<s>[INST] context: The picture shows a classic case of liver steatosis or fatty change, which results from accumulation of fat within hepatocytes. Alcohol is one of the most frequent causes of liver steatosis. At least in pa, the mechanism of alcohol-induced steatosis is due to acetaldehyde formation, which disrupts microtubules and increases the NADH/NAD+ ratio. Fatty change of the macrovesicular type is entirely reversible if the noxious stimulus (in this case, excessive alcohol intake) is removed. Acute hepatitis results from acute insults to the liver. Alcoholic hepatitis is characterized by hepatocyte necrosis, intracytoplasmic hyaline bodies (Mallory bodies), and neutrophilic infiltration. Usually, alcoholic hepatitis develops after a bout of heavy alcohol consumption. Fatty change may be superimposed on histologic signs of hepatitis, but steatosis does not evolve into hepatitis if alcohol intake is discontinued. Chronic hepatitis may result from long-term heavy alcohol consumption and is characterized by chronic inflammation of poal spaces and progressive fibrosis. Steatosis is usually associated with chronic hepatitis due to alcohol. Hyperplastic nodules represent a morphologic component of cirrhosis. Foci of hepatocyte hyperplasia develop as a compensatory mechanism to continuous loss of hepatocytes. [/INST] question: A 50-year-old man with a history of alcohol abuse is found to have elevated liver enzymes. A liver biopsy shows the microscopic features of steatosis. If the patient abstains from fuher drinking, this condition will most likely evolve into which of the following? | options: A: Acute hepatitis B: Chronic hepatitis C: Complete regression D: Hyperplastic nodules | answer: C </s>