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What is liver cirrhosis?
Cirrhosis is a chronic liver disease characterized by the presence of scar tissue (fibrosis) and widespread nodules (consisting of regenerating liver cells)
Normal hepatocytes are damaged and reduced, the consequence being a decrease in hepatic biochemical function.
What are the principle causes of liver cirrhosis?
Causes of cirrhosis are many, but the final result is the same.
Cirrhosis is an endpoint of many chronic liver diseases, because inflammation and cell death eventually yield to fibrosis and nodule formation.
Liver cirrhosis affects hundreds of millions of people worldwide.
There are many conditions that can lead to cirrhosis, and they are summarized in the following list.
| 1) |
Chronic hepatitis B |
| 2) |
Chronic hepatitis C |
| 3) |
Chronic hepatitis D |
| 4) |
Chronic autoimmune hepatitis |
| 5) |
Alcoholic liver disease |
| Less frequently |
| 6) |
Inborn abnormalities (hemocromatosis and Wilson's disease, abnormal handling by the body respectively of iron and copper)
|
| 7) |
Chronic bile duct diseases (e.g. biliary
cirrhosis) |
| 8) |
Drug-related liver disease |
| 9) |
Chronic congestive heart failure |
| 10) |
Parasitic infection (e.g. schistosomiasis) |
What are the consequences of liver
cirrhosis?
The fibrosis and nodule formation cause a distortion of normal structure of the liver with interference of blood flow through the
organ.
An important consequence is an increased pressure of the portal vein
(blood from the gut and the spleen enter the portal vein through which it is brought to the
liver).
This obstacled efflux of portal vein yields:
| a) |
Spleen enlargement with sequestration and destruction of blood cells
(reduction of leucocytes, platelets, erithrocytes)
|
| b) |
Blood flows backwards from the portal vein and this anormality can lead to varicoses varices in the stomach and esophagus
(gastric and esophageal varices) and rectum (hemorroids); rupture of varices can occur with massive bleeding
|
| c) |
Along with hormonal (aldosterone
increase), metabolic (albumin reduction) and kidney abnormalities can lead to fluid accumulation in the abdomen
(ascites) and peripheral tissue
(edema)
|
 Moreover abnormal liver functions may cause
decreased bilirubin secretion by the liver ( with jaundice)
reduction of albumin (ascites formation) and blood clotting (bleeding
complication) synthesis.
Finally in liver cirrhosis, especially in advanced cases, some
toxic metabolites, produced in the gut and normally removed from
the blood by the liver can reach the brain, the consequence
being encephalopathy (subtle mental changes advancing to
profound confusion and coma).
How is liver cirrhosis diagnosed?
Many patients may have no symptoms and the cirrhosis is diagnosed only by physical examination and laboratory tests or when a complication (ascites, hemorrage) occurs.
Other cirrhotics experience loss of appetite, jaundice, itching (due to bile products in the skin) weakness, occurrence of red palms, spider angiomata, hypertrophy of the parotid glands, gynecomastia or fibrosis of tendons in the palms. In advanced cirrhosis ascites, vomiting blood as a consequence of esophageal varices rupture and encephalopathy can occur.
Liver tests are always altered:
| a) |
Increase of liver enzymes in the blood (transaminases, alkaline phosphate, gammaGT), bilirubin, gammaglobulins
|
| b) |
Decrease of albumin, cholinesterase, coagulation factors (e.g.protrombin time)
|
| c) |
Derangement in the metabolism of tryglicerides, cholesterol and sugar. Cirrhosis can cause insulin resistence and diabetes
mellitus.
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As far as the cause is concerned, it is necessary to determine the presence of viral markers, autoantibodies, and to exclude iron or copper metabolism derangement, etc. Obviously a careful history of regular or eccessive alcohol intake must be investigated.
Liver biopsy, not always necessary, shows the presence of nodules with fibrosis and gives information about activity of the disease (inflammation and necrosis of liver cells).
Finally ultrasound or computed tomography shows enlarged liver and spleen, presence of initial ascites and excludes malignant nodules (hepatocellular carcinoma). Esophago-gastroscopy is important in order to evaluate the presence and extension of varices.
What is the risk for cirrhotic patients?
Over the years, if the patient continues drinking alcohol or if the activity of the virus involved is high, decompensation may appear (ascites, hemorrage from ruptured varices, encephalopathy etc.).
Hepatocellular carcinoma can occur in liver cirrhosis (3-4% yearly).
What is the treatment of liver cirrhosis?
Liver cirrhosis is irreversible but treatment of the underlying disease may slow or stop the progression. The therapy is related to the cause of the cirrhosis.
In alcoholic forms total abstinence from alcohol is mandatory.
In cirrhosis related to hepatitis B virus lamivudine is effective, even in advanced cases.
In cirrhosis due to hepatitis C virus interferon, interferon+ ribavirin can reduce inflammation, fibrosis and
probably the risk of hepatocellular carcinoma occurrence. The new pegylated interferon, under study , administered once a week for long time, might be the drug of choice for this aim in the future. These drugs cannot be administrated to advanced liver cirrhosis because of the side effects.
In these cases treatment must be directed at the complications.
Ascites and edema are treated with low sodium diet, water restriction and administration of diuretics. In non-responding patients paracenthesis has to be performed (evacuation by a needle of fluids from abdomen).
Bleeding esophageal varices are treated with endoscopic sclerotherapy or rubber band ligation. The rupture can be prevented by the administration of some drugs (e.g.betablockers).
Encephalopathy responds to low protein diet and lactulose.
Liver transplantation is highly effective for the treatment of end-stage cirrhosis.
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