Nonalcoholic steatohepatitis is a syndrome that develops in patients who consume no alcohol. The existing liver damage here is histologically can not be separated from that in an alcoholic hepatitis. It most often develops in patients with at least one of the following risk factors: obesity, dyslipidemia and glucose intolerance. The pathogenesis is poorly documented, but it seems to be related to insulin resistance (such. As in obesity and metabolic syndrome). Most patients are asymptomatic. Laboratory tests show an increase in transaminases. To confirm the diagnosis, a biopsy is necessary. Treatment includes elimination of causes and risk factors.

Nonalcoholic steatohepatitis is a syndrome that develops in patients who consume no alcohol. The existing liver damage here is histologically can not be separated from that in an alcoholic hepatitis. It most often develops in patients with at least one of the following risk factors: obesity, dyslipidemia and glucose intolerance. The pathogenesis is poorly documented, but it seems to be related to insulin resistance (such. As in obesity and metabolic syndrome). Most patients are asymptomatic. Laboratory tests show an increase in transaminases. To confirm the diagnosis, a biopsy is necessary. Treatment includes elimination of causes and risk factors.

See also liver structure and function and assessment of patients with liver disease.) The non-alcoholic steatohepatitis is a syndrome that develops in patients who consume no alcohol. The existing liver damage here is histologically can not be separated from that in an alcoholic hepatitis. It most often develops in patients with at least one of the following risk factors: obesity, dyslipidemia and glucose intolerance. The pathogenesis is poorly documented, but it seems to be related to insulin resistance (such. As in obesity and metabolic syndrome). Most patients are asymptomatic. Laboratory tests show an increase in transaminases. To confirm the diagnosis, a biopsy is necessary. Treatment includes elimination of causes and risk factors. (See American Society of Gastroenterology of the “Medical Position Statement” not alcohol-related fatty liver.) A NASH is diagnosed in patients between 40 and 60 years, most common, but can occur in all age groups. Many affected patients have obesity, type 2 diabetes mellitus (or glucose intolerance), dyslipidemia and / or metabolic syndrome. Pathophysiology Pathophysiology to include the accumulation of fat (steatosis), inflammation and variable occurring, fibrosis. Steatosis is the result of triglyceride accumulation in the liver. Possible mechanisms for the steatosis include a decreased synthesis of VLDL (very low density lipoproteins) and an increased synthesis of hepatic triglycerides (possibly as a result of reduced oxidation of fatty acids or of elevated free fatty acids that enter in the liver) a. Inflammation occurs as a result of cell membrane damage caused by lipid oxidation. These changes stimulate Kupffer cells, which ultimately leads to fibrosis. In the advanced state of NASH can cause cirrhosis and portal hypertension. Symptoms and signs Most patients are asymptomatic. However, some complain of fatigue and malaise and discomfort in the right upper abdomen. Hepatomegaly occurs in approximately 75% of patients. Splenomegaly may develop when an advanced fibrosis of the liver is available, it is usually the first sign of the existence of portal hypertension. Patients with cirrhosis due to NASH can be asymptomatic and let the signs of chronic liver disease miss. Diagnosis History (presence of risk factors, no excessive alcohol consumption) Serological tests that should hepatitis B and C preclude liver biopsy on the diagnosis be considered in patients with risk factors such as obesity, type 2 diabetes or dyslipidemia and in patients with unexplained laboratory abnormalities that a indicate liver disease. The most common pathological laboratory abnormalities exist in the elevation of transaminases. Unlike alcoholic liver disease, the ratio of AST / ALT in NASH is usually <1 Alkaline Phosphatase and gamma-glutamyl transferase (GGT) are occasionally increased. Hyperbilirubinemia, prothrombin time prolongation and hypoalbuminemia are rare. For diagnosis are strong indications necessary (such as the confirmation of the history of friends and relatives) that the consumption of alcohol excessively (z. B. is <20 g / day), and serological tests should show the absence of hepatitis B and C ( ie, hepatitis B surface antigen and hepatitis C virus antibodies should be negative). Liver biopsy shows damage similar to alcoholic hepatitis, usually including large fat droplets (coarse droplet fatty infiltration). Among the indications of a biopsy include unexplained signs of portal hypertension (eg. As splenomegaly, cytopenia) and an inexplicable increase in aminotransferase levels that lasts> 6 months in patients with diabetes, obesity or dyslipidemia. Imaging tests of the liver, including ultrasound, computed tomography, and especially MRI can reveal hepatic steatosis. However, these tests can not show the typical inflammation in NASH and it is not possible for NASH to distinguish from other causes of fatty liver. Prognosis The prognosis is difficult to make. Probably the majority of patients developed no liver failure or cirrhosis. Some drugs (cytotoxic drugs) and metabolic diseases associated with a more rapid formation of NASH. The prognosis is usually good if no complications (eg. As variceal bleeding) may occur. Therapy eliminate the causes and control of risk factors The only generally accepted treatment goal is the elimination of potential causes and risk factors. This may involve the treatment of hyperglycemia, the omission of drugs and toxins, weight loss and the specific treatment of Hyperlipid√§mieoder. There is preliminary evidence that thiazolidinediones and vitamin E support the normalization of biochemical and histological changes in NASH. Numerous other treatment trials (eg. As ursodeoxycholic acid, metronidazole, metformin, betaine, glucagon, glutamine infusion) have proven to be ineffective. Important points NASH causes histological liver damage similar to alcoholic hepatitis, but occurs in patients who are not alcoholics, who are often overweight or have type 2 diabetes mellitus, or dyslipidemia. Specific symptoms are not usually present, but some patients have right upper quadrant pain, show fatigue and / or discomfort. Signs of portal hypertension and cirrhosis can eventually occur and its first manifestations. Exclude alcoholism (based on a confirmed history), and hepatitis B and C (with serological tests). A liver biopsy is performed. If possible, the causes are to eliminate and control the risk factors.

Health Life Media Team

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