Pub Date : 2021-05-01DOI: 10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A2007
M. A. Ahmed, D. Verghese, Chenyu Sun, A. Mohan, D. Djondo
Coronavirus Disease 2019 (COVID-19) is known to have severe outcomes in patients with underlying comorbidities. Particularly, patients with compromised humoral immunity may face an increased risk for severe illness, as antibodies are essential for antiviral responses. Here, we present a COVID-19 patient with Bruton's X-linked agammaglobulinemia (XLA). A 46-year-old male with XLA receiving immunoglobulin replacement (IVIG) every three weeks, who contracted COVID-19 1-month ago, was admitted for 10-days of severe diarrhea and 3-days of exertional dyspnea. Repeat SARS-Co-V-2 PCR on admission was positive. Workup showed leukopenia and negative blood cultures. CT Chest Angiogram, performed for elevated D-dimer, revealed patchy bilateral ground-glass opacities, suggestive of viral/atypical pneumonia without pulmonary embolism. He received a 7-day course of Ceftriaxone and Azithromycin for community-acquired pneumonia and IVIG for low immunoglobulin levels. CT Abdomen and Pelvis, as well as a workup for infectious causes of diarrhea, were unremarkable. Colonoscopy ruled out microscopic and inflammatory colitis. Two stool SARS-Co-V-2 PCRs were negative. COVID IgG was negative, so he received COVID-19 Convalescent Plasma (CCP). Given his persistent fever spikes, bronchoscopy was performed, which was unremarkable;however, the bronchoalveolar lavage sample was positive for SARS-Co-V-2 PCR. The patient was hypoxemic and was started on Dexamethasone 6mg for 10-days. He was not a candidate for Remdesivir due to his delayed presentation. Tagged white blood cell (WBC) nuclear scan revealed mild pneumonia and mild sigmoid colonic WBC accumulation. The patient underwent prolonged hospitalization before improvement. As per the CDC's current recommendation to discontinue isolation 10-days from symptom onset, his isolation precautions were discontinued on the 16th day of hospitalization, 42 days after the first SARS-CoV-2 positive test. Given his underlying immunodeficiency, there was high suspicion that the patient was still infectious, putting frontline healthcare workers at risk. This was confirmed when an RT-PCR cell cycle threshold value (Ct) of 10.03 was obtained, which correlates to a highly culturable viral load and a highly infectious state. Isolation precautions were reinstated, and he was later discharged after another dose of CCP. Strict self-isolation for an additional ten days was advised. In summary, this patient with XLA had a lengthy hospital stay and prolonged viral shedding, likely due to an insufficient antibody response. In such patients, caution must be exercised when following the CDC recommendations for removing isolation precautions. RT-PCR Ct could be a valuable proxy in evaluating the state of infection and implementing appropriate infection control measures.
{"title":"The 'X' Factor: Exploring COVID-19 Viral Shedding in X-Linked Agammaglobulinemia. Can PCR Cell Cycle Threshold Play a Role?","authors":"M. A. Ahmed, D. Verghese, Chenyu Sun, A. Mohan, D. Djondo","doi":"10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A2007","DOIUrl":"https://doi.org/10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A2007","url":null,"abstract":"Coronavirus Disease 2019 (COVID-19) is known to have severe outcomes in patients with underlying comorbidities. Particularly, patients with compromised humoral immunity may face an increased risk for severe illness, as antibodies are essential for antiviral responses. Here, we present a COVID-19 patient with Bruton's X-linked agammaglobulinemia (XLA). A 46-year-old male with XLA receiving immunoglobulin replacement (IVIG) every three weeks, who contracted COVID-19 1-month ago, was admitted for 10-days of severe diarrhea and 3-days of exertional dyspnea. Repeat SARS-Co-V-2 PCR on admission was positive. Workup showed leukopenia and negative blood cultures. CT Chest Angiogram, performed for elevated D-dimer, revealed patchy bilateral ground-glass opacities, suggestive of viral/atypical pneumonia without pulmonary embolism. He received a 7-day course of Ceftriaxone and Azithromycin for community-acquired pneumonia and IVIG for low immunoglobulin levels. CT Abdomen and Pelvis, as well as a workup for infectious causes of diarrhea, were unremarkable. Colonoscopy ruled out microscopic and inflammatory colitis. Two stool SARS-Co-V-2 PCRs were negative. COVID IgG was negative, so he received COVID-19 Convalescent Plasma (CCP). Given his persistent fever spikes, bronchoscopy was performed, which was unremarkable;however, the bronchoalveolar lavage sample was positive for SARS-Co-V-2 PCR. The patient was hypoxemic and was started on Dexamethasone 6mg for 10-days. He was not a candidate for Remdesivir due to his delayed presentation. Tagged white blood cell (WBC) nuclear scan revealed mild pneumonia and mild sigmoid colonic WBC accumulation. The patient underwent prolonged hospitalization before improvement. As per the CDC's current recommendation to discontinue isolation 10-days from symptom onset, his isolation precautions were discontinued on the 16th day of hospitalization, 42 days after the first SARS-CoV-2 positive test. Given his underlying immunodeficiency, there was high suspicion that the patient was still infectious, putting frontline healthcare workers at risk. This was confirmed when an RT-PCR cell cycle threshold value (Ct) of 10.03 was obtained, which correlates to a highly culturable viral load and a highly infectious state. Isolation precautions were reinstated, and he was later discharged after another dose of CCP. Strict self-isolation for an additional ten days was advised. In summary, this patient with XLA had a lengthy hospital stay and prolonged viral shedding, likely due to an insufficient antibody response. In such patients, caution must be exercised when following the CDC recommendations for removing isolation precautions. RT-PCR Ct could be a valuable proxy in evaluating the state of infection and implementing appropriate infection control measures.","PeriodicalId":23189,"journal":{"name":"TP31. TP031 INTERESTING CASES ASSOCIATED WITH SARS-COV-2 INFECTION","volume":"21 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91011719","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-05-01DOI: 10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A1993
S. Golob, L. Winston, D. Manson, S. Fedyna
Introduction: Electronic-cigarette or vaping-product associated lung injury (EVALI) was first identified in August 2019, when U.S. public health officials noted a clinical syndrome of acute respiratory failure and systemic inflammation associated with the use of aerosolized nicotine and cannabinoids. The presence of lipid-laden macrophages on bronchiolar lavage is a specific but not sensitive histological finding of EVALI, which is often a diagnosis of exclusion. In 2020, the first cases of COVID-19, caused by SARS-CoV2 virus, were seen in the U.S. Both COVID-19 and EVALI can affect previously healthy individuals, manifesting with severe hypoxemia and systemic inflammation, posing diagnostic challenges in distinguishing the two syndromes. Secondary spontaneous pneumothorax is a well-described complication of COVID-19 yet is only rarely associated with EVALI, with only one published case report of EVALI complicated by pneumothorax. Here, we report a case of a 34-year-old man presenting with hypoxemic respiratory failure complicated by pneumothorax, initially thought to be from COVID-19 pneumonia, found ultimately to have EVALI associated diffuse alveolar damage. Case: In April 2020, a 34-year-old man presented with one week of myalgia, shortness of breath, and a reduced exercise tolerance. Social history was notable for extensive vaping. His exam was notable for hypoxemia requiring nonrebreather. Testing showed elevated inflammatory markers and diffuse bilateral opacities on chest radiography. Nasopharyngeal PCR was negative for SARS-CoV2. CT chest revealed dense consolidation with ground grass opacities and air bronchograms. Rheumatologic and infectious workup was unremarkable. Despite six negative SARS-CoV2 tests, he was treated for COVID-19 with empiric steroids and antibiotics for community-acquired pneumonia. On hospital day 3, he developed a right-sided pneumothorax requiring chest tube. On hospital day 12, he developed a left-sided pneumothorax and a second chest tube was placed. A presumptive diagnosis of pneumonitis and diffuse alveolar damage secondary to EVALI was made. Given non-healing bilateral pneumothoraces, on hospital day 32, he underwent chemical pleurodesis with doxycycline which was complicated by ARDS. He was intubated, suffered a PEA arrest from refractory hypoxemia, and emergently cannulated to VV ECMO. A head CT demonstrated diffuse cerebral edema suggestive of anoxic brain injury. After extensive goals of care discussions, care was withdrawn and the patient passed away. Discussion: EVALI, similar to COVID-19, is syndrome of severe acute hypoxemia and systemic inflammation. Both conditions have similar radiographic findings with ground glass opacities indicative of alveolar damage, histological findings of tracheobronchitis and diffuse alveolar damage, and can lead to secondary spontaneous pneumothoraces.
{"title":"E-Cigarette or Vaping-Product Associated Lung Injury Complicated by Spontaneous Pneumothoraces in the Setting of COVID-19 Pandemic","authors":"S. Golob, L. Winston, D. Manson, S. Fedyna","doi":"10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A1993","DOIUrl":"https://doi.org/10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A1993","url":null,"abstract":"Introduction: Electronic-cigarette or vaping-product associated lung injury (EVALI) was first identified in August 2019, when U.S. public health officials noted a clinical syndrome of acute respiratory failure and systemic inflammation associated with the use of aerosolized nicotine and cannabinoids. The presence of lipid-laden macrophages on bronchiolar lavage is a specific but not sensitive histological finding of EVALI, which is often a diagnosis of exclusion. In 2020, the first cases of COVID-19, caused by SARS-CoV2 virus, were seen in the U.S. Both COVID-19 and EVALI can affect previously healthy individuals, manifesting with severe hypoxemia and systemic inflammation, posing diagnostic challenges in distinguishing the two syndromes. Secondary spontaneous pneumothorax is a well-described complication of COVID-19 yet is only rarely associated with EVALI, with only one published case report of EVALI complicated by pneumothorax. Here, we report a case of a 34-year-old man presenting with hypoxemic respiratory failure complicated by pneumothorax, initially thought to be from COVID-19 pneumonia, found ultimately to have EVALI associated diffuse alveolar damage. Case: In April 2020, a 34-year-old man presented with one week of myalgia, shortness of breath, and a reduced exercise tolerance. Social history was notable for extensive vaping. His exam was notable for hypoxemia requiring nonrebreather. Testing showed elevated inflammatory markers and diffuse bilateral opacities on chest radiography. Nasopharyngeal PCR was negative for SARS-CoV2. CT chest revealed dense consolidation with ground grass opacities and air bronchograms. Rheumatologic and infectious workup was unremarkable. Despite six negative SARS-CoV2 tests, he was treated for COVID-19 with empiric steroids and antibiotics for community-acquired pneumonia. On hospital day 3, he developed a right-sided pneumothorax requiring chest tube. On hospital day 12, he developed a left-sided pneumothorax and a second chest tube was placed. A presumptive diagnosis of pneumonitis and diffuse alveolar damage secondary to EVALI was made. Given non-healing bilateral pneumothoraces, on hospital day 32, he underwent chemical pleurodesis with doxycycline which was complicated by ARDS. He was intubated, suffered a PEA arrest from refractory hypoxemia, and emergently cannulated to VV ECMO. A head CT demonstrated diffuse cerebral edema suggestive of anoxic brain injury. After extensive goals of care discussions, care was withdrawn and the patient passed away. Discussion: EVALI, similar to COVID-19, is syndrome of severe acute hypoxemia and systemic inflammation. Both conditions have similar radiographic findings with ground glass opacities indicative of alveolar damage, histological findings of tracheobronchitis and diffuse alveolar damage, and can lead to secondary spontaneous pneumothoraces.","PeriodicalId":23189,"journal":{"name":"TP31. TP031 INTERESTING CASES ASSOCIATED WITH SARS-COV-2 INFECTION","volume":"28 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74575052","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-05-01DOI: 10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A2009
J. Kirupakaran, D. Valentine, A. Idowu, M. Jiménez, M. Okaikoi, A. M. Thida, G. Bahtiyar, G. Aristide, G. Rodriguez
INTRODUCTION Coronavirus-19 disease (COVID-19) caused by the novel Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) continues to be a major cause of mortality worldwide. Advanced age and a number of chronic diseases have been investigated as risk factors for poor outcomes in patients with COVID-19. Likewise, Human Immunodeficiency Virus (HIV) has been proposed as a potential risk factor for COVID-19, however, the possible relationship between HIV and COVID-19 has remained difficult to fully elucidate due to a paucity of data. We describe a case series of 11 patients co-infected with HIV and SARS-CoV-2. CASE PRESENTATION Between March 20, 2020 and May 5, 2020, 11 patients with HIV were admitted for COVID-19at an underserved community hospital in Brooklyn, NY. . Patients ranged from 39 to 78 years of age. Seven patients were men and four patients were women. Seven patients were African American and four patients were Hispanic. All 11 patients possessed HIV RNA viral loads less than 40 copies/ml. The mean CD4 count was 556 cells/ml (range 171-1123 cells/ml). Nine patients were on antiretroviral therapy (ART). Six patients required invasive mechanical ventilation;five of the six patients died. Two of these five patients were not on ART, prior to admission and two of them developed acute respiratory distress syndrome during their hospital course. The mean length of stay was 10.9 days (range 2-21 days). Three of the six survivors were readmitted within 30 days for CHF exacerbation, bacterial pneumonia and COPD exacerbation. All three patients recovered without complications. At six-month follow-up, no mortalities were reported among the six surviving patients. DISCUSSION This case series presents a unique sample of African American and Hispanic patients co-infected with HIV and SARS-CoV-2. This is the first case series to report long term outcomes among minority population. The high mortality rate in this case series (45%) is also notable in comparison to prior research. This elevated mortality rate may reflect an increased burden of comorbidities in HIV patients. Further research is required to reveal if ART therapy reduces risk of poor outcomes, and if so, which regimen may confer protection against COVID-19.
{"title":"Clinical Features and Outcomes of Hospitalized Patients Co-Infected with COVID-19 and HIV: A Case Series","authors":"J. Kirupakaran, D. Valentine, A. Idowu, M. Jiménez, M. Okaikoi, A. M. Thida, G. Bahtiyar, G. Aristide, G. Rodriguez","doi":"10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A2009","DOIUrl":"https://doi.org/10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A2009","url":null,"abstract":"INTRODUCTION Coronavirus-19 disease (COVID-19) caused by the novel Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) continues to be a major cause of mortality worldwide. Advanced age and a number of chronic diseases have been investigated as risk factors for poor outcomes in patients with COVID-19. Likewise, Human Immunodeficiency Virus (HIV) has been proposed as a potential risk factor for COVID-19, however, the possible relationship between HIV and COVID-19 has remained difficult to fully elucidate due to a paucity of data. We describe a case series of 11 patients co-infected with HIV and SARS-CoV-2. CASE PRESENTATION Between March 20, 2020 and May 5, 2020, 11 patients with HIV were admitted for COVID-19at an underserved community hospital in Brooklyn, NY. . Patients ranged from 39 to 78 years of age. Seven patients were men and four patients were women. Seven patients were African American and four patients were Hispanic. All 11 patients possessed HIV RNA viral loads less than 40 copies/ml. The mean CD4 count was 556 cells/ml (range 171-1123 cells/ml). Nine patients were on antiretroviral therapy (ART). Six patients required invasive mechanical ventilation;five of the six patients died. Two of these five patients were not on ART, prior to admission and two of them developed acute respiratory distress syndrome during their hospital course. The mean length of stay was 10.9 days (range 2-21 days). Three of the six survivors were readmitted within 30 days for CHF exacerbation, bacterial pneumonia and COPD exacerbation. All three patients recovered without complications. At six-month follow-up, no mortalities were reported among the six surviving patients. DISCUSSION This case series presents a unique sample of African American and Hispanic patients co-infected with HIV and SARS-CoV-2. This is the first case series to report long term outcomes among minority population. The high mortality rate in this case series (45%) is also notable in comparison to prior research. This elevated mortality rate may reflect an increased burden of comorbidities in HIV patients. Further research is required to reveal if ART therapy reduces risk of poor outcomes, and if so, which regimen may confer protection against COVID-19.","PeriodicalId":23189,"journal":{"name":"TP31. TP031 INTERESTING CASES ASSOCIATED WITH SARS-COV-2 INFECTION","volume":"75 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86707232","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-05-01DOI: 10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A1986
Lisa N Glass, Pulmonary Disease, Sandrine Hanna, John P Lichtenberger, Ivana Milojevic, J. Ahari
Organizing pneumonia is a process of lung parenchymal injury caused by multiple etiologies. Although organizing pneumonia may be an idiopathic process, it usually occurs secondary to infection, aspiration, autoimmune disease, and after organ transplantation or radiation. We present a case of organizing pneumona after confirmed SARS-CoV-2 (COVID-19) infection manifesting as chronic cough. Keywords: Organizing pneumonia; COVID-19; Post-viral syndrome; Chronic cough.
{"title":"A Continuous Cough After COVID-19","authors":"Lisa N Glass, Pulmonary Disease, Sandrine Hanna, John P Lichtenberger, Ivana Milojevic, J. Ahari","doi":"10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A1986","DOIUrl":"https://doi.org/10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A1986","url":null,"abstract":"Organizing pneumonia is a process of lung parenchymal injury caused by multiple etiologies. Although organizing pneumonia may be an idiopathic process, it usually occurs secondary to infection, aspiration, autoimmune disease, and after organ transplantation or radiation. We present a case of organizing pneumona after confirmed SARS-CoV-2 (COVID-19) infection manifesting as chronic cough. Keywords: Organizing pneumonia; COVID-19; Post-viral syndrome; Chronic cough.","PeriodicalId":23189,"journal":{"name":"TP31. TP031 INTERESTING CASES ASSOCIATED WITH SARS-COV-2 INFECTION","volume":"89 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79019275","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2021-05-01DOI: 10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A2000
G. C. Chiang, T. Zaman, P. Noble
A 79-year-old male presented for evaluation of dyspnea and dry cough. Five months prior he was hospitalized with COVID-19 and a pulmonary embolus requiring 2L/min of supplemental oxygen, enoxaparin, hydroxychloroquine and remdesivir. He was discharged home with apixaban and supplemental oxygen. He had a 10 pack-per-year history of smoking and quit fifty years ago. He had no occupational or environmental exposures associated with pulmonary fibrosis. He had no family history of connective tissue disease or pulmonary fibrosis. On physical examination, he had normal vital signs and his saturation was 100% on room air. Pertinent positive exam findings were limited to bibasilar dry crackles. There were no skin, joint, or oral findings. Pulmonary function tests showed normal lung volumes with normal spirometry and a severely decreased diffusing capacity. A CT revealed improvement of ground glass opacities with persistent subpleural reticulations and honeycombing. Notably, lung images of the lower lobes from a CT scan of the abdomen six years prior to this evaluation showed bibasilar reticulations and ground glass infiltrates. Laboratory studies were notable for an elevated ANA titer in a speckled pattern, elevated CCP and elevated anti-SSA 52 kD. Additional autoimmune serologies were negative. Given the presence of interstitial lung abnormalities (ILAs) in prior imaging and elevated autoimmune markers, he was deemed to have had an exacerbation of previously subclinical ILD caused by COVID-19. The long-term effects of the inflammatory response from COVID-19 have not been characterized. Initial data of CT scans in patients show that up to 17% develop fibrotic changes during the course of the disease. It remains to be seen whether there will be a progressive fibrotic phenotype solely attributable COVID-19 itself. This has been described during the H1N1 and SARS-COV1 outbreaks in patients who developed ARDS but is not observed in post-ARDS pulmonary fibrosis caused by other etiologies. The key to differentiating between a primary ILD rather than post-COVID-19 hinges on antecedent history. The patient's prior radiographic findings meet the research construct of interstitial lung abnormalities (ILA) which refers to patterns of increased lung density in patients with no history of ILD. When post-COVID-19 pulmonary fibrosis is observed, due diligence must be taken to determine alternate etiologies of subclinical ILD that may have been unmasked by COVID-19, rather than caused by it. It remains unclear whether SARS-CoV-2 could activate a latent autoimmunity or potentially cause a de novo autoimmune lung disease as has been suggested.
{"title":"The Chicken or the Egg? Newly Diagnosed Interstitial Lung Disease (ILD) After Novel Coronavirus Pneumonia (COVID-19)","authors":"G. C. Chiang, T. Zaman, P. Noble","doi":"10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A2000","DOIUrl":"https://doi.org/10.1164/AJRCCM-CONFERENCE.2021.203.1_MEETINGABSTRACTS.A2000","url":null,"abstract":"A 79-year-old male presented for evaluation of dyspnea and dry cough. Five months prior he was hospitalized with COVID-19 and a pulmonary embolus requiring 2L/min of supplemental oxygen, enoxaparin, hydroxychloroquine and remdesivir. He was discharged home with apixaban and supplemental oxygen. He had a 10 pack-per-year history of smoking and quit fifty years ago. He had no occupational or environmental exposures associated with pulmonary fibrosis. He had no family history of connective tissue disease or pulmonary fibrosis. On physical examination, he had normal vital signs and his saturation was 100% on room air. Pertinent positive exam findings were limited to bibasilar dry crackles. There were no skin, joint, or oral findings. Pulmonary function tests showed normal lung volumes with normal spirometry and a severely decreased diffusing capacity. A CT revealed improvement of ground glass opacities with persistent subpleural reticulations and honeycombing. Notably, lung images of the lower lobes from a CT scan of the abdomen six years prior to this evaluation showed bibasilar reticulations and ground glass infiltrates. Laboratory studies were notable for an elevated ANA titer in a speckled pattern, elevated CCP and elevated anti-SSA 52 kD. Additional autoimmune serologies were negative. Given the presence of interstitial lung abnormalities (ILAs) in prior imaging and elevated autoimmune markers, he was deemed to have had an exacerbation of previously subclinical ILD caused by COVID-19. The long-term effects of the inflammatory response from COVID-19 have not been characterized. Initial data of CT scans in patients show that up to 17% develop fibrotic changes during the course of the disease. It remains to be seen whether there will be a progressive fibrotic phenotype solely attributable COVID-19 itself. This has been described during the H1N1 and SARS-COV1 outbreaks in patients who developed ARDS but is not observed in post-ARDS pulmonary fibrosis caused by other etiologies. The key to differentiating between a primary ILD rather than post-COVID-19 hinges on antecedent history. The patient's prior radiographic findings meet the research construct of interstitial lung abnormalities (ILA) which refers to patterns of increased lung density in patients with no history of ILD. When post-COVID-19 pulmonary fibrosis is observed, due diligence must be taken to determine alternate etiologies of subclinical ILD that may have been unmasked by COVID-19, rather than caused by it. It remains unclear whether SARS-CoV-2 could activate a latent autoimmunity or potentially cause a de novo autoimmune lung disease as has been suggested.","PeriodicalId":23189,"journal":{"name":"TP31. TP031 INTERESTING CASES ASSOCIATED WITH SARS-COV-2 INFECTION","volume":"84 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84284136","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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