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Captopril-induced cholestatic jaundice.

Drug Intelligence & Clinical Pharmacy

|March 1, 1984

Summary

Captopril therapy can cause liver injury, specifically cholestasis, in some patients. Discontinuation of the drug led to a complete recovery from this drug-induced hepatic dysfunction.

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Area of Science:

Hepatology
Pharmacology
Internal Medicine

Background:

Captopril is an angiotensin-converting enzyme (ACE) inhibitor commonly prescribed for hypertension.
Drug-induced liver injury (DILI) is a significant clinical concern, with various causative agents.
ACE inhibitors, including captopril, have been rarely associated with hepatic dysfunction.

Observation:

A 50-year-old female patient developed symptoms of hepatic dysfunction after one month of captopril therapy (25 mg three times daily).
Clinical presentation included jaundice, pruritus, anorexia, weight loss, hepatomegaly, and abdominal tenderness.
Liver biopsy revealed predominantly cholestasis with secondary hepatocellular changes.

Findings:

Laboratory tests showed markedly elevated liver enzymes: total bilirubin (506 mumol/L), alkaline phosphatase (737 U/L), lactate dehydrogenase (LDH) (319 U/L), and serum glutamic-oxaloacetic transaminase (SGOT) (100 U/L).
The hepatic dysfunction was attributed to captopril therapy.
Discontinuation of captopril resulted in a slow but complete recovery of liver function.

Implications:

This case highlights the potential for captopril to cause cholestatic liver injury.
Clinicians should consider captopril as a potential cause of hepatic dysfunction in patients presenting with relevant symptoms and laboratory abnormalities.
Prompt drug withdrawal is crucial for achieving full recovery from captopril-induced hepatotoxicity.

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