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Case Reports
. 2023 Mar 28;15(3):e36818.
doi: 10.7759/cureus.36818. eCollection 2023 Mar.

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

Affiliations
Case Reports

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

Marco Umberto Scaramozzino Sr et al. Cureus. .

Abstract

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.

Keywords: aipt; amiodarone; ground glass opacity; hyper-reactivity; ocs.

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Conflict of interest statement

The authors have declared that no competing interests exist.

Figures

Figure 1
Figure 1. A: Time zero chest CT scan showing areas of bilateral apical centrilobular consolidation with thickening of the pulmonary reticular interstitium of the intra- and interlobular septa, with predominance in the right apical areas. B: Time zero chest CT scan showing areas of bilateral apical centrilobular consolidation with thickening of the pulmonary reticular interstitium of the intra- and interlobular septa, with predominance at the right apical zones with presence in both lungs at the submantellar zones of solid centrilobular consolidations. C: Chest CT scan at time zero showing areas of right perilobular consolidation with thickening of the reticular pulmonary interstitium of the intra- and interlobular septa and prevalence in the right middle field of areas of solid centrilobular consolidation. D-E-F: Time-zero chest CT scan showing areas of peri- and mid-basal centrilobular consolidation prevailing on the right, thickening of the reticular pulmonary interstitium intra- and interlobular septa, and predominance in the mid-right field of areas of solid centrilobular consolidation. G-H-I: Chest CT scan carried out at three months of therapy with an oral corticosteroid, inhaled corticosteroid, and a long-acting bronchodilator, showing apical, middle, and basal areas almost complete regression of the areas of consolidation.
CT: computed tomography

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