UDCA Safety in Sepsis with Deranged LFTs
Ursodeoxycholic acid (UDCA) is hepatically safe in sepsis with deranged liver function tests and should be continued if already prescribed for an established cholestatic indication, as it provides hepatoprotective effects rather than hepatotoxicity. 1, 2
Evidence for Hepatic Safety
UDCA has not been associated with liver damage and actually decreases liver enzyme levels in liver disease rather than causing harm. 1 The FDA drug label explicitly states that "Ursodiol therapy has not been associated with liver damage" and that "Ursodiol has been shown to decrease liver enzyme levels in liver disease." 1
Mechanism Supporting Safety in Acute Illness
UDCA exerts direct cytoprotective effects on hepatocyte membranes by displacing toxic hydrophobic bile acids, which is particularly relevant when liver function is already compromised. 3, 4
The drug provides anti-apoptotic effects and protects against ongoing hepatocyte necrosis, making it potentially beneficial rather than harmful in acute settings with liver dysfunction. 2, 5
UDCA has been used successfully in acute viral hepatitis where it relieves cholestasis symptoms and arrests hepatocyte necrosis, demonstrating safety even in acute hepatic injury. 5
Clinical Application in Sepsis
If the patient is already on UDCA for a chronic cholestatic condition (PBC, PSC, intrahepatic cholestasis of pregnancy), continue the medication during sepsis. 6, 7
Monitoring Recommendations
Measure SGOT (AST) and SGPT (ALT) at baseline and monitor as clinically indicated, though abnormalities in liver enzymes have not been associated with UDCA therapy. 1
The deranged LFTs in sepsis are likely due to sepsis-induced cholestasis or hepatic hypoperfusion rather than UDCA toxicity. 3, 4
Important Caveats
Do not initiate UDCA during acute sepsis solely to treat deranged LFTs - there is no evidence supporting this indication, and the priority should be treating the underlying sepsis. 8, 6
In patients with hepatic decompensation or advanced cirrhosis, discontinuation may be necessary based on overall clinical status, though this relates to disease severity rather than UDCA toxicity. 7
Lithocholic acid (a metabolite of UDCA) is theoretically hepatotoxic, but humans efficiently sulfate this compound for detoxification, and clinical liver damage from this mechanism has not been documented. 1