Marco Umberto Scaramozzino

La Madonnina Pneumology Clinic, Italy

Title: Amiodarone-induced lung toxicity, a case initially not correctly framed

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. Comorbidities, oxygen therapy, invasive procedures, and surgical interventions can trigger the pulmonary symptoms. The risk of developing amiodarone-induced pulmonary fibrosis is directly related to the dosage and duration of administration. 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 amiodarone-induced pneumopathy; 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. This case report describes a patient with aipt who markedly improved after treatment with prednisone at a starting dose of 50mg/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.

Panel A: Time zero chest CT scan showing: areas of bilateral apical centrolobular consolidation with thickening of the pulmonary reticular interstitium of the intra- and interlobular septa, with predominance in the right apical areas.

Panel B: Time zero chest CT scan showing:1) Areas of bilateral apical centrolobular 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 centrolobular consolidations. 2) 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 centrolobular consolidation 3) Areas of peri- and mid-basal centrolobular 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 centrolobular consolidation.

Panel C: Chest CT scan carried out at 3 months of therapy with oral corticosteroid, inhaled corticosteroid, and long-acting bronchodilator, showing apical, middle and basal areas almost complete regression of the areas of consolidation.

Biography

Marco Umberto Scaramozzino works at La Madonnina Pneumology Clinic in Italy.

4th International Conference on Global Healthcare and Nutrition

Marco Umberto Scaramozzino

Title: Amiodarone-induced lung toxicity, a case initially not correctly framed

Abstract

Biography

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