Cirrhosis
Cirrhosis, irreversible liver damage characterized by scarring, or fibrosis, and widespread formation of nodules in the liver. If left untreated, the liver becomes unable to carry out its functions, resulting in complications that affect many different systems of the body.
Cirrhosis can result from virtually any chronic liver disease. When hepatocytes, the major liver cells, are damaged or die, they are replaced by scar tissue. Liver tissue may also regenerate in an abnormal pattern, forming tiny balls known as nodules.
A number of inherited metabolic diseases can cause cirrhosis, such as hemochromatosis (abnormal accumulation of iron), Wilson’s disease (inability to metabolize copper), and some forms of alpha-1-antitrypsin deficiency (inability to produce the alpha-1-antitrypsin protein). Cirrhosis can also result from certain autoimmune diseases in which the body’s immune system attacks and destroys liver tissue. In some parts of the world, parasitic infections are a common cause.
Especially in its early stages, cirrhosis is often symptomless. Some patients suffer from fatigue, particularly when they exercise. Some experience itching due to a buildup of bile, a yellowish brown liquid that aids in the digestion of fats, in the blood and skin. Later in the disease, the formation of nodules distorts the liver’s structure. This distortion slows the flow of blood through the liver, causing an increase of blood pressure in the portal vein, the main blood vessel that empties into the liver. This increase in blood pressure, known as portal hypertension, can lead to the formation of enlarged, twisted varicose veins in the stomach and esophagus. If these veins rupture, life-threatening internal bleeding can develop. Portal hypertension can also cause the spleen to become enlarged and trap platelets (tiny blood cells that aid in clotting), impairing the body’s ability to repair wounds.
As the liver's capacity to function is compromised, a variety of complications develop throughout the body. Jaundice results from the liver’s inability to process bilirubin, a pigment that forms as a result of the breakdown of old red blood cells. The buildup of this pigment causes the yellow discoloration of the skin and eyes characteristic of jaundice. Decreased production of a blood protein known as albumin, along with hormonal and kidney abnormalities, leads to retention of fluid, especially in the abdomen. Decreased production of clotting factors by the liver makes cirrhosis patients bruise and bleed easily. Inefficiency in breaking down toxins in the blood can cause neurological symptoms, including confusion, sleeplessness, and even coma. Cachexia, a general loss of weight and strength due to poor absorption of nutrients, can also develop.
The surest way to diagnose cirrhosis, especially in the earlier stages when symptoms are minimal, is by liver biopsy, in which a doctor uses a hollow needle to collect a small sample of liver tissue. In more advanced cases, symptoms such as jaundice, fluid in the abdomen, and generalized muscle wasting suggest a diagnosis of cirrhosis. Blood tests that show low albumin levels, elevated bilirubin levels, clotting problems, or other abnormalities can also point toward cirrhosis. Radiological tests such as ultrasound can sometimes detect advanced cases of cirrhosis.
Although cirrhosis is irreversible, treating the underlying cause of the liver damage can dramatically limit further destruction of liver tissue and help prevent the development of complications. For alcoholic cirrhosis, abstinence from alcohol is the key element of treatment. Damage from the hepatitis B or C virus can be limited with antiviral drugs such as alpha interferon. In patients with hemochromatosis, removal of blood to decrease iron levels in the body helps prevent liver damage. In advanced cases of cirrhosis, the goal of treatment is managing complications such as fluid retention, internal bleeding, and neurological symptoms. When drugs and other medical interventions can no longer control such complications, liver transplantation can be lifesaving.
Cirrhosis can result from virtually any chronic liver disease. When hepatocytes, the major liver cells, are damaged or die, they are replaced by scar tissue. Liver tissue may also regenerate in an abnormal pattern, forming tiny balls known as nodules.
A number of inherited metabolic diseases can cause cirrhosis, such as hemochromatosis (abnormal accumulation of iron), Wilson’s disease (inability to metabolize copper), and some forms of alpha-1-antitrypsin deficiency (inability to produce the alpha-1-antitrypsin protein). Cirrhosis can also result from certain autoimmune diseases in which the body’s immune system attacks and destroys liver tissue. In some parts of the world, parasitic infections are a common cause.
Especially in its early stages, cirrhosis is often symptomless. Some patients suffer from fatigue, particularly when they exercise. Some experience itching due to a buildup of bile, a yellowish brown liquid that aids in the digestion of fats, in the blood and skin. Later in the disease, the formation of nodules distorts the liver’s structure. This distortion slows the flow of blood through the liver, causing an increase of blood pressure in the portal vein, the main blood vessel that empties into the liver. This increase in blood pressure, known as portal hypertension, can lead to the formation of enlarged, twisted varicose veins in the stomach and esophagus. If these veins rupture, life-threatening internal bleeding can develop. Portal hypertension can also cause the spleen to become enlarged and trap platelets (tiny blood cells that aid in clotting), impairing the body’s ability to repair wounds.
As the liver's capacity to function is compromised, a variety of complications develop throughout the body. Jaundice results from the liver’s inability to process bilirubin, a pigment that forms as a result of the breakdown of old red blood cells. The buildup of this pigment causes the yellow discoloration of the skin and eyes characteristic of jaundice. Decreased production of a blood protein known as albumin, along with hormonal and kidney abnormalities, leads to retention of fluid, especially in the abdomen. Decreased production of clotting factors by the liver makes cirrhosis patients bruise and bleed easily. Inefficiency in breaking down toxins in the blood can cause neurological symptoms, including confusion, sleeplessness, and even coma. Cachexia, a general loss of weight and strength due to poor absorption of nutrients, can also develop.
The surest way to diagnose cirrhosis, especially in the earlier stages when symptoms are minimal, is by liver biopsy, in which a doctor uses a hollow needle to collect a small sample of liver tissue. In more advanced cases, symptoms such as jaundice, fluid in the abdomen, and generalized muscle wasting suggest a diagnosis of cirrhosis. Blood tests that show low albumin levels, elevated bilirubin levels, clotting problems, or other abnormalities can also point toward cirrhosis. Radiological tests such as ultrasound can sometimes detect advanced cases of cirrhosis.
Although cirrhosis is irreversible, treating the underlying cause of the liver damage can dramatically limit further destruction of liver tissue and help prevent the development of complications. For alcoholic cirrhosis, abstinence from alcohol is the key element of treatment. Damage from the hepatitis B or C virus can be limited with antiviral drugs such as alpha interferon. In patients with hemochromatosis, removal of blood to decrease iron levels in the body helps prevent liver damage. In advanced cases of cirrhosis, the goal of treatment is managing complications such as fluid retention, internal bleeding, and neurological symptoms. When drugs and other medical interventions can no longer control such complications, liver transplantation can be lifesaving.
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