Determining New Onset Pulmonary Involvement of Connective Tissue Disease in a Patient with Recently Diagnosed Coronavirus Disease 2019

M. Patel, J. Willoughby, M. Kousha
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Abstract

A 49-year-old female presented due to sore throat, productive cough, fever, shortness of breath with a past medical history significant for COVID-19 infection in 04/20, nonsmoker, NSTEMI and diabetes mellitus type 2. On admission, labs revealed leukocytosis 16.33 K/mcL with left shift, D-dimer 9660 ngFEU/mL, elevated troponin x 3, lactic acid 2.4 mmol/L. Repeat COVID-19 test was negative on 05/20. Patient had an abnormal chest CT with diffuse ground glass opacities which is compatible with COVID-19 related post infectious inflammation. HIV panel and respiratory viral panel were negative. Due to elevated troponins with wall motion abnormalities patient underwent cardiac catheterization which revealed no obstructive coronary artery disease however right ventricular dysfunction was noted with elevated right ventricle (44 mmhg) and right atrium pressures (42 mmhg), normal pulmonary capillary wedge pressure. RV dysfunction was likely related to post COVID myocarditis/hypoxemic respiratory failure. Patient was discharged home on a course of prolonged steroid taper and 3-4 L oxygen. Four months later in 09/20 the patient again presented with similar complaints of shortness of breath and chest pain. Due to an elevated D-dimer and tachycardia, a CTA was obtained which was negative for pulmonary embolism however showed diffuse ground glass opacities which appeared to be persistent;distribution attenuation was also similar to previous study with worsening basilar regions concerning for consolidation. Laboratory studies in 09/2020 remarkable for leukocytosis with left shift, elevated troponin and total CK, urine toxicology was negative. Patient completed treatment for CAP on both admissions with no significant improvement. Routine immunology workup positive for ANA, speckled pattern with titer greater than 1:1280, serial rheumatoid factor 336.5 Lunits/ml, RNP antibody greater than 8 Al, SmRNP antibodies > 8.0 Al. All other immunologic workup were negative and the patient had no signs of rheumatologic conditions. Patient was started on a prolonged steroid course due to concern for superimposed mixed connective tissue disease (MCTD) pulmonary involvement with underlying CT manifestation of COVID 19, which drastically reduced her oxygen requirement. Chest CT images in patients with underlying COVID-19 infection can resemble and obscure new onset rheumatologic conditions with pulmonary involvement, such as mixed connective tissue disease, systemic lupus erythematosus, rheumatoid arthritis and hence it may delay the diagnosis of progressive pulmonary conditions which require prompt treatment. CTA on 09/20 (right) on admission showing bilateral diffuse ground glass opacities throughout the lung parenchyma with predominantly dense lower lobe opacities and mild air bronchogram (Left 05/20).
确定2019年新诊断冠状病毒病患者新发结缔组织病肺部累及
患者49岁,女性,因喉咙痛、咳嗽、发热、呼吸短促就诊,既往有明显的2019冠状病毒病感染病史,不吸烟,非stemi和2型糖尿病。入院时,实验室示白细胞增多16.33 K/mcL左移,d -二聚体9660 ngFEU/mL,肌钙蛋白x 3升高,乳酸2.4 mmol/L。5月20日复查COVID-19检测呈阴性。患者胸部CT异常,弥漫性磨玻璃影,符合COVID-19相关感染后炎症。HIV和呼吸道病毒均为阴性。由于肌钙蛋白升高和壁运动异常,患者行心导管检查,未发现阻塞性冠状动脉疾病,但右心室升高(44 mmhg)和右心房压力升高(42 mmhg),肺动脉毛细血管楔压正常,出现右心室功能障碍。RV功能障碍可能与COVID - 19后心肌炎/低氧性呼吸衰竭有关。患者出院后接受延长类固醇减量治疗和3-4升氧气治疗。4个月后,即2009年9月,患者再次出现类似的呼吸急促和胸痛主诉。由于d -二聚体升高和心动过速,CTA显示肺栓塞阴性,但弥漫的磨玻璃影似乎持续存在;分布衰减也与先前的研究相似,基底区恶化,涉及实变。2020年9月实验室检查:白细胞增多左移,肌钙蛋白和总CK升高,尿毒理学阴性。患者在两次入院时均完成了CAP治疗,无明显改善。常规免疫检查ANA阳性,斑点型,滴度大于1:1280,系列类风湿因子336.5 Lunits/ml, RNP抗体大于8al, SmRNP抗体>所有其他免疫检查均为阴性,患者无风湿病症状。由于担心合并混合性结缔组织病(MCTD)肺部累及潜在的COVID - 19 CT表现,患者开始接受延长的类固醇疗程,这大大降低了她的需氧量。潜在的COVID-19感染患者的胸部CT图像可能类似和模糊新发的肺部受累的风湿病,如混合性结缔组织病、系统性红斑狼疮、类风湿性关节炎,因此可能延迟需要及时治疗的进行性肺部疾病的诊断。2009年9月(右)入院时的CTA显示双侧弥漫性磨玻璃影,贯穿肺实质,主要是密集的下肺叶影和轻度支气管充气征(左)。
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