Version June 2024
| Agent | Syndrome | Frequency | Potential mechanism |
| Procainamide | SLE-like syndrome | 50 to 90 percent of patients have positive ANA test; 10 to 20 percent become symptomatic; pleuritis, pleural effusion, and parenchymal infiltrates are common | Autoantibodies against histone H2A-H2B complex, potentially induced by interaction of drug metabolites with DNA, or drug-induced alteration in T-cell DNA methylation |
| Quinidine | SLE-like syndrome | Rare; pleuritis and pleural effusions are most common pulmonary signs; parenchymal infiltrates uncommon | Autoantibodies against histone H2A-H2B complex, potentially induced by interaction of drug metabolites with DNA, or drug-induced alteration in T-cell DNA methylation |
| Tocainide | Pneumonitis/fibrosis | Incidence is about 0.3 percent | Unknown |
| Flecainide | Pneumonitis/fibrosis | Rare | Unknown |
| Mexiletine | Pneumonitis/fibrosis | Rare | Unknown; interferes with theophylline metabolism and can cause toxic elevations in theophylline levels in serum |
| ACE inhibitors | Cough | Incidence is 5 to 15 percent; occurs with all ACE inhibitors; whether these agents precipitate bronchospasm in patients with asthma is controversial | Decreased degradation of irritant and bronchoconstrictive mediators (bradykinin and substance P); direct increase in sensitivity to irritant-induced cough; genetic predisposition (based on differences in ACE gene). |
| Angioneurotic edema | Rare; can lead to respiratory failure | Unknown | |
| Sotalol | Bronchospasm | Occurs in 2 percent of patients | Direct blockage of β2-receptors |
| Adenosine | Bronchospasm | Occurs with rapid infusion in 5 to 10 percent of patients; may trigger acute bronchospasm in patients with asthma or COPD. Reversible with aminophylline | Induction of mast cell mediator release |
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