Cirrhosis is a slowly progressing disease in
which healthy liver tissue is replaced with scar tissue, eventually
preventing the liver from functioning properly. This scarring of tissue
is irreversible and can be life threatening in advanced age.
In cirrhosis of the liver, scar tissue replaces normal, healthy tissue,
blocking the flow of blood through the organ and preventing it from
working as it should. Cirrhosis is the eighth leading cause of death by
disease, killing about 25,000 people each year.
Cirrhosis has many possible causes; sometimes more than one cause is
present in the same patient. In the Western World, chronic alcoholism
and hepatitis C are the most common causes.
- Alcoholic liver disease (ALD). Alcoholic cirrhosis develops
for between 10% and 20% of individuals who drink heavily for a decade
or more. There is great variability in the amount of alcohol needed
to cause cirrhosis (as little as 3-4 drinks a day in some men and 2-3
in some women). Alcohol seems to injure the liver by
blocking the normal metabolism of protein, fats, and carbohydrates.
Patients may also have concurrent alcoholic hepatitis with fever,
hepatomegaly, jaundice, and anorexia. AST and ALT are both elevated but
less than 300 IU/L with a AST:ALT ratio > 2.0, a value rarely
seen in other liver diseases. Liver biopsy may show hepatocyte
necrosis, Mallory bodies, neutrophilic infiltration with perivenular
- Chronic hepatitis C. Infection with the hepatitis C virus
causes inflammation of the liver and a variable grade of damage to the
organ that over several decades can lead to cirrhosis. Cirrhosis caused
by hepatitis C is the most common reason for liver transplant. Can be
diagnosed with serologic assays that detect hepatitis C antibody or
viral RNA. The enzyme immunoassay, EIA-2, is the most commonly used
screening test in the US.
- Chronic hepatitis B. The hepatitis B virus causes liver
inflammation and injury that over several decades can lead to
cirrhosis. Hepatitis D is dependent on the presence of hepatitis B, but
accelerates cirrhosis in co-infection. Chronic hepatitis B can be
diagnosed with detection of HBsAG > 6 months after initial
infection. HBeAG and HBV DNA are determined to assess whether patient
will need antiviral therapy.
- Non-alcoholic steatohepatitis (NASH). In NASH, fat builds
up in the liver and eventually causes scar tissue. This type of
hepatitis appears to be associated with diabetes, protein malnutrition,
obesity, coronary artery disease, and treatment with corticosteroid
medications. This disorder is similar to that of alcoholic liver
disease but patient does not have an alcohol history. Biopsy is needed
- Primary biliary cirrhosis. May be asymptomatic or complain
of fatigue, pruritus, and non-jaundice skin hyperpigmentation with
hepatomegaly. There is prominent alkaline phosphatase elevation as well
as elevations in cholesterol and bilirubin. Gold standard diagnosis is
antimitochondrial antibodies with liver biopsy as confirmation if
showing florid bile duct lesions. It is more common in women.
- Primary sclerosing cholangitis. PSC is a progressive
cholestatic disorder presenting with pruritus, steatorrhea, fat soluble
vitamin deficiencies, and metabolic bone disease. There is a strong
association with inflammatory bowel disease (IBD), especially
ulcerative colitis. Diagnosis is best with contrast cholangiography
showing diffuse, multifocal strictures and focal dilation of bile
ducts, leading to a beaded appearance. Non-specific serum
immunoglobulins may also be elevated.
- Autoimmune hepatitis. This disease is caused by the
immunologic damage to the liver causing inflammation and eventually
scarring and cirrhosis. Findings include elevations in serum globulins,
especially gamma globulins. Therapy with prednisone +/- azathioprine is
beneficial. Cirrhosis due to autoimmune hepatitis still has 10-year
survival of 90%+. There is no specific tool to diagnose autoimmune but
it can be beneficial to initiate a trial of corticosteroids.
- Hereditary hemochromatosis. Usually presents with family
history of cirrhosis, skin hyperpigmentation, diabetes mellitus,
pseudogout, and/or cardiomyopathy, all due to signs of iron overload.
Labs will show fasting transferrin saturation of > 60% and
ferritin > 300 ng/mL. Genetic testing may be used to identify
HFE mutations. If these are present, biopsy may not need to be
performed. Treatment is with phlebotomy to lower total body iron
- Wilson's disease. Autosomal recessive disorder
characterized by low serum ceruloplasmin and increased hepatic copper
content on liver biopsy. May also have Kayser-Fleischer rings in the
cornea and altered mental status.
- Alpha 1-antitrypsin deficiency (AAT). Autosomal recessive
disorder. Patients may also have COPD, especially if they have a
history of tobacco smoking. Serum AAT levels are low. Recombinant AAT
is used to prevent lung disease due to AAT deficiency.
- Cardiac cirrhosis. Due to chronic right sided heart failure
which leads to liver congestion.
- Glycogen storage disease type IV
- Cystic fibrosis
- Hepatotoxic drugs or toxins
- Certain parasitic infections (such as schistosomiasis)
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
- Loss of appetite
- Easy bruising from decreased production of blood clotting
factors by the diseased liver.
- Sudden weight loss or gain.
- Confusion, disorientation and personality changes.
Edema and ascites. When the liver loses its ability to make the protein
albumin, water accumulates in the leg (edema) and abdomen (ascites).
Bruising and bleeding. When the liver slows or stops production of the
proteins needed for blood clotting, a person will bruise or bleed
Jaundice. Jaundice is a yellowing of the skin and eyes that occurs when
the diseased liver does not absorb enough bilirubin.
Itching. Bile products deposited in the skin may cause intense itching.
Gallstones. If cirrhosis prevents bile from reaching the gallbladder, a
person may develop gallstones.
Toxins in the blood or brain. A damaged liver cannot remove toxins from
the blood, causing them to accumulate in the blood and eventually the
brain. This is known as hepatic encephalopathy. There, toxins can dull
mental functioning and cause personality changes, coma, and even death.
Signs of the buildup of toxins in the brain include neglect of personal
appearance, unresponsiveness, forgetfulness, trouble concentrating, or
changes in sleep habits.
Sensitivity to medication. Cirrhosis slows the liver's ability to
filter medications from the blood. Because the liver does not remove
drugs from the blood at the usual rate, they act longer than expected
and build up in the body. This causes a person to be more sensitive to
medications and their side effects.
Portal hypertension. Normally, blood from the intestines and spleen is
carried to the liver through the portal vein. But cirrhosis slows the
normal flow of blood through the portal vein, which increases the
pressure inside it. This condition is called portal hypertension.
Varices. When blood flow through the portal vein slows, blood from the
intestines and spleen backs up into blood vessels in the stomach and
esophagus. These blood vessels may become enlarged because they are not
meant to carry this much blood. The enlarged blood vessels, called
varices, have thin walls and carry high pressure, and thus are more
likely to burst. If they do burst, the result is a serious bleeding
problem in the upper stomach or esophagus that requires immediate
Problems in other organs. Cirrhosis can cause immune system
dysfunction, leading to infection. Ascites (fluid) in the abdomen may
become infected with bacteria normally present in the intestines, and
cirrhosis can also lead to kidney dysfunction and failure.
Hepatorenal Syndrome. The hepatorenal syndrome is defined as
progressive failure of the kidneys to clear substances from the blood
and produce adequate amounts of urine even 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
Other serious complications of cirrhosis of the liver include:
- Kidney failure.
- Reduced oxygen in the blood.
- Changes in blood counts.
- Increased risk of infections.
- Excessive bleeding and bruising.
- Breast enlargement in men.
- Premature menopause.
- Loss of muscle mass.
The diagnosis of cirrhosis is usually based on the presence of a risk
factor for cirrhosis, such as alcohol use or obesity, and is confirmed
by physical examination, blood tests, and imaging. The doctor will ask
about the person's medical history and symptoms and perform a thorough
physical examination to observe for clinical signs of the disease.
1.Complete blood count
2.Liver Function Test
5.Imaging- Ultrasonography, CT-scan, MRI.
Other laboratory studies performed in newly diagnosed cirrhosis may
- Serology for hepatitis viruses, autoantibodies (ANA,
anti-smooth muscle, anti-mitochondria, anti-LKM)
- Ferritin and transferrin saturation (markers of iron
overload), copper and ceruloplasmin (markers of copper overload)
- Immunoglobulin levels (IgG, IgM, IgA) - these are
non-specific but may assist in distinguishing various causes
- Cholesterol and glucose
- Alpha 1-antitrypsin
It must be-
1.Treating underlying cause.
2.Preventing further damage of liver tissue.
a.Avoid taking alcohol
b.Avoid mixing alcohol and drugs.
d.Take nutritious and balanced diet.
Role of homoeopathy-
Homeopathic medicines treat the underlying cause
of Cirrhosis of Liver as given above. It also helps in preventing
further damage to tissues, complications and transplantation unless
major pathology is not present. The medicine is selected after properly
considering all symptoms, which help in individualization.
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