Non-alcoholic fatty liver disease:mind the gaps: pathophysiology and non-invasive diagnosis

Non-alcoholic fatty liver disease (NAFLD) is the most common liver disease in western countries. Globally, NAFLD affects approximately 25% of the population. The term NAFLD includes both fatty liver disease (steatosis) and inflammation of the liver (NASH; non-alcoholic steatohepatitis). Fatty liver disease involves the accumulation of fat in the liver cells. If liver fattening persists, it can lead to liver inflammation. Liver inflammation occurs in about 30% of patients with fatty liver and can eventually lead to cirrhosis and liver cancer. With cirrhosis, there is severe damage to the liver that can lead to the liver not functioning properly over time. NAFLD results from an unhealthy lifestyle characterized by a high-calorie diet and little physical activity. Therefore, being overweight and obese are major risk factors for developing liver fatty degeneration. However, the exact way in which liver inflammation, or NASH, develops in patients with fatty liver is not yet fully known. This dissertation discusses three topics related to NAFLD, namely (i) factors that may play a role in the development of NASH, (ii) diagnosing NASH in a non-burdensome (non-invasive) way, and (iii) the role of the general practitioner in diagnosing NAFLD

Hyperferritinemia in Nonalcoholic Fatty Liver Disease:Iron Accumulation or Inflammation?

Hyperferritinemia, observed in inflammation, iron overload as well as in combination of both, is found in similar to 30% of nonalcoholic fatty liver disease (NAFLD) patients. The authors summarized the evidence regarding the potential cause of hyperferritinemia in NAFLD, as this may affect the indicated therapy. A systematic literature search was conducted in EMBASE, PubMed, MEDLINE, and the Cochrane library. In the majority of NAFLD patients, hyperferritinemia is due to inflammation without hepatic iron overload. In a smaller group, a dysmetabolic iron overload syndrome (DIOS) is found, showing hyperferritinemia in combination with mild iron accumulation in the reticuloendothelial cells. The smallest group consists of NAFLD patients with hemochromatosis. Phlebotomy is only effective with hepatocellular iron overload and should not be the treatment when hyperferritinemia is related to inflammation, whether or not combined with DIOS. Treatment with lifestyle changes is to date probably the more effective way until new medication is becoming available