits, I knew it was my liver. I was given tests and was told I have cirrhosis. I quit drinking as
soon as my abdomen was swelling. That has been seven weeks ago. So far, I have remained stable because of cutting out
the alcohol and following my diet and meds. I have faith that the part of my liver that is still functioning will carry me through.
I refuse to give up. My journey has just begun and I will do whatever it takes to prolong the inevitable. I look forward to
sharing my experiences. I am 60 and my cirrhosis was caused from alcohol abuse for the last eight years or so.
Comment from: concernedmom, 45-54 Male (Caregiver)Published: February 19
My son is 46 years old and was diagnosed with non-alcoholic cirrhosis and Hep C after being admitted to the ER for
a stress attack. He never drank but had taken over prescribed pain medication for over five years. His stress attack was
brought on by stopping all medication and this threw him into so much pain he just shut down. He is currently seeing a great
internist, has had his gallbladder out and is going to be evaluated for the transplant list sometime next week. Then he will
begin treatment. He was never a needle user and does not know he contacted Hep C. It looks like he has had it for over 20
years.


Patient Comments: Cirrhosis Of The Liver - Causes

1. Take the Liver Disease Quiz
2. Hepatitis Slideshow: A Visual Guide to Hepatitis
3. Take the Alcohol Quiz
What was the cause of your cirrhosis of the liver?
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Comment from: nottogood, 55-64 Female (Caregiver)Published: November 08
My husband cirrhosis of the liver was alcohol. He started by losing large masses of muscles. Then weight loss. Falls were
frequent. He had to start using a cane because of poor mobility. He now hasascites, edema in his legs, slurred speech. He
has no tolerance for cold drinks and can only eat small amounts of food. His legs and feet have turned red like a sunburn.
He has frequent bowel movements. In general his health is very poor.
Comment from: Brian, 45-54 Male (Patient)Published: May 07
I was diagnosed at age 40. I was a heavy drinker. I havehemochromatosis and had hepatitis C, which was cured thanks to
interferon. I am now 53 don't drink anymore. I do the blood-letting for hemochromatosis and get ultrasounds every six
months. Everything right now is good.
Related Medications: Interferon
Comment from: drjudy, 55-64 Female (Caregiver)Published: February 01
This is probably the most unusual case you ever read. I had Steven's Johnson syndrome as a result of the antibiotic Ceftin.
All my hair fell out and my scalp became colonized with impetigo (Staph). I am a physician and was a hospital pathologist at
that time. I used a strong solution of Minoxodil and Retin-A (Tretinoin) to regrow my hair. Big mistake, the Tretinoin got
systemically absorbed and caused a type of liver cirrhosis that looks like vitamin a induced cirrhosis on the labs and under
the microscope.
Related Medications: Tretinoin
Comment from: VSelo, 65-74 Female (Caregiver)Published: September 26
My mother had about 6-8 drinks daily (at least). She started by having frequent falls, fatty liver and then within days she was
dead of liver failure. It's no laughing matter, but to get an alcoholic to stop drinking is hard. Take this very seriously folks.
Comment from: Amy, 35-44 Female (Patient)Published: January 06
I was recently diagnosed with cirrhosis of the liver. I have never been a drinker. I am suffering with abdominal pain and
swelling, problems sleeping, and I am starting to get dizziness and confusion. I do not have any insurance and am unable to
get treatment if there is any.
Comment from: 55-64 Female (Caregiver)Published: October 13
My dad is 54 years old and he was diagnosed with cirrhosis of the liver. He found out when my mom and him where still
together that was about 10 years ago. I am just now getting to know my father. He also has hepatitis C from doing drugs in
the past. What is my concern is what can happen to him because he doesn't take care of himself like he's supposed to. He
doesn't drink anymore, but smokes and he hasemphysema and COPD and the doctors have told him to slow down
on smoking but he will go through at least a few cartons a month.
Comment from: Diana, 45-54 Female (Patient)Published: October 18
I was diagnosed with NASH, non-alcoholic cirrhosis 2.5 years ago when I woke up vomiting blood and not very coherent. I
was rushed to the Emergency room by my husband and daughter, I had 6 Pints of blood put in me and a TIPS / stent was
placed in my varices to keep me from having another episode. I go to a Liver Clinic every 6 months for MRIs and Blood
work, I was sent by my Gastro for a Liver Transplant, but so far my MELD blood work is at 8, so it has remained stable and I
don't need one now.


Patient Comments: Cirrhosis Of The Liver - Causes

1. Take the Liver Disease Quiz
2. Hepatitis Slideshow: A Visual Guide to Hepatitis
3. Take the Alcohol Quiz
What was the cause of your cirrhosis of the liver?
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Comment from: Ann, 55-64 MalePublished: June 05
My boyfriend of ten years just found out he has cirrhosis of the liver. He fell down a flight of stairs headfirst and had to be
taken to the hospital. After an MRI and a cat scan of his body, it showed the cirrhosis of the liver. He is a good eight drinks a
night person. Mostly alcohol in mixed drinks than anything else. He won't admit to being an alcoholic even now, he laughs at
what the doctor told him. He feels he can control the drinking and he will for a few days and then he feels he's been good
and deserves a drink and then he's back to it every night.
Comment from: Samantha, 25-34 Female (Patient)Published: January 05
My Cirrhosis is causes from my heart problems so they call it medical cirrhosis of the liver. Do to the back pressure of the
blood from the heart. Which mine cannot be fixed as easy I would have to get a heart transplant and the liver as well and
that is not happening any time soon I am only 29 years. old and now having to deal with this since birth a lot of people call
me a fighter and don't know how I do it every day!

I am 34 years old, and I went to the emergency room about week ago for extreme stomach pain. I had occasionally
vomited blood; I believed it was an ulcer. I didn't think anything about the dark color of my stool, except that I haven't
made a solid bowel movement in months, if not a year. I figured it was all related to my ulcer problem. Boy was I
wrong. At the ER, I underwent an ultrasound and three CT scans. I have been a heavy drinker since I was about 16
years old. The CT scan revealed my ulcer, which was no surprise, and then the ER doctor asked me to sit down. I
did, and he then revealed to me that I have cirrhosis of theliver. He told me in the best case, I have 17 to 24 months
to live. Since I don't have insurance, this is my fate. My hands are shaking as I type this. Sorry, I just can't believe that
I have just been given an expiration date like what's on a battery or a gallon of milk. The only thing I can say to this is:
If you have children and they like to party like I did, please inform them of the fate that might be in store for them.
Comment from: Em, 45-54 Female (Caregiver)Published: February 04
I am 32 years old and cannot remember a day when my mother did not have at least one drink. The summer of 2008,
she was diagnosed withhepatitis C and cirrhosis of the liver. She experienced rapid weight loss, jaundice, weakness,
swelling in her legs, redness of her hands and feet, and lethargy. Even after her diagnosis, she continued to drink.
She has since stopped drinking; however, the damage has been done. My days consist of shuffling my mom to and
from different doctor appointments to treat the different ailments that keep arising from her cirrhosis. Now that
sobriety has set in, she can understand the consequences of her actions. It is a shame that she has come to
awareness too little too late. My advice is this: Pay attention to your body, get regular check-ups, and if you suspect
something is wrong with your liver, insist on a blood test. It only takes one test to see if there is a problem. Early
detection and treatment is essential to living a long life.
Comment from: Widowed Caregiver, 45-54 Female (Caregiver)Published: June 05
My husband of 25 years died less than 4 months ago of cirrhosis that he acquired from Hep C and alcoholism. He
ignored his diagnosis of Hep C around three years ago. Did not get treatment for it and continued to drink everyday
after work and all weekend long. Let me make a long story short, he had his first severe fluid retention in May
followed by several hospitalizations. He quit cold turkey drinking so that he could be accepted to get on a liver
transplant list. He was accepted, did everything he was suppose to do, but nothing could stop the disease which took
over our lives. It is a horrible way to die. The progression takes over your entire body and mind, yes your mind. You
are dependent of someone else to do everything for you which that loved one is glad to do, but completely breaks
their heart and soul to watch their spouse go through. He was number 1 on the transplant list but his body was taken
over by constant blood infections, multiple organ failure, and death. Quitting drinking after your liver is damaged is too
late. I am now a widow and our daughter does not have a father and his mother lost her only son and his sisters lost
their only brother. He died at the age of 59. Trust me when I tell you that you do not want to die this way. It is brutal
and completely heartbreaking for your family and friends. Save a life register to become an organ donor today.
Comment from: worn out in Idaho, 55-64 Male (Caregiver)Published: June 02
I have just spent the last 4 hours wrestling someone into bed who is confused and disoriented. They tell me the
cause is an ammonia level of 84 in his blood stream. I got no explanation of what is "normal". He also has
extreme edema in both legs. Here is my problem. We went to a local hospital ER for his Gallbladder, which they
removed. During the course of laparoscopic surgery they discovered chronic hepatitis (which turned out to be C) and
early cirrhosis of the liver. They are telling me that ammonia levels and swelling are due to the "progression of hi s
disease, but he had none of this prior to the removal of his Gallbladder. Is there anyone out there who can explain
this to me?
Comment from: Vegas woman , 55-64 Female (Patient)Published: May 05
I am a 59-year-old woman with cirrhosis of the liver. My skin is yellowish and the whites of my eyes are yellowish.. I
believe my situation is fairly advanced, as I was first notified of my condition in preparation for ovarian cancer surgery
at the end of 2005 (three and a half years ago). I am now experiencing bruising on different areas of my body
including my arms and belly area. There was no apparent trauma or cause for the bruising, it just shows up.

My husband was diagnosed with Cirrhosis of the liver due to alcohol. He was told his liver was in the end stages as he was
being tapped forascites at least once a month, with gallons being extracted. He's also treated with an array of diuretics and a
beta blocker stopped consuming alcohol and eating healthy and after one year has made considerable progress - he's
gained most of his weight back and his energy levels are very good. The specialist tells us his liver has regenerated and
now they are cutting back on his medication. Given enough time, along with healthy living, the liver will regenerate. When it
comes to the liver there is a lot of hope.
Comment from: 45-54 Female (Patient)Published: April 01
This past August I entered the hospital for a typical hernia repair. I am 49 years old, and drank very little over the years, and
not at all for the past 6 years. However, during my hernia repair the surgeon noticed my liver was inflamed and did a biopsy,
which revealed cirrhosis of my liver. I have other health problems, such as degenerative arthritis, so the doctor believes the
cirrhosis was caused by my use of pain medications and combinations of medications for other health conditions. Other than
all of my teeth falling out, I had little or few symptoms at all of the cirrhosis, and since have developed portal hypertension,
for which I am now being treated with Nadolol. Other than that, my liver is still functional, so I am hopeful.
Related Medications: Nadolol
Comment from: 55-64 Male (Patient)Published: March 26
I am 59 years old and drank heavily most of my life, about 40 years. I went to the hospital with weight gain, an oversized
abdomen, swelling in the legs, and ankles. When I was diagnosed with cirrhosis, my right leg was two times larger then my
left. They had to take 7 liters of fluid from the abdomen. I have quit drinking, but it may be too little too late.
Comment from: Sissy, 35-44 Male (Caregiver)Published: February 04
My husband started losing weight for no reason. He had diarrhea most of the time. His stool was black for two months
before he ever told me about it. He started puking up a quart of blood at a time, and we found out the black stool was blood
too. I took him to the hospital, and they immediately put four bags of blood in him. They told us he has cirrhosis of the liver
from drinking too much alcohol. He would drink at least a case of beer a day for the past two and a half years that we have
been married, except for one week when he had to take medicine.
Comment from: Robert, 45-54 Male (Patient)Published: November 18
My cirrhosis was diagnosed when I was hospitalized with marked jaundice. I had been a long-standing alcoholic. For 18
months, I had experienced a loss of sex drive, a lot of weight gain around the abdomen, and a number of falls (when I had
not been drinking). I had been accustomed to walking a lot, but my calves began to feel as if they were carrying lead
weights. There was also a small amount of blood in my stools. (That rapidly worsened.) Within a week of going to the
hospital, I developed hepatorenal syndrome and ended up in intensive care. That was more than three years ago. I no
longer drink, and I am much healthier. Fortunately, no transplant was necessary.
Comment from: Peacock, 25-34 Female (Patient)Published: October 16
I have suffered from JRA and IgE immune problems since the age of 2 resulting with me being in and out of the hospital
most of my early childhood and on some sort of medication. I was diagnosised with PBC a year ago. I was extremely tried,
irritable, constantly having sever sinus infections, feeling of food just sitting on my stomach which followed with vomiting,
problems going to the bathroom, itching all over my torso, arms, legs, hands and feet, to the point where I was scratching
myself bloody and crying at night because I couldn't make it stop which resulted in me not sleeping. It was horrible. I am gl ad
that they found the problem and I am doing much better now after being prescribed Urso Forte.

I have been with my boyfriend for 10 years now. He has always drank beer every night after work. At least 18 beers a night.
He used to start drinking at 3:30 and within a few years it moved up to 2:00. He is almost 38 years old now. He has been
drinking since he was about 20. He drinks until it's time for bed and than wakes up in the middle of the night to eat. He qui t
drinking a week ago. He has that belly of course, but he also has yellow eyes (jaundice). He has pins and needles of the feet
and fatigue. His liver is so fat the doctor told him he could see it through his belly. They are sending him for a biopsy in the
next few weeks. He has lost an incredible amount of weight and kind of looks sickly. I just don't know what to do for him, I
hope it isn't too late.
Comment from: ligiaheldy, 65-74 Female (Patient)Published: May 28
I was wondering if cirrhosis of the liver (non-alcoholic) can cause fingernail disorders such as nail separation. ?
Comment from: lm1, 75 or over Male (Caregiver)Published: June 26
I have just learned that my father has cirrhosis. He has severe fluid retention now in both legs and his abdomen. He has
severe fatigue and general malaise. He is having some mental issues as well. All the doctor had to say was I am in for a
hard time taking care of him. What does that mean?! I am trying to get more information. I want to know how long he has.
He is 81. Evidently, he has had it for a couple of years.
Comment from: Bill, (Caregiver)Published: June 26
My daughter is 41 years old. She took all types of drugs for 20 years. Now she has cirrhosis of the liver. I took her to the
emergency room, and she was in the hospital for five days. The doctor put her on fluid medications, antibiotics and beta
blockers. She lost 30 pounds of fluid. He told her to see her family doctor. She does not have one. I have called four
different doctors and none of them will see her. I was going to pay for the office visit. I hope I can find a doctor to see her to
refill her prescriptions. If not, I will have to take her back to the emergency room. My daughter got hooked on pain killers
when she was hit in the eye and lost her sight in that eye. When the doctor would not give her anymore pain killers, she
turned to street drugs. I am sure this is how a lot of people get started.
Related Medications: Beta Blockers
Comment from: SadWife, 45-54 Female (Caregiver)Published: June 26
My husband has cirrhosis (stage 4). His eyes are yellowish, his breath awful. He has sleepless nights, and itchy blotchy skin.
He is always tired and grumpy. He has taken pain killers for many years, and he has been a regular beer drinker since his
teen years. His MELD score is 11 at the moment. He's on beta blockers. We only found out a few months ago when he had
pain in his stomach and chest area. Now he has three doctors who say his condition is not severe enough for a transplant. I
can't believe how upset he gets over the smallest of things.
Comment from: 45-54 Female (Caregiver)Published: April 22
I'm a wife of one that has hepatitis C, and we just found out that now he has cirrhosis of the liver. I have found that my
husband's memory is very different from mine. He doesn't remember one minute to the next at times. Or sometimes he
doesn't remember what I told him five minutes before. I found out that memory loss can be one of the side effects from
cirrhosis. We have two small kids that I worry for as well.
Comment from: Debbie, 55-64 MalePublished: April 22
My husband has been drinking for years. He is 55 years old and has other family members that have past away because of
their drinking problems. Now he is having all types of problems because of his cirrhosis. His ankles seem to swell more often
now, and the prednisone seems to be doing nothing to help him.