Amiodarone-Associated Pulmonary Toxicity: A Clinical and Pathologic Study of Eleven Cases

Dean, Philip A. W.; Groshart, Kenneth; Porterfield, James G.; Iansmith, David H.; Golden, Emmel

doi:10.1093/ajcp/87.1.7

Cited by 100 publications

(40 citation statements)

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“…10 The dose and duration of amiodarone therapy has not been significantly different in patients with amiodarone toxicity and those with amiodarone effect. 10,11 However, other studies suggest that patients taking daily maintenance doses of 400 mg or higher and those over 60 yr of age are more likely to develop lung toxicity.…”

Section: Discussionmentioning

confidence: 99%

Amiodarone lung toxicity in a cardiac transplant candidate initially diagnosed by fine‐needle aspiration: Cytologic, histologic, and electronmicroscopic findings

Ömeroğlu

Kalugina

Erşahin

et al. 2006

Diagnostic Cytopathology

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A cardiac transplant candidate with ischemic cardiomyopathy developed bilateral small parenchymal opacities in lower lobes of the lung. A fine-needle aspiration (FNA) was performed that revealed changes characteristic of amiodarone toxicity. Subsequently performed lung biopsies and electron microscopic studies confirmed the initial FNA diagnosis. The patient has been successfully transplanted with marked improvement in his clinical findings. This is the first case of amiodarone lung toxicity where the diagnosis was initially suggested based on the FNA findings. We also describe the clinical, cytological, histological, and electron microscopic (EM) findings of amiodarone-related pulmonary toxicity and provide a review of the literature.

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Section: Discussionmentioning

confidence: 99%

Amiodarone lung toxicity in a cardiac transplant candidate initially diagnosed by fine‐needle aspiration: Cytologic, histologic, and electronmicroscopic findings

Ömeroğlu

Kalugina

Erşahin

et al. 2006

Diagnostic Cytopathology

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“…It is important that upon termination of drug administration or exposure, PLDsis is generally reversible with the drug effluxing from the cell, the phospholipid levels returning to normal and morphological changes diminishing or disappearing [35][36][37][38][39][40] . The time course of the reversal is dependent on the dissociation rate of a CAD from the phospholipid and on the elimination rate of the CAD from the tissue, through the accumulation and efflux of active metabolites must also be considered 38,41 .…”

Section: Reversibilitymentioning

confidence: 99%

Drug-induced Phospholipidosis -Pathological Aspects and Its Prediction

Nonoyama

Fukuda

2008

J Toxicol Pathol

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Drug-induced phospholipidosis (PLDsis) is an excessive accumulation of polar phospholipids in cells or tissues/organs caused by xenobiotics. Numerous drugs and chemicals are capable of inducing the storage disorder in animals and humans; however, despite their diverse pharmacological activities, each of these drugs shares common physicochemical properties: a hydrophobic aromatic ring structure on the molecule and a hydrophilic side chain with a charged cationic amine group and therefore are in the group of cationic amphiphilic drugs. In affected cells the appearance of membrane-bound inclusions, primarily lysosomal in origin, with a lamellar structure (lamellar bodies) is a definitive morphologic hallmark. Massive accumulations can occur in animal tissues such as the lung with little effect on organ function. The inducing drug also accumulates in association with the excess phospholipid. Although these alterations are generally reversible after cessation of drug treatment, PLDsis is of regulatory concern and an issue for drug safety for pharmaceutical companies. Thus, the assessment of potential target organ dysfunction and the identification of clinical biomarkers are important objectives for new drug development. Recent advances in biotechnology such as metabonomics and toxicogenomics have been providing novel tools to elucidate the mechanisms of PLDsis and to establish biomarkers for screening tests in the preclinical stages and for monitoring in the clinical phases in addition to conventional approaches such as morphology (lamellar bodies) and biochemical methods including assays of specific metabolites and phospholipase inhibition. (J Toxicol Pathol 2008; 21: 9-24)

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“…This fact is not indicative of pulmonary toxicity. 10,18,19 We were not able to perform BAL because of the patient's severe hypoxemia.…”

Section: Discussionmentioning

confidence: 99%

Acute amiodarone toxicity causing respiratory failure

Kaya

Deger

Hacievlıyagıl

et al. 2017

Rev. Assoc. Med. Bras.

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A 66-year-old male patient was referred to our clinic with severe pneumonia. Bronchoscopy was performed due to clinical worsening despite antibiotics and diuretic therapy, respiratory failure and radiographic progression. Because bacterial cultures of the bronchoalveolar lavage fluid were negative and after using amiodarone for almost one month, we eliminated amiodarone from his medication regimen due to suspicion of amiodarone toxicity. Accordingly, we also initiated systemic steroid therapy. Chest X-ray done after 72 hours showed a significant resolution of lung consolidations and the patient exhibited significant clinical improvement, with decline of his oxygen requirements.

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Amiodarone-Associated Pulmonary Toxicity: A Clinical and Pathologic Study of Eleven Cases

Cited by 100 publications

References 0 publications

Amiodarone lung toxicity in a cardiac transplant candidate initially diagnosed by fine‐needle aspiration: Cytologic, histologic, and electronmicroscopic findings

Amiodarone lung toxicity in a cardiac transplant candidate initially diagnosed by fine‐needle aspiration: Cytologic, histologic, and electronmicroscopic findings

Drug-induced Phospholipidosis -Pathological Aspects and Its Prediction

Acute amiodarone toxicity causing respiratory failure

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