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 |