COP Out诊断:一例罕见的巨细胞病毒肺炎和covid - 19组织性肺炎

J. Khosa, I. C. Jun, K. Wei
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引用次数: 0

摘要

巨细胞病毒(CMV)肺炎在免疫功能低下的危险人群中是一种危及生命的疾病,并与隐源性组织性肺炎(COP)的发展有关。我们报告了一例独特的巨细胞病毒肺炎合并与最近的sars冠状病毒19 (covid - 19)感染相关的COP。临床医生必须认识到潜在的转移注意力或潜在的锚定偏见,以区分包括继发性机会性感染在内的covid - 19后遗症。描述:一位55岁的男士表现为发烧、咳嗽、呼吸困难和肌痛,持续9天,进展为急性低氧性呼吸衰竭。胸部CT示弥漫性磨玻璃空腔病变伴肺门淋巴结病变及左下基底实变(图1)。考虑的诊断鉴别包括社区获得性肺炎和covid - 19支气管肺炎。开始使用经验性抗生素、阿那白和全身性类固醇。最初的微生物学研究在细菌、真菌或病毒病因方面呈阴性,对自身免疫性疾病的血清学检测也呈阴性。5份拭子核酸扩增探针检测结果均为阴性。患者未能在临床上得到改善,最终被转介进行手术肺活检。活检显示核内病毒包涵体和慢性纤维化间质性肺炎合并巨细胞病毒肺炎。血清CMV聚合酶链反应(PCR)显示病毒载量为2520 IU/mL,随后发现COVID-19特异性血清IgG阳性。患者给予治疗剂量的更昔洛韦治疗两周,并给予较长的类固醇疗程治疗组织性肺炎。经过长时间的住院治疗后,患者出院回家,使用逐渐减少的强的松和补充氧气。讨论:据我们所知,迄今已有另一起病例报告了covid - 19和巨细胞病毒肺炎共存(1,3)。我们推测,以IgG阳性为证据的covid - 19感染可能是导致组织性肺炎发展的煽动事件。全身性类固醇可诱导相对免疫抑制状态,易发生机会性感染,如巨细胞病毒肺炎。另外,巨细胞病毒可以在危重患者中重新激活(2)。值得注意的是,该病例显示了混淆诊断和锚定偏差的危险,因为我们的患者在继发感染巨细胞病毒的情况下,可能对COP的全身类固醇治疗没有临床反应。这一病例突出表明,当患者对经验性治疗反应不充分时,有必要在诊断covid - 19后遗症时考虑其他可能的混杂因素,并对covid - 19患者进行更多的组织病理学或尸检检查。
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The COP Out Diagnosis: A Rare Case of CMV Pneumonitis and COVID19 Organizing Pneumonia
Introduction: Cytomegalovirus (CMV) pneumonitis is well known as a life-threatening condition in immunocompromised risk groups and has been implicated in the development of cryptogenic organizing pneumonia (COP). We present a unique case of CMV pneumonitis confounded by COP related to a recent SARS-Coronavirus 19 (COVID19) infection. It is important for clinicians to recognize underlying red herrings or potential anchoring bias in the differential of COVID19 sequelae including secondary opportunistic infections. Description: A fifty-five year old gentleman presented with fevers, cough, dyspnea, and myalgias for nine days which progressed to acute hypoxemic respiratory failure. Computed tomography (CT) of the chest showed diffuse ground glass airspace disease with hilar lymphadenopathy and left lower basal consolidation (Figure 1). Diagnostic differentials considered included community acquired pneumonia and COVID19 bronchopneumonia. Empiric antibiotics, Anakinra, and systemic steroids were started. Initial microbiologic studies were negative for bacterial, fungal or viral etiologies, as were serologic testing for autoimmune diseases. COVID19 nucleic acid amplification probes were negative on five separate swabs. The patient failed to clinically improve and ultimately was referred for surgical lung biopsy. The biopsy revealed intranuclear viral inclusions and findings of chronic fibrosing interstitial organizing pneumonia with CMV pneumonitis. Serum CMV polymerase chain reaction (PCR) showed a viral load of 2,520 IU/mL and COVID-19 specific serum IgG was later found to be positive. The patient was treated with therapeutic dose of ganciclovir for two weeks and given a longer steroid course for the organizing pneumonia. After a prolonged hospital stay, the patient was discharged home with tapered prednisone and supplemental oxygen. Discussion: The coexistence of COVID19 and CMV pneumonitis has reported to date in one other case to our knowledge (1,3). We hypothesize that COVID19 infection as evidenced by positive IgG could have served as the inciting event leading to the development of organizing pneumonia. Systemic steroids can induce a relative immunosuppressed state which predisposes to opportunistic infections like CMV pneumonitis. Alternatively, CMV can reactivate in critically ill patients (2). Of note, this case demonstrates the perils of confounding diagnoses and anchoring bias as our patient likely failed to respond clinically to systemic steroid therapy for COP while secondarily infected with CMV. This case highlights the need to consider other possible confounders in the diagnostic differential for COVID19 sequalae when patients are not responding adequately to empiric treatment and to evaluate more histopathologic or post-mortem examinations of COVID19 patients.
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