Pulmonary Fibrosis Related to Amiodarone—Is It a Standard Pathophysiological Pattern? A Case-Based Literature Review

Budin, Corina Eugenia; Cocuz, Iuliu Gabriel; Sabău, Adrian Horaţiu; Niculescu, Raluca; Ianosi, Ingrid Renata; Ioan, Vladimir; Cotoi, Ovidiu Simion

doi:10.3390/diagnostics12123217

Cited by 8 publications

(5 citation statements)

References 52 publications

(125 reference statements)

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“…Currently, there are no clear diagnostic criteria for lung injury caused by amiodarone, and ruling out such a diagnosis is the main focus. Differential diagnoses include infectious diseases, collagen diseases, congestive heart failure, and pulmonary infarction (5). In the present case, there were no serological findings suggestive of collagen disease.…”

Section: Discussioncontrasting

confidence: 46%

Autopsy of Drug-induced Lung Injury with Atypical Diffuse Alveolar Disorder due to Amiodarone: A Case Report

Mamizu,

Kohda,

Tomita

et al. 2024

Intern. Med.

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Amiodarone, a prominent antiarrhythmic drug, may cause lung injury. We herein report the case of an 87year-old man who had been taking amiodarone for 5 years and was subsequently referred due to respiratory failure. Chest computed tomography revealed multiple consolidations with air bronchograms in both lungs. Despite administering steroid pulse therapy, his respiratory failure worsened, and he died 3 days later. Autopsy revealed hyaline membrane formation and organic formation with fibrin deposition. Drug-induced lung injury caused by amiodarone was confirmed by autopsy. Caution is therefore required when fibrin deposition in the alveolar spaces is observed in such cases, which are prone to suffer a rapid deterioration.

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Section: Discussioncontrasting

confidence: 46%

Autopsy of Drug-induced Lung Injury with Atypical Diffuse Alveolar Disorder due to Amiodarone: A Case Report

Mamizu,

Kohda,

Tomita

et al. 2024

Intern. Med.

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“…Lung injuries are caused by the accumulation of phospholipid complexes in histocytes and type II pneumocytes, the medication can lead to mild to severe lung injuries, involving both the parenchyma and the pleura [9], and may cause respiratory failure. Reducing the dosage of amiodarone considerably decreases the incidence of these complications, however, AIPT can be life-threatening and there can be acute cases [10].…”

Section: Discussionmentioning

confidence: 99%

Amiodarone-Induced Lung Toxicity: A Case Initially Not Correctly Framed

Scaramozzino¹,

Sapone²,

Plastina³

et al. 2023

Cureus

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Amiodarone-induced pulmonary toxicity (AIPT) is one of the most serious adverse effects of amiodarone and is one of the leading causes of death associated with its use. The onset of AIPT depends on dosage, patient's age, and pre-existing pulmonary pathologies; typically, the adverse effects stop progressing when a cumulative dose higher than 150 mg is reached. The risk of developing amiodarone-induced pulmonary fibrosis is directly related to the dosage and duration of administration. In this case report, the effect of a prolonged overdose of amiodarone taken at doses of 200 mg/day for two years is reported, with symptoms and instrumental evidence of respiratory pathology induced by amiodarone drug toxicity. Comorbidities, oxygen therapy, invasive procedures, and surgical interventions can trigger pulmonary symptoms. Despite significant advances in understanding AIPT, its etiology and pathogenesis remain poorly understood. The role of steroids in the treatment of AIPT is still under debate as most reports of improvement after amiodarone withdrawal differ little from those in which concomitant steroid therapy was used. In clinical practice, therapeutic doses of corticosteroids may be indicated for patients with AIPT; usually, a starting dose of prednisone from 40 to 60 mg daily, which is then gradually reduced, is prescribed. The pharmacodynamics of amiodarone determines a treatment period of four to 12 months.The patient with AIPT in this case report, who markedly improved after treatment with prednisone at a starting dose of 50 mg/day, which was then gradually tapered. At the end of the therapy, the computed tomography (CT) scan revealed the disappearance of most of the scattered ground-glass opacities and of the thickening indicating bi-apical pulmonary fibrosis.The case report is unique because: 1) Bronchoalveolar lavage (BAL)/transbronchial biopsy was not used for diagnosis.2) The case was framed based on the patient's laboratory and clinical data.3) The pathology is normally prevalent in men rather than women.

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“…Amiodarone induces pulmonary toxicity through a direct cytotoxic effect, an indirect damage through an immunological reaction or through accumulation of phospholipid complexes within the lung parenchyma and/or the pleura. 6 , 8 , 9 It has also been found to increase the production of toxic-free radicals in tissues. 10 APT is less frequent than thyroid and eye complications, but it is deemed to be the most dangerous of all possible complications.…”

Section: Discussionmentioning

confidence: 99%

“…The effects of amiodarone on the lung can take on an acute, subacute or a chronic form. 9 Some initial pulmonary specific events are bronchospasm, exacerbation of obstructive airway diseases, interstitial pneumonias, acute respiratory distress syndromes, pleural effusion, interstitial thickenings, and diffuse alveolar haemorrhages. 3 , 6 , 10 , 11 Masses and nodules are typically formed in later stages of APT.…”

Section: Discussionmentioning

confidence: 99%

Too Little, Too Late: A Case of a Swift Fatal Culmination of Amiodarone Induced Pulmonary Toxicity in an Adult Male

Tan,

Kumar

2023

IMCRJ

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Amiodarone is a commonly prescribed antiarrhythmic drug. It can cause a myriad of complications associated with its long-term use, with amiodarone induced pulmonary toxicity being the worst. Amiodarone does this through its destructive properties and its’ ability to accumulate if taken for extended periods of time or in high cumulative doses. Albeit uncommon, the management of amiodarone induced pulmonary toxicity can be straightforward if recognized early. Otherwise, it can lead to severe respiratory failure causing death. In this case report, we aim to highlight the importance of vigilance with clinicians prescribing amiodarone and to spark interests into research for alternative management options of amiodarone induced pulmonary toxicity. This will be done through the description of a case of a 64-year-old male presenting with cough and dyspnoea, who has been on a large dose of amiodarone daily for the past 11 months. He was diagnosed too little, too late, which unfortunately culminated in his rapid fatality. This case is unique for two reasons. The diagnosis of amiodarone induced pulmonary toxicity was through the clinical picture – without the use of invasive investigations. In addition, the futile cessation of amiodarone and use of high dose systemic corticosteroids as a management – which to our knowledge is uncommon in literature.

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Pulmonary Fibrosis Related to Amiodarone—Is It a Standard Pathophysiological Pattern? A Case-Based Literature Review

Cited by 8 publications

References 52 publications

Autopsy of Drug-induced Lung Injury with Atypical Diffuse Alveolar Disorder due to Amiodarone: A Case Report

Autopsy of Drug-induced Lung Injury with Atypical Diffuse Alveolar Disorder due to Amiodarone: A Case Report

Amiodarone-Induced Lung Toxicity: A Case Initially Not Correctly Framed

Too Little, Too Late: A Case of a Swift Fatal Culmination of Amiodarone Induced Pulmonary Toxicity in an Adult Male

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