Non-alcoholic steatohepatitisK75.8

Syndrome associated with chronic non-alcoholic fatty liver disease (NAFDL; K76.0), which develops in (non-alcoholic) patients with liver cell damage that cannot be separated histologically from alcoholic hepatitis (alcoholic fatty liver hepatitis ASH; alcohol consumption >20g/day).

NASH is most commonly diagnosed in patients between 40 and 60 years of age, but can occur in all age groups; w>m;

NASH develops in 80% of cases in patients with any of the following risk factors:

• Obesity (see also Obesity and skin lesions).
• Dyslipidaemia
• glucose intolerance.

The pathogenesis is poorly understood, but it seems to be related to insulin resistance (as in obesity and metabolic syndrome).

50% of patients are asymptomatic. Occasionally there are complaints of tiredness and a feeling of sickness as well as sensations of discomfort in the right upper abdomen. Hepatomegaly develops in about 75% of the patients. Splenomegaly can develop when there is advanced fibrosis of the liver. It is usually the first sign of portal hypertension. Patients with liver cirrhosis due to NASH may be asymptomatic and lack the signs of chronic liver disease.

Laboratory tests show (in contrast to the pure fatty liver) a moderate or significant increase in transaminases. De ritis quotient (GOT/GPT in NASH often < 1). Possible indications of diabetes mellitus type 2 or of dyslipidemia.

The knowledge of NASH as a separate nosological entity is important because it can be the cause of transaminase elevations of unclear etiology. The diagnosis consists of a medical history (presence of risk factors, alcohol consumption <20g/day), serological tests that exclude hepatitis B and C and a liver biopsy to confirm the diagnosis.

Imaging procedures of the liver, including ultrasound, computer tomography and in particular MRI, can reveal hepatosteatosis. However, these procedures cannot show the typical inflammation in NASH and it is not possible to distinguish NASH from other causes of fatty liver.

• Alcoholic steatohepatitis (ASH K70.0)
• Viral hepatitis
• Hepatitis. autoimmunological
• Toxic liver damage
• Wilson's disease
• alpha-1-antitrypsin deficiency

Elimination of causes and control of risk factors.

The only generally accepted treatment goal is elimination of potential causes and risk factors. Possible reduction of medications and alcohol, weight reduction, treatment of present hyperlipidemia or and hyperglycemia.

Evidence suggests that thiazolidinediones and vitamin E support normalization of biochemical and histological changes in NASH. Numerous other treatment attempts (e.g. ursodeoxycholic acid, metronidazole, metformin, betaine, glucagon, glutamine infusion) have proven ineffective.

The majority of patients (95%) do not develop liver failure or liver cirrhosis (often misdiagnosed as cryptogenic liver cirrhosis) within 10 years. Some drugs (cytotoxic drugs) and metabolic diseases are associated with a faster development of NASH. NASH and liver cirrhosis have an increased risk of HCC (hepatocellular carcinoma).