Fatty liver and liver chirrosis

Fatty liver and liver chirrosos: Description: Fatty liver is an abnormal accumulation of certain fats (triglycerides) inside liver cells. Fatty liverThese conditions cause fat to accumulate in liver cells either by causing the body to synthesize more fat or by processing (metabolizing) and excreting fat more slowly. As a result, fat accumulates and is then stored inside liver cells. Just consuming a high-fat diet does not result in fatty liver. Microvesicular steatosis, a rare form of fatty liver, can develop in certain genetically susceptible women during pregnancy. The fatty liver may or may not be inflamed. Inflammation may then develop into scarring (fibrosis). Fibrosis often progresses into cirrhosis. Fatty liver (with or without fibrosis) due to any condition except alcoholism is called nonalcoholic steatohepatitis. This disorder develops most often in people with the metabolic syndrome. Symptoms: Cirrhosis takes years to develop. In the early stages of cirrhosis, many people experience no symptoms. However, as the disease progresses and fatty liver function deteriorates, symptoms may develop. The most common signs and symptoms include: 1. Loss of appetite 2. Weight loss 3. Nausea 4. Weakness 5. Fatigue or exhaustion 6. Loss of interest in sex Evidence of cirrhosis may not develop until a patient experiences complications of the disease. When this happens, signs and symptoms that may be present include: 1. Spider-like veins (spider angiomas) that develop under the skin 2. Abdominal pain from an enlarged liver 3. Yellowing of the skin and whites of the eyes (jaundice) 4. Dark, cola-colored urine. 5. Fluid in the abdominal cavity (ascites). 6. Swelling of the legs and feet (edema) 7. Vomiting of blood. 8. Increased sensitivity to drugs 9. Itching of the hands and feet that spread to other parts of the body. 10. Mental confusion, such as forgetfulness or difficulty concentrating, or brain damage (encephalopathy). 11. Abnormal nerve function (peripheral neuropathy) 12. Enlarged breasts in men (gynecomastia). 13. Shrinking (atrophy) of testicles in men. 14. Gallstones. 15. Excessive or prolonged bleeding 16. Bruising easily. 17. Esophageal vein bleeding. Treatment: There is no cure for cirrhosis. The liver is capable of repairing some damage, but it is limited. The focus of treatment is to prevent or delay further progression of the disease and to reduce complications. This may involve treating the underlying cause of the disease. All patients, including those with cirrhosis caused by alcohol abuse, must stop drinking alcohol. Some patients require assistance to help them quit, which may involve a chemical dependency evaluation, intervention, counseling, support groups, outpatient treatment program or inpatient residential program. Other drugs that may be related to liver damage should also be avoided. These include acetaminophen, some other over-the-counter drugs and certain vitamin supplements. Patients with cirrhosis, regardless of the cause of the disease, must follow a healthy diet because the liver requires nutrients to heal. In addition, patients should avoid eating raw seafood because of the potential presence of bacteria. A diet that restricts salt may also be recommended because of the potential for swelling (edema) and fluid in the abdomen (ascites). Patients with cirrhosis caused by hepatitis may be treated with medication, such as interferon for viral hepatitis or corticosteroids for autoimmune hepatitis. Treatment may also involve treating complications of the disease, including: Portal hypertension: Medications that lower blood pressure, such as beta blockers, may be prescribed to lower pressure in the portal vein. Bleeding blood vessels: Medications may be prescribed to reduce bleeding from blood vessels. Patients may also undergo medical procedures to stop bleeding. Fluid retention: Patients may be treated with medications called diuretics to reduce fluid buildup in the legs or abdomen. Some patients require fluid to be removed from the abdominal cavity with a needle using local anesthetic. Patients may require antibiotics to lessen the possibility of bacterial peritonitis. Itching: Patients may be treated with antihistamines to help stop itching. Hepatic encephalopathy: Patients may be treated with lactulose, a medication that helps lower blood ammonia, or antibiotics, which reduce the amount of ammonia-producing bacteria in the intestines. Fatty liver Transplant: When the liver is so severely damaged that it does not function, patients need a liver transplant. This involves removing the damaged liver and replacing it with one from an organ donor. Though liver transplantation is successful in a large number of patients, the number of patients who need a new liver is much larger than the number of donated organs. In addition, newer technologies, such as living donors who donate a portion of their liver to another person, are being performed. These transplants may become increasingly available to people seeking a liver. Causes and Risk factors: In the United States, the leading cause of cirrhosis is chronic alcoholism. Alcoholic cirrhosis usually occurs after a decade or more of heavy drinking, although the amount of alcohol that results in damage to the liver varies among individuals. Some people who drink occasionally (social drinkers) may also develop cirrhosis. The liver breaks down alcohol into highly toxic chemicals, some of which trigger inflammation that eventually destroys liver cells. Other, less common, causes of cirrhosis include: Autoimmune hepatitis: A liver disease in which the immune system attacks liver cells. This causes inflammation of the liver, which may be severe and chronic and result in cirrhosis. Nonalcoholic steatohepatitis (NASH): Inflammation and excessive fat buildup in the liver that is not associated with alcohol use. This can lead to inflammation and the development of scar tissue. Inherited diseases: These include diseases that cause high levels of certain minerals to accumulate in the liver, such as Wilson's disease (which causes copper buildup) or hemochromatosis (which causes iron buildup). Cystic fibrosis (a chronic disease characterized by the buildup of thick sticky mucus in the lungs and digestive tract), glycogen storage diseases (which hinder the body's use of sugar) and alpha 1-antitrypsin deficiency (a disorder in which the liver produces an abnormal amount of a protective protein) can also lead to cirrhosis. Blocked or inflamed bile ducts: Certain diseases, such as primary biliary cirrhosis and primary sclerosing cholangitis, can cause bile ducts to become inflamed, blocked or scarred. Bile ducts transport bile (which is produced in the liver) to the gallbladder and small intestine. There is chronic inflammation and eventual scarring of the biliary system with subsequent liver cell damage and cirrhosis. Primary sclerosing cholangitis can also lead to bile duct cancer. Parasitic infection: Infection with schistosoma, a parasite that occurs mainly in tropical countries, may lead to liver damage and result in cirrhosis. Cardiac cirrhosis: This type of heart failure can lead to liver congestion or damage. Prolonged exposure to toxins: People who are exposed to environmental toxins, such as arsenic, face a higher risk of developing cirrhosis. Diagnosis: Cirrhosis may be diagnosed by a physician during a physical examination that includes a medical history and list of medications. A physician can sometimes identify early stages of cirrhosis by gently pressing the abdomen to determine whether the liver is enlarged and firm. During later stages of the disease the liver shrinks, causing an enlarged spleen which a physician may also identify by gently touching the abdomen. If a patient is suspected to have cirrhosis, blood tests may be performed. These can detect changes in the body that occur as a result of cirrhosis. The tests include: Hematology Tests: The patient with cirrhosis is often anemic and also tends to have larger-than-normal spleens, which leads to abnormally low platelet counts. The loss of functioning liver leads to less clotting protein production and abnormal coagulation labs. Liver Function Test: When a liver is damaged, it releases enzymes, which may be detected with a blood test. Bilirubin Test: Bilirubin (substance formed from the breakdown of red blood cells that gives bile its color) is processed in the liver and excreted in urine. When the liver is damaged, it cannot process bilirubin, leading to high levels of bilirubin in the blood. Imaging tests that detect liver damage may also be performed. They include: Ultrasound: An imaging technology that uses sound waves to produce images of the shape and outline of various tissues and organs of the body. CAT scan: A test that allows for multiple x-rays to be taken from different angles around the patient. It creates images of organs and bones within the body. MRI: Safe and noninvasive or minimally invasive imaging test that can help physicians diagnose diseases of numerous organs and vessels. It uses powerful magnets to produce images on a computer screen and film. Liver Scan: A radioactive substance (radioisotope) that highlights the liver is injected into a vein. After the liver absorbs the substance, the liver is scanned and images are displayed on a computer screen. Laparoscopy: A laparoscope (thin, lighted tube with a tiny video camera) is inserted into the abdomen through a small incision. Images are displayed on a computer screen.. Liver Biopsy: A liver biopsy is often performed to confirm a diagnosis of cirrhosis. During this procedure, a needle is inserted into the abdomen and a tiny sample of liver tissue is removed. The tissue is examined under a microscope for the presence of scarring or other signs of disease. Medicine and medication: Large amounts of SAMe (S-adenosylmethionine) may improve survival and fatty liver function in alcoholic liver cirrhosis. A double-blind trial found that 1,200 mg of SAMe per day for two years significantly decreased the overall death rate and the need for liver transplantation in people with alcoholic liver cirrhosis, particularly in those with less advanced fatty liver disease. Preliminary trials suggest that lower amounts of SAMe (180 mg per day in one trial12 and 800 mg per day in another13) may improve liver function in people with liver cirrhosis. SAMe supplementation has been shown to reverse the depletion of glutathione, an important antioxidant required for liver function.14. It has also been shown to aid in the resolution of blocked bile flow (cholestasis), a common complication of liver cirrhosis. In addition to protein deficiency as discussed above, liver cirrhosis is characterized by low blood levels of branched-chain amino acids (BCAAs) in relation to other amino acids. This imbalance may contribute to the development of PSE. BCAA supplementation could be a way to correct this problem, as well as to provide a source of needed protein, but its effectiveness is unclear. BCAAs (isoleucine, leucine, and valine) represent a good protein source for people with cirrhosis because they are less likely to induce PSE. A controlled study of protein-intolerant people with cirrhosis showed that BCAA supplementation corrected abnormal protein metabolism about as well as an equivalent amount of dietary protein without inducing PSE as frequently. In a small double-blind trial, people with liver cirrhosis taking 5 grams per day of BCAAs had significant improvement in their ability to process protein. However, treatment trials using BCAAs alone or in solutions containing other amino acids in people with cirrhosis and PSE have reported conflicting results. It may be that certain people with liver cirrhosis can benefit from supplementation with BCAAs while others cannot, for reasons that are unclear. In a double-blind trial, people with liver cirrhosis and PSE received 0.24 grams per 2.2 pounds body weight (approximately 16-17 grams per day) of BCAAs for 15 days, after which most experienced significant improvement in brain function, mental status, and protein metabolism. Those who continued taking BCAAs for three months also had mild improvement in liver function tests. Therapeutic effects of oral BCAAs have also been shown in children with fatty liver failure and in adults with cirrhosis of the liver without PSE.29. Overall, it appears that BCAA supplementation does not always help in cirrhosis, but some people with and without PSE may benefit. A qualified doctor must closely supervise such BCAA supplementation. In a study of people with cirrhosis, supplementing with 10 grams of fermentable fiber per day (containing equal parts of beta-glucan, insulin, pectin, and resistant starch) for 30 days resulted in an improvement in liver function. The impaired brain function that often accompanies cirrhosis of the liver (hepatic encephalopathy) also improved. Phosphatidylcholine (PC) breaks down scar tissue in the liver and may be able to reverse tissue changes that cause cirrhosis. Alcoholic fatty liver cirrhosis is associated with zinc deficiency, zinc acetate supplementation (200 mg three times daily, providing a total of 215 mg of elemental zinc per day), given to cirrhosis patients for seven days, significantly improved portal-systemic encephalopathy (PSE). A second trial achieved similar results after three months of treatment. People with cirrhosis sometimes have impaired taste function, and it has been suggested that zinc deficiency may be the cause of this abnormality. Although one study demonstrated that taste problems in cirrhosis are due to the disease process itself and not to zinc deficiency, a double-blind trial showed that 200 mg three times per day of zinc sulfate (providing 135 mg of elemental zinc per day) for six weeks significantly improved taste function in people with alcoholic liver cirrhosis. A doctor should supervise long-term supplementation of zinc in these amounts. People with cirrhosis have decreased secretion of bile acids. Supplementation with bile acids (such as ursodeoxycholic acid and tauroursodeoxycholic acid) may improve the composition of bile and delay disease progression in primary biliary cirrhosis (PBC). In one trial, people with PBC were followed for five to nine years. Those who took 13-15 mg per 2.2 pounds body weight of ursodeoxycholic acid (about 900-1200 mg) per day had improved liver function tests and significantly delayed progression to cirrhosis. Several other trials have confirmed that bile acids improve liver function in people with PBC. Commercial supplements of bile acids are available as ox bile concentrates. However, these ox bile preparations contain other types of bile acids than those used in PBC research. The effectiveness and appropriate amount of ox bile concentrates in the treatment of PBC is unknown. L-ornithine-L-aspartate (OA) is a nutritional supplement that has been investigated as a treatment for cirrhosis and hepatic encephalopathy. In a double-blind trial, participants taking 18 grams of OA for 14 days had significant improvements in liver function, mental status, and brain function. Similar benefits have also been demonstrated using injections of OA L-carnitine injections have been used to improve circulation to the liver in people with cirrhosis, but trials of the oral supplement are lacking. Vitamin E has been shown to decrease damage in cirrhotic livers and may reduce immune abnormalities that contribute to the development of the disease. However, a study reported that supplementation of 500 IU per day of vitamin E for one year failed to influence laboratory tests, liver function survival or hospitalization rates in people with alcoholic cirrhosis. Further clinical trials are needed to determine if any benefits may be expected from vitamin E supplementation in people with liver cirrhosis. Selenium levels have been found to be low in people with liver cirrhosis55 and the need for antioxidants has been found to be increased. A small, preliminary trial suggested that 100 mcg per day of selenium may improve liver function in people with alcoholic cirrhosis. People with primary biliary cirrhosis are at increased risk of bone loss. In a preliminary trial, supplementation with 0.5 micrograms of calcitriol (a prescription form of vitamin D) twice daily for 12 months prevented a loss in bone mineral density.58 Whether regular vitamin D might also prevent bone loss in people with PBC is unknown. DISCLAIMER: This information should not substitute for seeking responsible, professional medical care.  


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