Non-alcoholic fatty liver

The term NAFL ("nonalcoholic fatty liver") refers to simple or plain fatty liver in which no inflammatory changes are histologically detectable apart from small or coarse-dropped fatty deposits.

In Europe, the prevalence of NAFL in the population is about 20-30 % (Younossi ZM et al. 2011). In children, the prevalence of NAFL is about 10%. It increases with increasing age, with girls having a significantly higher prevalence than boys (16.3% versus 10.1%). Sonographically, the diagnosis rate varies between 17% and 46% depending on the population studied.

This is probably due to the increase in metabolic risk factors, also in connection with the ageing of the population. In fatty liver patients, the prevalence of obesity is between 30 and 100 %, while that of type 2 diabetes mellitus is between 10 and 75 %.

A major risk factor for NAFLD is obesity, type 2 diabetes (a prevalence of 69% is found in type 2 diabetics). Furthermore fat metabolism (often elevated triglyceride and decreased HDL cholesterol levels).

Medication: Amiodron (leads to NASH in ca.25%); glucocorticoids, nifedipine, diltiazem, tamoxifen, synthetic estrogens, highly active retroviral therapy(HAART).

Further dependence is found on factors such as age (higher age is predisposing), gender (m>w) and ethnicity (higher proportion in patients with Hispanic descent).

Genetic factors: Patients with point mutations in the nPNPLA3 gene show an increased predisposition to NAFL (further also to liver cirrhosis and hepatocellular carcinoma).

The patients are usually free of symptoms and the laboratory parameters are frequent. Some complain of increased fatigue or a feeling of pressure in the right upper abdomen.

In fatty liver, gamma-GT is often increased, and in fatty liver hepatitis there is an additional increase in transaminases. Possibly increased ferritin level (50% of patients) or increased transferrin saturation (in 6-11% of patients). In contrast to the situation in hemochromatosis, however, the iron content of the liver is typically within the normal range. The combined test procedures and apoptosis markers (cytokeratin-18 fragments) have so far not been of major importance in clinical routine.

Screening by non-invasive examination method (ultrasound: sensitivity 60-94 %, specificity 66-97 %). The accuracy of sonography decreases with lower degrees of steatosis. The degree of fibrosis of the liver can be assessed non-invasively using various elastography techniques (Fibroscan and Acoustic Radiation Force Impulse). Ultimately, the liver biopsy is still the gold standard for purely formal diagnosis of NASH.

The relationship between weight gain and incidence or between weight reduction and regression of fatty liver disease could be proven prospectively over 7 years. A weight reduction of up to 4 % of body weight is already sufficient to bring about a reduction in fatty liver in 56 % of patients (reduction in the NAFLD activity score). Further intensive lifestyle modification with increase in exercise, optimal adjustment of possibly existing diabetes mellitus,

So far, there is no long-term effective drug that would favourably influence the course of fibrosis. The effects of metformin are doubtful, as is the effect of pioglitazone. Positive results are available for vitamin E in non-diabetic NAFL patients.

NAFL is reversible in principle; weight reduction plays a major role in this. After bariatric surgery, fatty liver deposits are reduced and the proportion of patients with fibrosis also decreases.

Between 5 and 20 % of NAFL patients develop NASH (non-alcoholic steatohepatitis) in the course of the disease; in about 10-20 % of patients, this changes into higher grade fibrosis, in < 5 % cirrhosis occurs.

Patients with NASH also have an increased risk of hepatocellular carcinoma (HCC), although this risk is usually limited to those with advanced fibrosis and HCC. If cirrhosis is present, there is an approximately 2%/year risk of HCC. NAFL is also an independent cardiovascular and nephrological risk factor.

The term "nonalcoholic fatty liver disease" (NAFLD) refers to a steatosis of the liver with a fat content of more than 5-10 % of the liver weight or a macrosteatosis of the hepatocytes of the same extent, which is not significantly caused by increased alcohol consumption (women: ≤ 20 g/d, men ≤ 30 g/d).

Hybrid forms between NAFLD and alcoholic fatty liver disease (AFLD) are possible.

1. Firneisz G (2018) Non-alcoholic fatty liver disease and type 2 diabetes mellitus: the liver disease of our age? World J Gastroenterol 20: 9072-9089.

2. Ertle J et al (2011): Non-alcoholic fatty liver disease progresses to hepatocellular carcinoma in the absence of apparent cirrhosis. Int J Cancer 128: 2436-43

3. Younossi ZM et al (2011): Changes in the prevalence of the most common causes of chronic liver diseases in the United States from 1988 to 2008, Clin Gastroenterol Hepatol 9: 524-530.Younossi ZM et al (2011): Changes in the prevalence of the most common causes of chronic liver diseases in the United States from 1988 to 2008, Clin Gastroenterol Hepatol 9: 524-530.