COVID-19是罪魁祸首吗?快速进展性组织性肺炎1例抗mda5抗体阳性

L. Mcnamara, V. A. Brady
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引用次数: 2

摘要

组织性肺炎是间质性肺疾病(ILD)的一个组织学亚型。虽然是对肺损伤的非特异性反应,但它可能与感染、自身免疫或药物毒性有关,也可能被定性为特发性。与COVID-19感染的关联仍在积极调查中。除了在COVID-19中看到的初始病毒血症之外,以过度活跃的宿主免疫反应为特征的后续阶段还不太清楚。抗黑色素瘤分化相关基因5 (MDA5)抗体与自身免疫性病理有关,包括皮肌炎和快速进行性ILD,并在一些COVID-19患者中呈阳性。我们描述了一例快速进展的组织性肺炎,抗mda5阳性,可能是由早期的COVID-19感染引起的。病例:一位70岁的男性,几个月前有COVID-19感染史,出现亚急性呼吸困难。他没有因COVID-19感染而住院,但随后出现缓慢进行性呼吸困难、喘息和炎症性迁移性多发性关节炎。每日口服甲基强的松龙32mg的门诊治疗改善了他的关节炎,然而,尽管额外吸入皮质类固醇和受体激动剂,他的呼吸症状并没有改善。入院影像显示新的双侧上肺叶主要磨玻璃影,外周间质网状和支气管扩张(图1)。感染性检查,包括SARS-CoV-2检测,均为阴性。风湿病检查显示类风湿因子、抗核抗体(1:160,弥漫性)和抗mda5抗体阳性。患者接受了广谱抗菌素和利尿治疗,但急性低氧血症/高碳呼吸衰竭恶化,需要插管和机械通气、俯压和神经肌肉阻滞。脉冲剂量类固醇与静脉注射甲基强的松龙每6小时250毫克,试验了几天没有改善。行视频辅助胸腔镜手术,活检显示闭塞性细支气管炎和组织性肺炎伴纤维化区,无透明膜形成或可见微生物。该患者不适合体外膜氧合,当上述活检结果出现时,他转移到舒适的重点护理,并死亡。尸检显示弥漫性肺泡损伤,伴透明膜形成,早期纤维增生灶和鳞状化生,组织实质瘢痕。讨论:抗mda5抗体阳性与快速进展的ILD有关,通常对类固醇等常规治疗难以治疗。虽然该患者的病理表现为组织性肺炎,但不幸的是,类固醇治疗没有改善。本例患者先前感染了COVID-19,随后在抗mda5抗体的情况下出现了快速进展的ILD,这引起了对病毒介导的自身免疫性ILD的关注。这凸显了了解SARS-CoV-2与宿主免疫反应和随后自身抗体发展的相互作用的紧迫性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Is COVID-19 the Culprit? A Case of Anti-MDA5 Antibody Positivity in a Rapidly Progressive Organizing Pneumonia
Introduction: Organizing pneumonia is a histologic subsect of interstitial lung disease (ILD). While a non-specific reaction to lung injury, it can be associated with infection, autoimmunity, or medication toxicity, or be characterized as idiopathic. Association with COVID-19 infection remains under active investigation. Beyond the initial viremia seen in COVID-19, the subsequent phase, characterized by an over-active host immune response, is less well understood. Anti-melanoma differentiation-associated gene 5 (MDA5) antibodies have been implicated in autoimmune pathology, including dermatomyositis and rapidly progressive ILD, and found to be positive in some patients with COVID-19. We describe a case of rapidly progressive organizing pneumonia with anti-MDA5 positivity, perhaps precipitated by earlier COVID-19 infection. Case: A 70-year-old gentleman with history of COVID-19 infection several months earlier presented with subacute dyspnea. He had not required hospitalization for COVID-19 infection, but subsequently developed slowly progressive dyspnea, wheezing, and inflammatory, migratory polyarthritis. Outpatient management with oral methylprednisolone 32mg daily, improved his arthritis, however, his respiratory symptoms did not improve despite additional inhaled corticosteroids and beta agonists. Admission imaging showed new bilateral upper lobe predominant ground glass opacities, reticulation of peripheral interstitium and bronchiectasis (Figure 1). Infectious workup, including SARS-CoV-2 testing, was negative. Rheumatologic workup revealed positive rheumatoid factor, anti-nuclear antibody (1:160, diffuse pattern) and anti-MDA5 antibody. The patient received broad spectrum antimicrobials and diuresis, but developed worsening acute hypoxemic/hypercarbic respiratory failure, requiring intubation and mechanical ventilation, proning, and neuromuscular blockade. Pulse dose steroids with intravenous methylprednisolone 250mg every six hours, were trialed for several days without improvements. Video assisted thorascopic surgery was performed and biopsy revealed bronchiolitis obliterans and organizing pneumonia with areas of fibrosis, without hyaline membrane formation or visible micro-organisms. The patient was not a candidate for extracorporeal membrane oxygenation and by the time the aforementioned biopsy resulted, he transitioned to comfort focused care, and died. Post-mortem examination revealed progression to diffuse alveolar damage with hyaline membrane formation, foci of early fibroplasia and squamous metaplasia and organizing parenchymal scars. Discussion: Anti-MDA5 antibody positivity has been implicated in rapidly progressive ILD often refractory to conventional treatments like steroids. While this patient's pathology showed organizing pneumonia, there was unfortunately no improvement with steroids. This case, of a patient with prior COVID-19 infection, who subsequently presented with rapidly progressive ILD in the setting of anti-MDA5 antibody, raises concern for viral-mediated autoimmune ILD. This highlights the urgency to understand SARS-CoV-2's interaction with the host immune response and subsequent autoantibody development.
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