Amiodarone pulmonary toxicity

Kennedy JI Jr. Clinical aspects of amiodarone pulmonary toxicity. Clin Chest Med 1990 ll(l) 119-29. 

Gonzalez-Rothi RJ, Hannan SE, Hood Cl, Franzini DA. Amiodarone pulmonary toxicity presenting as bilateral exudative pleural effusions. Chest 1987 92(l) 179-82. 

Kudenchuk PJ, Pierson DJ, Greene HL, Graham EL, Sears GK, Trobaugh GB. Prospective evaluation of amiodarone pulmonary toxicity. Chest 1984 86(4) 541-8. 

Siniakowicz RM, Narnia D, Suster B, Steinberg JS. Diagnosis of amiodarone pulmonary toxicity with high-resolution computerized tomographic scan. J Cardiovasc Electrophysiol 2001 12(4) 431-6. 

Duke PK, Ramsay MAE, Herndon JC, Swygert TH, Cook AO. Acute ojqrgen induced amiodarone pulmonary toxicity after general anaesdiesia. Anesthesiology (1991) 75, A228. 

Kay GN, Epstein AE, Kirklin JK, Diethelm AG, Graybar G, Plumb VI Fatal postoperative amiodarone pulmonary toxicity. Am J Cardiol (1988) 62, 490-2. 

Herndon JC, Cook AO, Ramsay AE, Swygert TH, Capehart J. Postoperative unilateral pulmonary edema possible amiodarone pulmonary toxicity. Anesthesiology (1992) 76, 308-12. 

Nalos PC, Kass RM, Gang ES, Fishbein MC, Mandel WJ, Peter T. Life-direatening postoperative pulmonary complications in patients with previous amiodarone pulmonary toxicity undergoing cardiothoracic operations. J Thorac Cardiovasc Surg (1987) 93,904-12. 

Pulmonary toxicity may occur in about 10% of patients given amiodarone. Pulmonary toxicity due to cyclophosphamide may occur between 1 to 6 months after exposure or occttr as a more insidiotts form after about 6 months. The early onset of symptorrrs in the patients described above suggests accelerated mechanisms of ptrlmonary toxicity. Both cyclophosphamide and amiodarone pulmonary toxicity appear to be erthanced by oxygen and the combination of cyclophosphamide with amiodarone may enhance oxidative stress and therefore ptrlmonary toxicity. 

Martin WJ, Rosenow EC. Amiodarone pulmonary toxicity. Recc nition and pathogenesis (Part 1). Chest (1988) 93, 1067-75. 

Kosseifl SG, Halawa A, Bailey B, Micklewright M, Roy TM, Byrd RP Jr. Reduction of amiodarone pulmonary toxicity in patients treated with angiotensinconverting enzyme inhibitors and angiotensin receptor blocker. Ther Adv Respir Dis 2009 3(6) 289-94. 

Respiratory Amiodarone pulmonary toxicity has been described after lung transplantation [28 ]. 

Diaz-Guzman E, Mireles-Cabodevila E, Arrossi A, Kanne JP, Budev M. Amiodarone pulmonary toxicity after lung transplantation. J Heart Lung Transplant 2008 27(9) 1059-63. 

J. Reasor and S. Kacew, Amiodarone pulmonary toxicity morphologic and biochemical features, Proc. Soc. Exp. Biol. Med., 1991, 96, 1-7. 

Oral- Amiodarone may cause a clinical syndrome of cough and progressive dyspnea accompanied by functional, radiographic, gallium scan, and pathological data consistent with pulmonary toxicity. The frequency varies from 2% to 17% fatalities occur in about 10% of cases. However, in patients with life-threatening arrhythmias, discontinuation of amiodarone therapy due to suspected drug-induced pulmonary toxicity should be undertaken with caution. 

Chronic oral therapy with amiodarone is associated with several side effects, including pulmonary toxicity (fibrosis and probably immunologically mediated pneumonitis), hepatotoxicity, thyroid gland dysfunction, corneal microdeposits, blue-grey skin discoloration and neurological disturbances. 

Dronedarone is a structural analog of amiodarone and lacks iodine atoms. The design was intended to eliminate action of the parent drug on thyroxine metabolism and to modify the half-life of the drug. Dronedarone has multiple actions like amiodarone, blocking IKr, IKs, ICa, INa, and adrenoceptors. The drug has a half-life of 24 hours and was administered twice daily in the initial clinical trials. No thyroid or pulmonary toxicity has been noted during early use. 

An initial increase in cardiac arrhythmias (proarrhythmic effect) may occur when class III drugs are instituted. The most important proarrhythmia is known as torsades de pointes, which is a form of ventricular tachycardia that can be fatal.11,40 Specific class III agents are associated with various other side effects. Amiodarone, for example, is associated with pulmonary toxicity and liver damage. Other class III drugs may have a more favorable side-effect profile but may not be as effective as amiodarone in controlling arrhythmias. Side effects of class HI drugs there-... 

Cardiac side effects Torsade de pointes (<0.5%), severe bradycardia (one-year risk of bradycardia 2.4% on amiodarone vs. 0.8% on placebo). Non-cardiac side effects Pulmonary toxicity I % per year with fatal cases discontinue and treat symptomatically, hepatotoxicity... 

Dusman RE, Stanton MS, Miles WM, Klein LS, Zipes DP, Fineberg NS, Heger JJ. Clinical features of amiodarone-induced pulmonary toxicity. Circulation 1990 82(l) 51-9. 

Kaushik S, Hussain A, Qarke P, Lazar HL. Acute pulmonary toxicity after low-dose amiodarone therapy. Ann Thorac Surg 2001 72(5) 1760-1. 

Alter P, Grimm W, Maisch B. Amiodaron-induzierte Pneumonitis bei dilatativer Kardiomyopathie. [Amiodarone induced pulmonary toxicity.] Pneumologie 2002 56(l) 31-5. 

Kanji Z, Sunderji R, Gin K. Amiodarone-induced pulmonary toxicity. Pharmacotherapy 1999 19(12) 1463-6. 

Bums KE, PUiotis E, Garcia BM, Ferguson KA. Amiodarone pulmonary, neuromuscular and ophthahnolo-gical toxicity. Can Respir J 2000 7(2) 193-7. 

Esato M, Sakurada H, Okazaki H, Kimura T, Nomizo A, Endou M, Tamura T, Hiyoshi Y, Mishizaki M, Teshima T, Yanase O, Hiraoka M. Evaluation of pulmonary toxicity by CT, pulmonary function tests, and KL-6 measurements in amiodarone-treated patients. Ther Res 2001 22 867-73. 

Nicholson AA, Hayward C. The value of computed tomography in the diagnosis of amiodarone-induced pulmonary toxicity. Clin Radiol 1989 40(6) 564-7. 

Dirlik A, Erinc R, Ozcan Z, Atasever A, Bacakoglu F, Nalbantgil S, Ozhan M, Burak Z. Technetium-99m-DTPA aerosol scintigraphy in amiodarone induced pulmonary toxicity in comparison with Ga-67 scintigraphy. Ann Nucl Med 2002 16(7) 477-81. 

It is unknown whether thyroid dysfunction (hypothyroidism or hyperthyroidism) is a result of the amiodarone, the iodine contained in the amiodarone, or another mechanism. The production of amiodarone-phospholipid complexes within organs has been proposed as the mechanism for some of this drug s adverse effects. The mechanism of the pulmonary toxicity seen following chronic use is also uncertain but is the result of a hypersensitivity reaction in some. 

Burns KEA, Piliotis E, and Garcia BM (2000) Amiodarone pulmonary, neuromuscular and ophthalmological toxicity. Canadian Respiratory Journal 7 193-197. 

Olshansky B (1997) Amiodarone-induced pulmonary toxicity. New England Journal of Medicine 337 1814. 

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