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 inflammation.
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 for diagnosis.
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 levels.
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
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 easily.
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 medical attention.
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 liver fails.
Other serious complications of cirrhosis of the liver include:
Reduced oxygen in the blood.
Changes in blood counts.
Increased risk of infections.
Excessive bleeding and bruising.
Breast enlargement in men.
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 include:
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
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 proper scanning of all symptoms which help in individualization.