Key result
Low-dose amiodarone treatment for 10 months induced pulmonary toxicity, which was successfully treated with drug withdrawal and steroids.
Case Report (n=1)
Even low-dose amiodarone therapy can induce severe pulmonary toxicity, which may be reversible with prompt drug discontinuation and steroid treatment.
Clinicians should monitor for pulmonary toxicity even with low-dose amiodarone; case reports leave open true incidence and optimal management.
Amiodarone is a potent antiarrythmic agent used in the treatment of refractory tachyarrythmias and premature ventricular contractions. Amiodarone may be responsible for the frequent and various side effects including corneal deposits, abnormal liver function test, hyperthyriodism or hypothyroidism, bluish discoloration of the skin, neuropathies, and the others. However, pulmonary toxicity is most serious adverse reaction limiting the clinical efficacy. Rescently, we experienced a case of pulmonary toxicity induced by low dose 10-month amiodarone treatment for atrial fibrilation with rapid ventricular response. Lung biopsy reveals interstitial inflammation, fibrosis, hyperplasia of pneumocytes, and foamy macrophages. Respiratory symptoms and abnormal chest X-ray findings were nearly complete cleared after using steroid and withdrawal of amiodarone. We report a case of amiodarone-induced pulmonary toxicity with literature review.
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A 1994 study conducted a case report in Atrial fibrillation with rapid ventricular response (n=1). Amiodarone was evaluated on Pulmonary toxicity. Low-dose amiodarone treatment for 10 months induced pulmonary toxicity, which was successfully treated with drug withdrawal and steroids.
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