27 July, 2017
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Life Expectancy of Cirrhosis of the Liver
When your liver becomes damaged due to disease, a condition known as cirrhosis, scar tissue builds up in your liver and keeps it from functioning properly. Unlike some of your body's organs---your spleen and gall bladder, for example---you cannot live without your liver. It filters out toxins in your blood and creates essential nutrients. Though a mildly damaged liver can usually repair itself, severe cirrhosis will shorten your lifespan.
When your liver becomes damaged due to disease, a condition known as cirrhosis, scar tissue builds up in your liver and keeps it from functioning properly. Unlike some of your body’s organs—your spleen and gall bladder, for example—you cannot live without your liver. It filters out toxins in your blood and creates essential nutrients. Though a mildly damaged liver can usually repair itself, severe cirrhosis will shorten your lifespan.
Because the liver is such a vital organ, your life can be substantially shortened if your liver becomes too damaged to function properly. As with any life-threatening condition, the number of years lost will vary from person to person, depending on whether there are any other complicating conditions present. If you have cirrhosis of the liver due to heavy alcohol use and you stop drinking and begin a healthy lifestyle with plenty of nutritious food and exercise, you will have a high likelihood of reversing or at least halting the progress of your liver damage. If however, you continue with excessive drinking and an unhealthy lifestyle, the probability of an early death from liver disease is greatly increased.
Like high blood pressure, cirrhosis is often a silent killer. Often there are no symptoms until the condition is serious or even irreversible. People who do experience symptoms may be fatigued, have swelling in their legs and abdomen, feel nauseated, bruise or bleed easily, and have an unexpected loss of appetite and weight loss. Although you may not feel any symptoms, a simple blood test at regular intervals (during your yearly physical exam, for instance) can detect potential liver problems. Discovering liver damage early can help extend your lifespan.
There are several diseases that contribute to cirrhosis. The most prevalent are long-term alcohol abuse and Hepatitis B and C. Too much iron or copper in the body can also result in liver damage, while cystic fibrosis, fatty liver disease, and inadequate or damaged bile ducts can also cause cirrhosis. In some developing countries, parasites can contribute to liver disease. In all these conditions, scar tissue builds up in the liver over time and can drastically shorten life expectancy.
Risk factors for cirrhosis include the long-term abuse of alcohol. Intravenous drug users are also at high risk for cirrhosis since Hepatitis B and C can be contracted through sharing needles. These diseases can also be passed along through unsanitized tattoo or piercing needles. In earlier years, surgery patients sometimes contacted Hepatitis C through blood transfusions, but the blood supply in the U.S. today is screened to prevent this. Other risk factors for cirrhosis include genetic factors such as the malformation or dysfunction of bile ducts, as well as conditions like cystic fibrosis.
Although cirrhosis itself cannot be cured, treatment of the conditions and diseases that caused it can help the liver repair itself to some degree. If you have Hepatitis B or C, antiviral treatments can assist in managing these conditions and limiting the injury to your liver. Ending the use of alcohol is imperative and if you find it difficult, seek out a program that will assist you. When cirrhosis has advanced too far, a liver transplant is the only solution. Though this surgery requires a whole liver from an organ donor, it requires only a partial liver from a compatible living person, perhaps a child or sibling. By either reducing the danger to your liver in mild cirrhosis or replacing your liver in advanced cirrhosis, your chances for a longer lifespan is greatly increased.