Acute transaminitis after initial days of starting haloperidol

Area of Science:

• Hepatology
• Psychopharmacology
• Clinical Case Reports

Background:

• Haloperidol, a first-generation antipsychotic, is known for its lipophilicity and hepatic metabolism.
• Elevated liver enzymes occur in approximately 2.4% of patients on haloperidol, typically with chronic use.
• Distinguishing drug-induced liver injury from other causes is crucial for patient management.

Purpose of the Study:

• To report a case of acute liver enzyme elevation following short-term haloperidol initiation.
• To investigate the potential link between haloperidol and transaminitis in the absence of viral or autoimmune hepatitis.
• To demonstrate the successful management and psychiatric stabilization by switching to clozapine.

Main Methods:

• A detailed clinical case presentation of a patient experiencing adverse liver enzyme elevation.
• Laboratory investigations including hepatic viral serology and autoimmune markers were performed.
• Treatment modification from haloperidol to clozapine with subsequent monitoring of liver function and psychiatric status.

Main Results:

• The patient developed elevated liver enzymes (alanine transaminase > aspartate transaminase) within 1-2 days of starting haloperidol on two separate occasions.
• Peak alanine transaminase levels reached 288 U/L, with negative viral and autoimmune serology.
• Discontinuation of haloperidol and initiation of clozapine led to transaminitis recovery and psychiatric stabilization.

Conclusions:

• Haloperidol can cause acute, short-term liver enzyme elevation, even in the absence of confounding hepatic conditions.
• Clozapine appears to be a viable and well-tolerated alternative in patients experiencing haloperidol-induced liver injury.
• Prompt recognition and management are essential for preventing severe hepatic complications and ensuring psychiatric care continuity.