Raised alanine aminotransferase and alkaline phosphatase level due to drug induced liver injury is resolved spontaneously in some cases through a process of adaptation. What is/are the underlying mechanisms for these adaptations? Is it due to scavenging effects of dietary antioxidants?
The best resolution way of DILI lesione is stopping definitively the administration of the ofending drug
Depending on the duration of injury and the histological location of damage, drug-induced liver injury (DILI) is categorized as acute or chronic, and either as hepatitis, cholestatic, or a mixed pattern of injury. The hepatitis pattern is characterized by hepatocyte necrosis and is associated with a poor prognosis. There are three types of acute cholestatic drug-induced injury: bland cholestasis is the result of abnormal biliary secretion, and is not accompanied by significant hepatocellular damage; cholestatic hepatitis (mixed type) refers to cholestasis with concomitant hepatic parenchymal damage; and the third form of acute cholestasis is defined by the presence of bile duct injury or cholangiolitis. Medications may cause chronic cholestasis through two additional mechanisms: through the obliteration of bile ducts, also known as the vanishing bile duct syndrome, or by extrahepatic biliary obstruction, known as secondary sclerosing cholangitis.
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