The term "hepatitis" means inflammation, and liver cells can become inflamed because of infection.

Hepatitis A is a viral infection that is spread primarily through the fecal-oral route when small amounts of infected fecal matter are inadvertently ingested. Hepatitis A causes an acute inflammation of the liver which generally resolves spontaneously. The hepatitis A vaccine can prevent this infection. Thorough handwashing, especially when preparing food is the best way to prevent the spread of hepatitis A.

Hepatitis B is spread by exposure to body fluids (needles from drug abusers, contaminated blood, and sexual contact) and can cause an acute infection, but can also progress to cause chronic inflammation (chronic hepatitis) that can lead to cirrhosis and liver cancer. The hepatitis B vaccinecan prevent this infection.

Hepatitis C causes chronic hepatitis. An infected individual may not recall any acute illness. Hepatitis C is spread by exposure to body fluids (needles from drug abusers, contaminated blood, and sexual contact). Chronic hepatitis C may lead to cirrhosis and liver cancer. At present, there is no vaccine against this virus.

Cirrhosis

• Cirrhosis is scarring of the liver and poor liver function. It is the final phase of chronic liver disease.

  Causes

  Cirrhosis is the end result of chronic liver damage caused by chronic liver diseases. Common causes of chronic liver disease in the United States include:

  • Hepatitis C infection (long-term infection)
  • Long-term alcohol abuse (see alcoholic liver disease)

  Other causes of cirrhosis include:

  • Autoimmune inflammation of the liver
  • Disorders of the drainage system of the liver (the biliary system), such as primary biliary cirrhosis andprimary sclerosing cholangitis
  • Hepatitis B (long-term infection)
  • Medications
  • Metabolic disorders of iron and copper (hemochromatosis and Wilson's disease)
  • Nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH)

  Symptoms

  Symptoms may develop gradually, or there may be no symptoms.

  When symptoms do occur, they can include:

  • Confusion or problems thinking
  • Impotence, loss of interest in sex, and breast development (gynecomastia) in men
  • Loss of appetite
  • Nausea and vomiting
  • Nosebleeds or bleeding gums
  • Pale or clay-colored stools
  • Small, red spider-like blood vessels on the skin
  • Swelling or fluid buildup of the legs (edema) and in the abdomen (ascites)
  • Vomiting blood or blood in stools
  • Weakness
  • Weight loss
  • Yellow color in the skin, mucus membranes, or eyes (jaundice)

Possible Complications

• Bleeding disorders (coagulopathy)
• Buildup of fluid in the abdomen (ascites) and infection of the fluid (bacterial peritonitis)
• Enlarged veins in the esophagus, stomach, or intestines that bleed easily (esophageal varices)
• Increased pressure in the blood vessels of the liver (portal hypertension)
• Kidney failure (hepatorenal syndrome)
• Liver cancer (hepatocellular carcinoma)
• Mental confusion, change in the level of consciousness, or coma (hepatic encephalopathy)

  Prevention

  Don't drink alcohol heavily. If you find that your drinking is getting out of hand, seek professional help.

  Measures for preventing the transmission of hepatitis B or C include:

  • Avoid sexual contact with a person who has acute or chronic hepatitis B or C.
  • Use a condom and practice safe sex.
  • Avoid sharing personal items, such as razors or toothbrushes.
  • Do not share drug needles or other drug paraphernalia (such as straws for snorting drugs).
  • Clean blood spills with a solution containing 1 part household bleach to 10 parts water.

Alcoholic liver disease

Alcoholic liver disease is a term that encompasses the hepatic manifestations of alcohol over consumption, including fatty liver, alcoholic hepatitis, and chronic hepatitis with hepatic fibrosis or cirrhosis. 

It is the major cause of liver disease in Western countries. Although steatosis (fatty liver) will develop in any individual who consumes a large quantity of alcoholic beverages over a long period of time, this process is transient and reversible. Of all chronic heavy drinkers, only 15–20% develop hepatitis or cirrhosis, which can occur concomitantly or in succession.

 

How alcohol damages the liver is not completely understood. 80% of alcohol passes through the liver to be detoxified. Chronic consumption of alcohol results in the secretion of pro-inflammatory cytokines (TNF-alpha, IL6 and IL8), oxidative stress, lipid peroxidation, and acetaldehyde toxicity. These factors cause inflammation, apoptosis and eventually fibrosis of liver cells. Why this occurs in only a few individuals is still unclear. Additionally, the liver has tremendous capacity to regenerate and even when 75% of hepatocytes are dead, it continues to function as normal.

 

The risk factors presently known are:

• Quantity of alcohol taken: consumption of 60–80g per day (about 75–100 ml/day) for 20 years or more in men, or 20g/day (about 25 ml/day) for women significantly increases the risk of hepatitis and fibrosis by 7 to 47%

 

• Pattern of drinking: drinking outside of meal times increases up to 2.7 times the risk of alcoholic liver disease.

 

• Gender: females are twice as susceptible to alcohol related liver disease, and may develop alcoholic liver disease with shorter durations and doses of chronic consumption. The lesser amount of alcohol dehydrogenase secreted in the gut, higher proportion of body fat in women, and changes in fat absorption due to the with menstrual cycle may explain this phenomenon.

 

• Hepatitis C infection: a concomitant hepatitis C infection significantly accelerates the process of liver injury.

 

• Genetic factors: genetic factors predispose both to alcoholism and to alcoholic liver disease. Monozygotic twins are more likely to be alcoholics and to develop liver cirrhosis than dizygotic twins. Polymorphisms in the enzymes involved in the metabolism of alcohol, such as ADH, ALDH, CYP4502E1, mitochondrial dysfunction, and cytokine polymorphism may partly explain this genetic component. However, no specific polymorphisms have currently been firmly linked to alcoholic liver disease.

 

• Iron overload (hemochromatosis) Diet: malnutrition, particularly vitamin A and E deficiencies, can worsen alcohol-induced liver damage by preventing regeneration of hepatocytes. This is particularly a concern as alcoholics are usually malnourished because of a poor diet, anorexia, and encephalopathy.