Case Report of Severe Pulmonary Fibrosis as a Sequelae of Covid-19 Infection

Abstract

Though acute pulmonary manifestations of COVID-19 infection are well documented, the long-term sequelae from this viral infection are unclear. We report a case of a patient presenting with persistent respiratory failure after recovery from COVID-19 infection with imaging showing evidence of new onset pulmonary fibrosis. CASE PRESENTATION: 56 year-old Hispanic male with Diabetes Mellitus presents to ED for shortness of breath on exertion after recent hospitalization 16 days ago for Covid-19 infection. He reports progressive dyspnea since discharge, interfering with daily activities including walking to the bathroom and preparing food. He denies dyspnea at rest, cough, constitutional symptoms, or exposure to sick contacts. On his last visit, he was hospitalized for 24 days for Covid-19 pneumonia, and finished a course of antibiotics, hydroxychloroquine and steroids. PaO2/Fio2 ratio was 250, and oxygen requirements were met with nasal cannula, with gradual improvement to 95% saturation on room air. He denied previous hospitalizations, family history, occupational exposures and substance abuse. Vital Signs showed blood pressure 137/91 mmHg, Pulse 116 BPM, RR 22 Temperature 98.4 F. Physical exam was pertinent for fine velcro-like inspiratory and expiratory crackles auscultated at lung bases, saturating 94% on room air at rest but desaturating to 85% after walking 5 steps. Labs revealed chest x-ray showed patchy opacities diffusely worsened from previous visit. CTPE showed no pulmonary embolism, but diffuse bilateral patchy infiltrates with ground glass opacities and bronchiectasis. WBC was 8.64 [K/mm3], absolute lymphocyte count 1.73 K/mm3. BNP, procalcitonin, lactate, autoimmune workup and Echocardiogram were normal. Inflammatory markers were elevated but decreased from last admission. Quantiferon Gold was positive with three negative AFB smears suggesting latent tuberculosis. PFTs showed a moderate restrictive pattern. He was treated with methylprednisolone and oxygen to prevent further fibrosis in areas of active inflammation and isoniazid for latent TB. After symptomatic improvement, he was discharged on home oxygen and steroid taper with outpatient follow up.

Clinical Outcomes of Individuals with COVID-19 and Tuberculosis during the Pre-Vaccination Period of the Pandemic: A Systematic Review

“…Second, corticosteroid therapy was used in some persons with COVID-19 and TB co-infection. Some reports cited a TB-specific indication for corticosteroids, namely central nervous system TB [ 42 , 43 ], while others reported the use of corticosteroids as primary therapy for COVID-19 [ 33 , 38 , 45 ]. Third, persons with COVID-19 and TB co-infection presented with various comorbidities (HIV, diabetes mellitus, chronic kidney disease) [ 34 , 37 , 44 , 46 ] and complications: hepatotoxicity [ 33 , 35 ]; extension of the duration of standard TB treatment to 9 months [ 32 ]; drug-resistant TB [ 34 , 47 , 48 ]; extrapulmonary TB [ 42 , 43 , 48 ]; and death [ 33 , 38 , 48 ].…”

“…A vast majority of these patients received hydroxychloroquine, which is no longer the standard of care for COVID-19 directed treatment and could have possibly contributed to adverse outcomes [ 83 ]. A Among 4 persons coinfected with TB and COVID-19 who received corticosteroid therapy for COVID-19, two deaths were reported [ 33 , 38 , 45 ]. The use of corticosteroids for severe/critically ill, hospitalized persons with COVID-19 [ 84 ] raises the question about whether TB outcomes might, in fact, be worsened among persons coinfected with active TB and COVID-19 [ 38 ].…”

Tissue protective role of Ganetespib in SARS-CoV-2-infected Syrian golden hamsters

“…Reports have characterized the development of fibrotic lungs in COVID-19 patients, which may progress even after disease resolution, with virus eradication [67][68][69] . Monocytes and profibrotic macrophages play a critical role in the pathogenesis and progression of both ARDS and lung fibrosis [70][71][72] and a pronounced infiltration of monocyte-derived macrophages, which have a profibrotic nature, was seen in the lung of severe COVID-19 patients 16 .…”

TRIM2, S100A14, CYP4B1, LMO7, and SFN are signature genes in the progression of idiopathic pulmonary fibrosis epithelial cells to their lung adenocarcinoma comorbidities: a comprehensive analysis based on single-cell RNA sequencing data and RNA transcriptome data

“…And 6 categories of IPF-related cell types were identified, including Monocyte (cluster 0, 5,7,10, 13, 15, 16), Tissue_stem_cells (cluster 1, 6), Endothelial_cells (cluster 2, 9), Fibroblasts (cluster 3, 14), Macrophage (cluster 4, 8, 17), Epithelial_cells (cluster11, 12) (Figures 7G, H, I). As for LUADassociated cells, we annotated them into 4 categories, including Epithelial_cells (cluster 0, 1, 3,4,6,11,13,18,19,20,22,23,24), Tissue_stem_cells (cluster 2, 9, 10, 12), Macrophage (cluster 5,7,8,14,15,16,17,21,25), and Endothelial_cells (cluster 26) (Figures 7P, Q, R). In the study, we referenced 13 cell types for marker genes, including Cancer stem cells (PROM1, CD34, and CD90), Monocyte (CD14), M1 macrophages (CD16, FCGR3B, and FCGR1A), M2 macrophages (MSR1, CD163, MRC1, and CSF1R), CD8+ T cells (GZMK, CD8A, and CD8B), CD4+ memory cells (IL7R, CD27, and CCR7), B cells (CD79A and CD37), Regulatory T cells (LAG3, ITGA2, FOXP3, HELIOS, and NRP1), NK cells (CD160, NKG7, GNLY, CD247, CCL3, and GZMB), Fibroblasts (FGF7 and MME), Endothelial cells (PECAM1 and VWF), Neurons (ENO2), and Epithelial_cells (cD24, CDH1, and CLDN4).…”

“…[20]. Accumulating evidence suggests that the prevalence of pulmonary fibrosis is significantly higher in COVID-19 patients than in normal subjects [21][22][23]. Worse still, as of today (5 July 2023, 10:01 pm GMT+8), the WHO has counted a cumulative total of 767,726,861 confirmed cases of COVID-19, which would be the most important source of patients with IPF.…”