From the Guidelines

Paracetamol can affect AST and ALT levels, particularly at high doses or with prolonged use, as evidenced by a study published in 2022 1.

At therapeutic doses (up to 4000mg per day for adults), paracetamol is generally safe for most people and causes minimal liver enzyme elevation.
However, exceeding the recommended dose can lead to significant increases in AST and ALT, indicating liver injury.
A daily dose of 2–3 g of acetaminophen was reported to have no association with decompensation in patients with liver cirrhosis 1.
Even regular therapeutic doses can occasionally cause mild elevations in some individuals, particularly those with pre-existing liver conditions, those who consume alcohol regularly, or those who are fasting or malnourished.

If you're taking paracetamol regularly and need liver function tests, inform your healthcare provider about your medication use.
Patients with liver cirrhosis are at risk of metabolic disorder and prolonged half-life of acetaminophen, and a daily dose of 2–3 g is generally recommended for acetaminophen 1.
NSAIDs prescribed to patients with liver disease have a higher concentration of free compounds and are more likely to cause side effects and toxicity, and their use must be avoided as much as possible 1.

A study published in 2022 found that amounts of less than 4 g per day of acetaminophen are very unlikely to cause clinically significant hepatotoxicity 1.
Another study published in 2007 found that therapeutic ingestions of APAP may result in mild elevations of serum transaminases of unknown significance 1.

From the Research

Paracetamol overdose can cause significant elevations in aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels, indicating hepatic toxicity 2, 3.
Studies have shown that AST and ALT levels rise in similar proportions after paracetamol overdose, but later decline at different rates, with AST falling more rapidly than ALT 2, 3.
The AST/ALT ratio can be used to indicate recovery after acute paracetamol poisoning, with a ratio less than or equal to 0.4 being highly predictive of recovery in patients treated with N-acetylcysteine (NAC) 2.

The kinetics of AST and ALT release into and disappearance from the circulation following paracetamol overdose have been described, with AST activity falling with a half-life of 15.1 hours and ALT activity falling with a half-life of 39.6 hours 3.
The use of AST rather than ALT to determine when to discontinue NAC treatment could result in antidotal treatment being stopped earlier, potentially measured in days 3.

N-acetylcysteine (NAC) has been shown to have hepatoprotective effects against paracetamol-induced liver damage, and its use has been compared to other antioxidants such as N-acetyl-methionine (NAM) and N-acetylglucosamine (NAG) 4, 5.
NAG and NAC have been found to significantly improve paracetamol-induced hepatic and blood biochemical and histopathological disturbances 4.
Erdosteine has also been shown to be effective in preventing liver damage induced by paracetamol intoxication, and its use has been compared to NAC administration 5.

Paracetamol overdose is a common cause of acute liver injury, and hepatotoxicity from paracetamol overdose remains a global issue 6.
The clinical and pathophysiologic features of hepatotoxicity secondary to paracetamol have been described, and current available knowledge and treatment options have been updated 6.