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Amiodarone‐Induced Neuropathy with chronic inflammatory demyelinating polyneuropathy‐like presentation
Author(s) -
Okhovat Ali Asghar,
Saffar Hiva,
Fatehi Farzad
Publication year - 2020
Publication title -
neurology and clinical neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.125
0ISSN - 2049-4173
DOI - 10.1111/ncn3.12373
Subject(s) - medicine , amiodarone , pulmonary toxicity , polyneuropathy , pathology , peripheral neuropathy , pathological , pulmonary fibrosis , riluzole , fibrosis , lung , endocrinology , amyotrophic lateral sclerosis , disease , diabetes mellitus , atrial fibrillation
Long‐term administration of amiodarone may have various neurological complications and systemic involvement. Herein, we report a 46‐year‐old male patient who was admitted as a result of paresthesia and progressive four‐limb weakness started six months before. Spiral chest CT scan showed bilateral hyper‐dense consolidations predominately seen in peripheral and lower lobes. We checked the serum level of amiodarone that was 3.1 mg/L (therapeutic range: 1.5 and 2.5 µg/mL). According to the characteristic pulmonary findings in lung CT scan, demyelinating polyneuropathy, and lack of response to treatment, with the suspicion of amiodarone toxicity, CT‐guided percutaneous core needle biopsy was performed. The pathological assessment revealed chronic interstitial inflammation and fibrosis, and exudation of macrophages with finely cytoplasmic vacuolization associated with hyperplasia of type II pneumocytes in alveoli with necrosis. These findings are consistent with amiodarone‐induced pulmonary toxicity. Chronic use of amiodarone may present as a CIDP‐like presentation, which may be overlooked if clinical suspicion is not high upon presentation.