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Assistant Professor Department of Cardiology Ege University School of Medicine Izmir, Turkey
Associate Professor Department of Chest Diseases Ege University School of Medicine
Associate Professor Department of Cardiology Ege University School of Medicine
Assistant Professor Department of Cardiology Ege University School of Medicine Bornova 35100 Izmir, Turkey fax 0090-232-343-53-92 canrfca{at}yahoo.com
Published Online, January 11, 2005. www.theannals.com, DOI 10.1345/aph.1E388
Case Report. A 67-year-old male physician presented with a one-week history of shortness of breath, wheezing, and dry cough. His past medical history was significant for coronary artery disease. He had undergone coronary artery bypass graft surgery 11 years earlier and was having frequent episodes of palpitations since then. Several Holter monitorings showed frequent (>10/h), symptomatic PVCs and couplets. A recent thallium-201 study demonstrated a fixed defect in the inferior wall and no reversible ischemia. Transthoracic echocardiography showed left-ventricular ejection fraction of 45%. Several medications, including the selective ß1-receptor blocker metoprolol 50 mg/day, the nonselective ß-receptor blocker carvedilol 6.25 mg twice a day, and mexiletine 200 mg 3 times a day had been tried previously with partial success for his symptomatic PVCs.
Based on these findings, the patient was placed on amiodarone 400 mg/day for one week, 200 mg/day the next 3 weeks, and finally 100 mg/day. By the end of the third month of low-dose amiodarone treatment, he started reporting shortness of breath both at rest and on exertion, nonproductive cough, and wheezing, but denied chest discomfort, fever, or chills. Because of the progressively increasing severity of his symptoms, the man was hospitalized for further evaluation. On admission, he was in moderate respiratory distress, and physical examination revealed clear lungs except for bilateral, diffuse expiratory wheezing. There were no signs of heart failure.
Based on serial workup (Table 1), the temporal relationship between amiodarone treatment, and the patient's signs and symptoms in the presence of documented bronchial hyperreactivity, the diagnosis of amiodarone-induced bronchial asthma was made. Amiodarone was discontinued on admission. Inhaled corticosteroid therapy (budesonide 320 µg twice a day), inhaled ß2-agonist bronchodilator (formoterol 9 µg twice a day), intravenous corticosteroid (methylprednisolone 40 mg/day), and intravenous theophylline 400 mg/day were started.
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By the third hospital day, the patient was breathing more comfortably. Intravenous corticosteroid therapy and theophylline were continued for one week. In 2 weeks, forced expiratory volume in 1 second increased to 2.87 L (87%) with inhaled corticosteroid and ß2-agonist bronchodilator therapy. He was asymptomatic in long-term follow-up (6 mo). The patient is currently maintained on inhaled corticosteroid therapy and did not need to continue inhaled ß2-agonist bronchodilator therapy. We did not rechallenge with amiodarone due to its attending risks and the patient's refusal. No treatment for the PVCs was restarted after amiodarone discontinuation. Causality assessment using the Naranjo probability scale revealed that the adverse drug event was probable.3
Discussion. Several types of pulmonary toxicity of amiodarone have been described, with a frequency of 2–7%.4 Amiodarone-induced bronchial asthma has been reported in 3 patients.1,5 One of the patients had a history of chronic bronchitis and the other 2 patients had a history of bronchial asthma. Patients were receiving a wide range of doses of amiodarone (100, 200, 600 mg/day) at the time of diagnosis of bronchial asthma.
Interestingly, in our case, there was no history of asthma, exposure to
common asthma triggers (eg, new pets), nasal polyps and/or chronic allergic
rhinitis, gastroesophageal reflux disease, or smoking, and the patient had
been on ß-blocker therapy previously without any signs of bronchial
hyperreactivity. As a result, clinicians should be aware that new-onset
bronchial asthma can be induced by low-dose amiodarone (
200 mg/day).
References
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