Kohli Akshay, Sharma Avinash V
Internal Medicine, MedStar Washington Hospital Center, Washington DC, USA.
Cardiology, University of California, San Francisco, Fresno, USA.
Cureus. 2020 Oct 12;12(10):e10913. doi: 10.7759/cureus.10913.
Amiodarone is widely used as an antiarrhythmic agent for the treatment of both supraventricular and ventricular arrhythmias in various inpatient as well as outpatient settings. Classified as a class III antiarrhythmic agent, it acts mainly by inhibition of potassium channels in the cardiac muscle. Adverse effects are quite common and usually involve pulmonary, gastrointestinal, endocrine, dermatologic, or neuromuscular systems. Although hematologic side effects including thrombocytopenia have also been reported, amiodarone-induced neutropenia is quite rare. We present a case of amiodarone-induced neutropenia in a 66-year-old Caucasian gentleman. He presented to our hospital with cardiac arrest due to ventricular-fibrillation and had received amiodarone as a part of his therapy. His hospital course was complicated by neutropenia which was found to have a clear temporal relation with amiodarone. His initial white blood cell count was 6400/mm3 with an absolute neutrophil count (ANC) of 4800/mm3. His ANC started to downtrend and reached a nadir of 400/mm3 at day six of therapy. This improved significantly after stopping amiodarone, without any change in other medications. Given the rapid improvement of his neutropenia with the discontinuation of amiodarone, further workup with a bone marrow biopsy was not performed. Severe selective neutropenia, also known as agranulocytosis, is a life-threatening condition due to increased risk of severe infections. Antiarrhythmic agents such as tocainamide, procainamide, and flecainide are generally known to cause agranulocytosis. The mechanism of agranulocytosis or neutropenia is thought to be mediated by either immune-mediated destruction or direct and indirect toxicity to myeloid precursors. Although amiodarone has been in use for over 20 years in the management of tachyarrhythmias, agranulocytosis as a direct side effect of amiodarone therapy has been rarely reported. It is important to keep in mind this rare but potentially life-threatening adverse effect of amiodarone when initiating therapy.
胺碘酮作为一种抗心律失常药物，广泛应用于各类住院及门诊患者，用于治疗室上性和室性心律失常。它被归类为Ⅲ类抗心律失常药物，主要通过抑制心肌中的钾通道发挥作用。不良反应相当常见，通常累及肺、胃肠道、内分泌、皮肤或神经肌肉系统。虽然也有包括血小板减少在内的血液学副作用的报道，但胺碘酮所致中性粒细胞减少相当罕见。我们报告一例66岁白种男性因胺碘酮导致中性粒细胞减少的病例。他因心室颤动导致心脏骤停入院，接受胺碘酮治疗作为其治疗的一部分。他的住院病程因中性粒细胞减少而复杂化，发现该情况与胺碘酮有明确的时间关系。他最初的白细胞计数为6400/mm³，绝对中性粒细胞计数（ANC）为4800/mm³。他的ANC开始下降，在治疗第6天降至最低点400/mm³。停用胺碘酮后，情况显著改善，其他药物未作任何改变。鉴于停用胺碘酮后他的中性粒细胞减少迅速改善，未进行骨髓活检等进一步检查。严重的选择性中性粒细胞减少，也称为粒细胞缺乏症，是一种因严重感染风险增加而危及生命的疾病。一般已知抗心律失常药物如妥卡尼、普鲁卡因胺和氟卡尼会导致粒细胞缺乏症。粒细胞缺乏症或中性粒细胞减少的机制被认为是由免疫介导的破坏或对髓系前体细胞的直接和间接毒性介导的。虽然胺碘酮已用于治疗快速性心律失常20多年，但胺碘酮治疗直接导致粒细胞缺乏症的情况很少报道。开始治疗时牢记胺碘酮这种罕见但可能危及生命的不良反应很重要。
