Cirrhosis liver how long can you live

Life expectancy by stage Increasing life expectancy Coping with diagnosis Cirrhosis of the liver is one of the final stages of liver disease. Share on Pinterest Image credit: Getty Images. Life expectancy by stage. CTP class 3-month survival rate 1-year survival rate 2-year survival rate Class A Increasing life expectancy. Coping with a diagnosis.

Exposure to air pollutants may amplify risk for depression in healthy individuals. Costs associated with obesity may account for 3. Related Coverage. Everything you need to know about cirrhosis. Medically reviewed by Daniel Murrell, MD. What is liver fibrosis? What to know about liver failure and liver disease stages. Diet for jaundice: What to eat for a healthy liver. Medically reviewed by Natalie Olsen, R. Statistical testing was performed using R-software.

The Mann—Whitney U -test was used to test for differences between groups. A p-value of less than 0. The survival curves were estimated by the Kaplan-Meier estimator, using years as the time-scale and taking delayed entry into account. Differences between groups were investigated by Wald test in Cox proportional hazards model, with age as the time-scale, adjusting for gender, calendar year of diagnosis and age of diagnosis.

The primary end-point was death from all causes. Overall liver biopsies were performed at the University Hospital of Iceland during the study period. A total of patients with at least one index biopsy were identified by the computerized search in the pathology database as having fatty liver on biopsy.

Those who were misclassified and did not have fatty liver on review were excluded Figure 1. A total of patients were excluded for other reasons than based on histopathology Figure 1.

The remaining study group of patients had no signs of viral hepatitis in the index liver biopsy and did not receive any medication known to be associated with the development of steatosis. Medical records from these patients were traced and the biopsies reviewed by experienced pathologists. Clinical and biochemical data at the time of index liver biopsy in the patients of the two study groups Table 1. No significant difference was found in the BMI between the two groups Table 1.

The clinical data on other diseases associated with the metabolic syndrome at the time of index liver biopsy and at the end of follow-up period in the two study groups are shown in Table 2. The two groups had also similar morbidity in terms of conditions associated with metabolic syndrome both at baseline and at follow-up Table 2. The histological characteristics in the index liver biopsy are summarized in Table 3.

Patients developing liver cirrhosis and liver related complications are demonstrated in Table 4. The median survival was Median follow-up time for the non-alcoholic group was 9. There was no significant difference in overall survival between the two study groups and no significant difference between genders data not shown. The hazard ratio for women in the AFLD group was 1. Kaplan Meier survival plots showing survival from day of birth after correcting for age, gender and year of diagnosis for the none to mild fibrosis group green line and moderate to severe fibrosis group red line.

In the AFLD group six men and three women died of liver-related disease. In the AFLD group, 4 died of breast cancer and one each of renal cancer, malignant brain tumor, colon cancer, nasopharyngeal cancer and pancreas cancer.

In the NAFLD group, two died of breast cancer and one each of prostate cancer, multiple myeloma, endometrial cancer and one of small cell lung cancer. Few studies have determined the natural history of biopsy-proven fatty liver disease and compared the long-term prognosis of these two major groups of fatty liver disease due to alcoholic and non-alcoholic fatty liver disease. Our study has several methodological strengths. First, all patients had biopsy proven fatty liver disease and histology was re-evaluated based on validated scores.

The fact that all the patients underwent a liver biopsy is also a weakness, especially when evaluating disease outcome. Previous studies have shown that NAFLD patients diagnosed with liver biopsy have a worse prognosis compared with patients diagnosed with ultrasonography. Therefore, studying patients recruited from the pathology registry involves a selection bias. The main limitation of the study was its retrospective design and data was not systematically registrered and was therefore sometimes missing or unavailable.

In addition the search for the code M fatty liver is limiting in itself as the more serious steatosis with fibrosis and even cirrhosis might be coded as something else than just fatty liver. Since this was a retrospective study on liver biopsies it is not possible to standardize the size of the needle biopsies.

Therefore the size is very variable and the range can be considerable, but should be similar to the standards observed in pathology departments in general. Samples less than 2 mm in diameter would have been excluded from the study, but no such samples came into the study.

The slides used for pathological estimation were the original slides and recuts or restaining of slides was not done except for a few exceptional cases where the original slides were unavailable or when a Masson-Trichrome stain had not been performed originally. Occationally the colours of the slides had faided somewhat. This however we do not anticipate having significant effect on the results, especially since ballooning degeneration increases cell size and this is not greatly affected by fading colours.

Another limitation is the small number of hard endpoints with only four patients in the NAFLD group who developed cirrhosis over the follow-up period. There is also a potential uncertainty in the non-histological diagnosis of cirrhosis which must be taken into consideration when reviewing the results.

One of the main findings in this study was that patients with fatty liver disease showed a markedly higher risk of developing liver-related death compared to the general population. These findings are in contrast with liver-related death rate in Iceland [ 13 ] which was a mean of 0.

As in other studies it is a challenge to classify patients into non-alcoholic and alcoholic group. We tried to minimize the misclassification by regrouping those without a known alcohol etiology if the patients were found to have an alcoholic related diagnosis later as for instance alcohol pancreatitis and alcohol dependence. People who have had varices in the past may need to take medicine to prevent future episodes.

Hepatic encephalopathy is treated by cleansing the bowel with lactulose-a laxative given orally or in enemas. Antibiotics are added to the treatment if necessary. Patients may be asked to reduce dietary protein intake. Hepatic encephalopathy may improve as other complications of cirrhosis are controlled.

Some people with cirrhosis who develop hepatorenal failure must undergo regular hemodialysis treatment, which uses a machine to clean wastes from the blood.

Medications are also given to improve blood flow through the kidneys. Other treatments address the specific causes of cirrhosis. Treatment for cirrhosis caused by hepatitis depends on the specific type of hepatitis. For example, interferon and other antiviral drugs are prescribed for viral hepatitis, and autoimmune hepatitis requires corticosteroids and other drugs that suppress the immune system. Medications are given to treat various symptoms of cirrhosis, such as itching and abdominal pain.

When is a liver transplant indicated for cirrhosis? A liver transplant is considered necessary when complications cannot be controlled by treatment. Liver transplantation is a major operation in which the diseased liver is removed and replaced with a healthy one from an organ donor.

A team of health professionals determines the risks and benefits of the procedure for each patient. Survival rates have improved over the past several years because of drugs that suppress the immune system and keep it from attacking and damaging the new liver. The number of people who need a liver transplant far exceeds the number of available organs.

A person needing a transplant must go through a complicated evaluation process before being added to a long transplant waiting list. Generally, organs are given to people with the best chance of living the longest after a transplant.

Survival after a transplant requires intensive follow-up and cooperation on the part of the patient and caregiver. What causes cirrhosis? Most people who consume alcohol do not suffer damage to the liver. But heavy alcohol use over several years can cause chronic injury to the liver.

The amount of alcohol it takes to damage the liver varies greatly from person to person. For women, consuming two to three drinks-including beer and wine-per day and for men, three to four drinks per day, can lead to liver damage and cirrhosis. In the past, alcohol-related cirrhosis led to more deaths than cirrhosis due to any other cause.

Deaths caused by obesity-related cirrhosis are increasing. Chronic hepatitis C The hepatitis C virus is a liver infection that is spread by contact with an infected person's blood. Chronic hepatitis C causes inflammation and damage to the liver over time that can lead to cirrhosis. Chronic hepatitis B and D The hepatitis B virus is a liver infection that is spread by contact with an infected person's blood, semen, or other body fluid. Hepatitis B, like hepatitis C, causes liver inflammation and injury that can lead to cirrhosis.

The hepatitis B vaccine is given to all infants and many adults to prevent the virus. Hepatitis D is another virus that infects the liver and can lead to cirrhosis, but it occurs only in people who already have hepatitis B. This increasingly common liver disease is associated with obesity, diabetes, protein malnutrition, coronary artery disease, and corticosteroid medications. Autoimmune hepatitis This form of hepatitis is caused by the body's immune system attacking liver cells and causing inflammation, damage, and eventually cirrhosis.

Researchers believe genetic factors may make some people more prone to autoimmune diseases. About 70 percent of those with autoimmune hepatitis are female. Diseases that damage or destroy bile ducts Several diseases can damage or destroy the ducts that carry bile from the liver, causing bile to back up in the liver and leading to cirrhosis. In adults, the most common condition in this category is primary biliary cirrhosis, a disease in which the bile ducts become inflamed and damaged and, ultimately, disappear.

Secondary biliary cirrhosis can happen if the ducts are mistakenly tied off or injured during gallbladder surgery.

Primary sclerosing cholangitis is another condition that causes damage and scarring of bile ducts. In infants, damaged bile ducts are commonly caused by Alagille syndrome or biliary atresia, conditions in which the ducts are absent or injured.

Inherited diseases Cystic fibrosis, alpha-1 antitrypsin deficiency, hemochromatosis, Wilson disease, galactosemia, and glycogen storage diseases are inherited diseases that interfere with how the liver produces, processes, and stores enzymes, proteins, metals, and other substances the body needs to function properly.

Cirrhosis can result from these conditions. Drugs, toxins, and infections Other causes of cirrhosis include drug reactions, prolonged exposure to toxic chemicals, parasitic infections, and repeated bouts of heart failure with liver congestion.

Complications of Cirrhosis Because the liver becomes lumpy and stiff in cirrhosis, blood cannot flow through it easily, so pressure builds up in the vein that brings blood to the liver. Edema and ascites When liver damage progresses to an advanced stage, fluid collects in the legs, called edema, and in the abdomen, called ascites.

Ascites can lead to bacterial peritonitis, a serious infection. Bruising and bleeding When the liver slows or stops producing the proteins needed for blood clotting, a person will bruise or bleed easily.

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, which increases the pressure in the portal vein. This condition is called portal hypertension. Esophageal varices and gastropathy When portal hypertension occurs, it may cause enlarged blood vessels in the esophagus, called varices, or in the stomach, called gastropathy, or both.

Enlarged blood vessels are more likely to burst due to thin walls and increased pressure. If they burst, serious bleeding can occur in the esophagus or upper stomach, requiring immediate medical attention. Am J Gastroenterol. AME Medical Journal. Morgan TR. Treatment of alcoholic liver disease. Gastroenterol Hepatol. Cleveland Clinic. Cirrhosis of the liver. Updated November 1, Fairbanks KD.

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I Accept Show Purposes. Table of Contents View All. Table of Contents. Recap In the early stages of alcoholic liver disease, you may have no symptoms.

Recap Your prognosis is based on your individual lab results. Frequently Asked Questions What is the life expectancy of someone with cirrhosis of the liver? Your doctor will score your liver disease based on number of factors, including: Bilirubin Protein in the blood How long it takes blood to clot Fluid build-up Hepatic encephalopathy, a nervous system disorder caused by toxins building up in your body Your healthcare provider will estimate your two-year survival rate based on these scores.

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