The Chicken or the Egg? Newly Diagnosed Interstitial Lung Disease (ILD) After Novel Coronavirus Pneumonia (COVID-19)

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.