Severe lobular infiltration of polymorphonuclear leukocytes (neutrophils) is abundantly present in this condition in contrast to most other types of hepatitis where mononuclear cells localize around portal triads. This stage is known as alcoholic hepatitis. Eosinophilic fibrillar material (Mallory hyaline or Mallory-Denk bodies) forms in swollen (ballooned) hepatocytes. On further progression, there is marked steatosis, hepatocellular necrosis, and acute inflammation.
Fatty liver is generally considered a reversible condition.
The altered intracellular redox potential leads to the accumulation of intracellular lipids. It involves the accumulation of small fat droplets around liver cells, specifically around the venules, and approaches the portal tracts. Histopathology at Different States of Alcoholic Hepatitis: Patatin-like phospholipase domain-containing protein 3 (PNPLAP3) is associated with alcoholic liver cirrhosis. Concurrent hepatitis C infection is associated with younger age of onset, more advanced histological damage, and decreased survival. Obesity and high-fat diet also increase the risk of alcoholic liver disease. Quantity and duration of the patient's alcohol intake are the highest risk factors for the development of liver disease. If the consumption of alcohol does not stop at this stage, it sometimes leads to alcoholic hepatitis. With continued alcohol consumption, the alcoholic liver disease progresses to severe damage to liver cells known as "alcoholic cirrhosis." Alcoholic cirrhosis is the stage described by progressive hepatic fibrosis and nodules. The initial stage involves the accumulation of fat in the liver cells, commonly known as fatty liver or steatosis. The liver tolerates mild alcohol consumption, but as the consumption of alcohol increases, it leads to disorders of the metabolic functioning of the liver. Different factors, such as metabolic, genetic, environmental, and immunological, collectively play a role in alcoholic liver disease.
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