Golimumab-Associated Myocarditis with Progressive Eosinophilia after Route Switch in Rheumatoid Arthritis

Area of Science:

• Cardiology
• Rheumatology
• Pharmacology

Background:

• Tumour necrosis factor-alpha (TNF-α) inhibitors are widely used for rheumatoid arthritis (RA).
• While generally safe for cardiovascular health, rare instances of drug-induced myocarditis are reported.
• Pharmacovigilance data on TNF-α inhibitor-associated myocarditis is limited.

Purpose of the Study:

• To report a case of suspected drug-induced hypersensitivity myocarditis linked to golimumab in a rheumatoid arthritis patient.
• To highlight the potential for cardiotoxicity with TNF-α inhibitors, particularly after dose escalation or route change.
• To emphasize the importance of pharmacovigilance for rare adverse events.

Main Methods:

• A case study of a 51-year-old male with RA on intravenous golimumab presenting with acute chest pain.
• Clinical evaluation including high-sensitivity troponin I, echocardiography, and coronary angiography.
• Monitoring for viral infections, inflammatory markers, and peripheral eosinophilia.
• Causality assessment using established algorithms (WHO-UMC, Naranjo).

Main Results:

• The patient presented with acute myocardial injury (troponin I 32,419 ng/l) and mildly reduced ejection fraction.
• Coronary angiography showed non-obstructive arteries; viral serology and inflammatory markers were negative.
• Progressive eosinophilia was observed, supporting a hypersensitivity reaction.
• Left ventricular function normalized after golimumab discontinuation, coinciding with drug elimination.

Conclusions:

• The case supports drug-induced hypersensitivity myocarditis due to golimumab, with a 'probable' causality.
• Switching to intravenous golimumab increased peak serum concentration significantly, potentially contributing to sensitization.
• Peripheral eosinophilia in acute myocardial injury without viral prodrome warrants suspicion for drug-induced myocarditis.