Fatty liver or steatosis is a common finding in human liver biopsies. It is a condition where fat has accumulated within liver cells (hepatocytes) without causing any specific symptoms. (It has been defined either as more than 5% of cells containing fat droplets or total lipid exceeding 5% of liver weight.).
Fatty liver as a longstanding chronic condition can occur in association with a wide range of diseases, toxins and drugs, although in clinical practice, the majority of cases are due to alcohol excess, diabetes and obesity. Much less common are occurrences of acute fatty liver of pregnancy and as a response to administration of tetracyclines, acetaminophen and other drugs and toxins.
The understanding of steatosis has advanced considerably in recent years. Fatty liver was believed to be a benign reversible condition. Careful clinical studies, however, demonstrate that that fatty liver of either alcoholic or non-alcoholic origin can lead to inflammation, cell death and fibrosis (steatohepatitis), and eventually even cirrhosis. Cirrhosis is the irreversible end result of fibrous scarring, a response of the liver to a variety of long-standing inflammatory, toxic, metabolic and congestive damage.
Alcohol is by far the commonest cause both steatosis and cirrhosis in the Western world. As we know it, however, there is a considerable inter-individual difference in the degree of liver damage produced by excessive alcohol intake. There seems to be no correlation between the incidence and severity of fatty liver and either the amount, type or duration of alcohol abuse. It has been unclear why in some individuals steatosis, whatever its etiology, never progresses to steatohepatitis and cirrhosis.
A growing body of evidence supports a role for lipid peroxidation in the further development of liver damage. In other words it requires additional exposure to toxins that produce free radical damage.
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