A 58-year-old man started on amiodarone 6 months ago for recurrent ventricular tachycardia presents with progressive dry cough and exertional dyspnea. Chest CT shows bilateral basal interstitial infiltrates. Which mechanism best explains this adverse effect?
- A Type I hypersensitivity reaction with eosinophilic infiltration
- B Direct phospholipid accumulation and cytotoxic effect of amiodarone on alveolar cells ✓
- C Inhibition of surfactant production by type II pneumocytes only
- D Oxidative injury from the iodine moiety of the drug
Correct answer: B. Direct phospholipid accumulation and cytotoxic effect of amiodarone on alveolar cells
Explanation
Amiodarone accumulates in lung tissue and causes direct phospholipidosis plus cytotoxic injury, producing interstitial pneumonitis that can progress to fibrosis. The risk is dose related and appears after months of therapy. The best distractor, hypersensitivity, describes methyldopa or penicillamine patterns; amiodarone lung disease is not immune mediated. Basal predominance on imaging and the temporal link to therapy support drug induced rather than infective or heart failure etiology.
Reference: Katzung's Basic and Clinical Pharmacology, 16th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
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