If you have cirrhosis

It is vitally important that patients with liver disease maintain a balanced diet, one which ensures adequate calories, carbohydrates, fats and proteins. Such a diet will aid the liver in the regeneration of liver cells. Nutrition that supports this regeneration is a means of treatment of some liver disorders.

Patients with cirrhosis, for example, who are malnourished, require a diet rich in protein and providing 2,000 – 3,000 calories per day to help the liver re-build itself. However, some cirrhotic patients have protein intolerance. Too much protein will result in an increased amount of ammonia in the blood, while too little protein can reduce healing of the liver. Doctors must carefully prescribe a specific amount of protein that will not elevate the blood ammonia. Lactulose and neomycin are two drugs that help keep the ammonia down.

It is believed that the risk of gallbladder disorders can be reduced by avoiding high fat and cholesterol foods and preventing obesity. The gallbladder is a storage sac for the bile produced by the liver. During digestion, the gallbladder releases bile into the small intestine through the common bile duct. Most gallbladder problems are caused by gallstones and 80-90% of all gallstones are produced from excessive cholesterol which crystallizes and forms stones. By maintaining a well-balanced diet and avoiding high cholesterol intake, the incidence of gallstone formation may be lowered.

If you have cirrhosis, be careful to limit additional liver damage:

  • Don’t drink alcohol. Whether your cirrhosis was caused by chronic alcohol use or another disease, avoid alcohol. Drinking alcohol may cause further liver damage.
  • Eat a low-sodium diet. Excess salt can cause your body to retain fluids, worsening swelling in your abdomen and legs. Use herbs for seasoning your food, rather than salt. Choose prepared foods that are low in sodium.
  • Eat a healthy diet. People with cirrhosis can experience malnutrition. Combat this with a healthy plant-based diet that includes a variety of fruits and vegetables. Choose lean protein, such as legumes, poultry or fish. Avoid raw seafood.
  • Avoid infections. Cirrhosis make sit more difficult for you to fight off infections. Protect yourself by avoiding people who are sick and washing your hands frequently. Get vaccinated for hepatitis A and B, influenza, and pneumonia.
  • Use over-the-counter medications carefully. Cirrhosis makes it more difficult for your liver to process drugs. For this reason, ask your doctor before taking any medications, including nonprescription drugs. Avoid drugs such as aspirin and ibuprofen (Advil, Motrin IB). If you have liver damage, your doctor may recommend you avoid acetaminophen (Tylenol, others) or take it in low doses for pain relief.

People with cirrhosis may need more extra calories and protein. They may lose their appetite and experience nausea, vomiting, and severe weight loss. This can lead to shortage of the minerals calcium and magnesium (signs include muscle cramps, fatigue, weakness, nausea, and vomiting), or a shortage of zinc (signs include reduced ability to taste, changes in taste).

It can help to eat small, frequent meals (4 to 7 times a day), including an evening snack.

When the scarring from cirrhosis prevents blood from passing through the liver, pressure increases in the veins entering the liver. This is called portal hypertension. The body is forced to reroute the blood away from the liver and into the general blood circulation. This causes large blood vessels, called “varices,” to form.

Because the rerouted blood bypasses the liver, it contains high levels of amino acids, ammonia, and toxins that normally would have been handled by the liver. When these substances reach the brain, they can cause confusion and temporary loss of memory (a condition called “hepatic encephalopathy”).

Amino acids and ammonia come from protein in the diet. Some evidence shows that patients with cirrhosis do better when they get their protein from vegetables (such as beans, lentils, and tofu) and from dairy products (eggs, milk, yogurt) instead of from meats.

General recommendations for patients with severe liver disease include:

  • Eat large amounts of carbohydrate foods. Carbohydrates should be the major source of calories in this diet.
  • Eat a moderate intake of fat, as prescribed by the health care provider. The increased carbohydrates and fat help prevent protein breakdown in the liver.
  • Have about 1 gram of protein per kilogram of body weight. This means that a 154-pound (70-kilogram) man should eat 70 grams of protein per day. This does not include the protein from starchy foods and vegetables. A person with a badly damaged liver may need to eat less protein. Talk to your doctor about your protein needs.
  • Take vitamin supplements, especially B-complex vitamins.
  • Reduce the amount of salt you consume (typically less than 1500 milligrams per day) if you are retaining fluid.

Hepatitis

Hepatitis (plural: hepatitides) is a medical condition defined by the inflammation of the liver and characterized by the presence of inflammatory cells in the tissue of the organ. Hepatitis may occur with limited or no symptoms, but often leads to jaundice, poor appetite and malaise. Hepatitis is acute when it lasts less than six months and chronic when it persists longer. The condition can be self-limiting (healing on its own) or can progress to fibrosis (scarring) and cirrhosis.

Worldwide,  causes include autoimmune diseases and ingestion of toxic substances (notably alcohol, certain medications, some industrial organic solvents, and plants).

Viral hepatitis is the most common cause of hepatitis worldwide.[5] Other common causes of non-viral hepatitis include toxic and drug-induced, alcoholic, autoimmune, fatty liver, and metabolic disorders.[6] Less commonly some bacterial, parasitic, fungal, mycobacterial and protozoal infections can cause hepatitis.[7][8] Additionally, certain complications of pregnancy and decreased blood flow to the liver can induce hepatitis.[7][9] Cholestasis (obstruction of bile flow) due to hepatocellular dysfunction, biliary tract obstruction, or biliary atresia can result in liver damage and hepatitis.[10][11]

The term is derived from the Greek hêpar (ἧπαρ), meaning “liver,” and the suffix -itis (-ῖτις), meaning “inflammation” (c. 1727).[2]

Non-alcoholic fatty liver disease (NAFLD) is one cause of a fatty liver, occurring when fat is deposited (steatosis) in the liver not due to excessive alcohol use. It is related to insulin resistance and the metabolic syndrome and may respond to treatments originally developed for other insulin-resistant states (e.g. diabetes mellitus type 2) such as weight loss, metformin and thiazolidinediones.[1] Non-alcoholic steatohepatitis (NASH) is the most extreme form of NAFLD, and is regarded as a major cause of cirrhosis of the liver of unknown cause.[2]

Most patients with NAFLD have few or no symptoms. Patients may complain of fatigue, malaise, and dull right-upper-quadrant abdominal discomfort. Mild jaundice may be noticed although this is rare. More commonly NAFLD is diagnosed following abnormal liver function tests during routine blood tests. By definition, alcohol consumption of over 20 g/day (about 25 ml/day of net ethanol) excludes the condition.[1]

NAFLD is associated with insulin resistance and metabolic syndrome (obesity, combined hyperlipidemia, diabetes mellitus (type II) and high blood pressure).[1][2]

Common findings are elevated liver enzymes and a liver ultrasound showing steatosis. An ultrasound may also be used to exclude gallstone problems (cholelithiasis). A liver biopsy(tissue examination) is the only test widely accepted as definitively distinguishing NASH from other forms of liver disease and can be used to assess the severity of the inflammationand resultant fibrosis.[1]

Non-invasive diagnostic tests have been developed, such as FibroTest, that estimates liver fibrosis,[7] and SteatoTest, that estimates steatosis,[8] however their use has not been widely adopted.[9] Apoptosis has been indicated as a potential mechanism of hepatocyte injury as caspase-cleaved cytokeratin 18 (M30-Apoptosense ELISA) in serum/plasma is often elevated in patients with NASH; however, as the role of oncotic necrosis has yet to be examined it is unknown to what degree apoptosis acts as the predominant form of injury.[10][11]

Other diagnostic tests are available. Relevant blood tests include erythrocyte sedimentation rate, glucose, albumin, and renal function. Because the liver is important for making proteins used in coagulation some coagulation related studies are often carried out especially the INR (international normalized ratio). Blood tests (serology) are usually used to rule out viral hepatitis (hepatitis A, B, C and herpes viruses like EBV or CMV), rubella, and autoimmune related diseases. Hypothyroidism is more prevalent in NASH patients which would be detected by determining the TSH.[12]

It has been suggested that in cases involving overweight patients whose blood tests do not improve on losing weight and exercising that a further search of other underlying causes be undertaken. This would also apply to those with fatty liver who are very young or not overweight or insulin-resistant. In addition those whose physical appearance indicates the possibility of a congenital syndrome, have a family history of liver disease, have abnormalities in other organs, and those that present with moderate to advanced fibrosis or cirrhosis.[13]

Management

A large number of treatments for NAFLD have been studied. While many appear to improve biochemical markers such as alanine transaminase levels, most have not been shown to reverse histological abnormalities or reduce clinical endpoints:[1]

  • Treatment of nutrition and excessive body weight:
    • Nutritional counseling: Diet changes have shown significant histological improvement.[14] Specifically, avoiding food containing high-fructose corn syrup and trans-fats is recommended.[15]
    • Weight loss: gradual weight loss may improve the process in obese patients; rapid loss may worsen NAFLD. Specifically, walking or some form of aerobic exercise at least 30–45 minutes daily is recommended.[15] The negative effects of rapid weight loss are controversial: the results of a meta-analysis showed that the risk of progression is very low.[16]
    • A recent meta-analysis presented at the Annual Meeting of the American Association for the Study of Liver Diseases (AASLD) reported that weight-loss surgery leads to improvement and or resolution of NASH in around 80% of patients.[17]
  • Insulin sensitisers (metformin[18] and thiazolidinediones[19]) have shown efficacy in some studies.
  • ursodeoxycholic acid and lipid-lowering drugs, have little benefit.[citation needed]
  • Vitamin E: Vitamin E can improve some symptoms of NASH and was superior to insulin sensitizer in one large study. In the Pioglitazone versus Vitamin E versus Placebo for the Treatment of Nondiabetic Patients with Nonalcoholic Steatohepatitis (PIVENS) trial, for patients with NASH but without diabetes mellitus, the use of very high dosages of vitamin E (800 IU/day) for four years was associated with a significantly higher rate of improvement than placebo (43% vs. 19%) in the primary outcome. The primary outcome was an improvement in certain histological features as measured by biopsy—but it did not improve fibrosis. Pioglitazone, an insulin sensitizer, improved some features of NASH but not the primary outcome, and resulted in a significant weight gain (mean 4.7 kilograms) which persisted after pioglitazone was discontinued.[20]
  • Statin: Improvements in liver biochemistry and histology in patients with NAFLD through treatment with statins have been observed in numerous cases, although these studies were carried out on a relatively small sample of patients.[21] Statins have also been recommended for use in treating dyslipidemia for patients with NAFLD.
  • Modest wine drinking: In a study using the NHANES III dataset, it has been shown that mild alcohol consumption (one glass of wine a day) reduces the risk of NAFLD by half.[22]

Epidemiology

The prevalence of non-alcoholic fatty liver disease ranges from 9 to 36.9% of the population in different parts of the world.[23][24][25] Approximately 20% of the United States population suffers from non-alcoholic fatty liver, and the prevalence of this condition is increasing.[26] The prevalence of non-alcoholic fatty liver disease is higher in Hispanics, which can be attributed to high rates of obesity and type 2 diabetes in Hispanic populations.[27] Non-alcoholic fatty liver disease is also more common among men than women in all age groups until age 60, where the prevalence between sex equalize. This is due to the protective nature of estrogen.[28]