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1.
Eur Respir Rev ; 30(162)2021 Dec 31.
Article in English | MEDLINE | ID: covidwho-1575132

ABSTRACT

Acute manifestations of SARS-CoV-2 infection continue to impact the lives of many across the world. Post-acute sequelae of coronavirus disease 2019 (COVID-19) may affect 10-30% of survivors of COVID-19, and post-acute sequelae of COVID-19 (PASC)-pulmonary fibrosis is a long-term outcome associated with major morbidity. Data from prior coronavirus outbreaks (severe acute respiratory syndrome and Middle East respiratory syndrome) suggest that pulmonary fibrosis will contribute to long-term respiratory morbidity, suggesting that PASC-pulmonary fibrosis should be thoroughly screened for through pulmonary function testing and cross-sectional imaging. As data accumulates on the unique pathobiologic mechanisms underlying critical COVID-19, a focus on corollaries to the subacute and chronic profibrotic phenotype must be sought as well. Key aspects of acute COVID-19 pathobiology that may account for increased rates of pulmonary fibrosis include monocyte/macrophage-T-cell circuits, profibrotic RNA transcriptomics, protracted elevated levels of inflammatory cytokines, and duration of illness and ventilation. Mechanistic understanding of PASC-pulmonary fibrosis will be central in determining therapeutic options and will ultimately play a role in transplant considerations. Well-designed cohort studies and prospective clinical registries are needed. Clinicians, researchers and healthcare systems must actively address this complication of PASC to minimise disability, maximise quality of life and confront a post-COVID-19 global health crisis.


Subject(s)
COVID-19 , Pulmonary Fibrosis , Humans , Pandemics , Prospective Studies , Pulmonary Fibrosis/diagnosis , Pulmonary Fibrosis/epidemiology , Quality of Life , SARS-CoV-2
2.
Respir Med ; 188: 106602, 2021 11.
Article in English | MEDLINE | ID: covidwho-1401830

ABSTRACT

INTRODUCTION: Survivors of COVID-19 infection may develop post-covid pulmonary fibrosis (PCF) and suffer from long term multi-system complications. The magnitude and risk factors associated with these are unknown. OBJECTIVES: We investigated the prevalence and risk factors associated with PCF and other complications in patients discharged after COVID-19 infection. METHODS: Patients had phone assessment 6 weeks post hospital discharge after COVID-19 infection using a set protocol. Those with significant respiratory symptoms were investigated with a CTPA, Pulmonary Function Tests and echocardiogram. Prevalence of myalgia, fatigue, psychological symptoms and PCF was obtained. Risk factors associated with these were investigated. RESULTS: A large number of patients had persistent fatigue (45.1%), breathlessness (36.5%), myalgia (20.5%) and psychological symptoms (19.5%). PCF was seen in 9.5% of the patients and was associated with persistent breathlessness at 6 weeks and inpatient ventilation [adjusted OR 5.02(1.76-14.27) and 4.45(1.27-15.58)] respectively. It was more common in men and in patients with peak CRP >171.5 mg/L, peak WBC count ≥12 × 10 9/L, severe inpatient COVID-19 CXR changes and CT changes. Ventilation was also a risk factor for persisting fatigue and myalgia, the latter was also more common in those with severe cytokine storm and severe COVID-19 inpatient CXR changes. CONCLUSIONS: All the patients discharged after COVID-19 should be assessed using a set protocol by a multidisciplinary team. Patients who had severe COVID-19 infection particularly those who were intubated and who have persistent breathlessness are at risk of developing PCF. They should have a CT Chest and have respiratory follow-up.


Subject(s)
COVID-19/complications , Lung/physiopathology , Pandemics , Patient Discharge/trends , Pulmonary Fibrosis/etiology , SARS-CoV-2 , Adult , COVID-19/epidemiology , Humans , Male , Middle Aged , Prevalence , Pulmonary Fibrosis/diagnosis , Pulmonary Fibrosis/physiopathology , Respiratory Function Tests , Risk Factors , United Kingdom/epidemiology
3.
JCI Insight ; 6(14)2021 07 22.
Article in English | MEDLINE | ID: covidwho-1320461

ABSTRACT

BACKGROUNDIndividuals recovering from COVID-19 frequently experience persistent respiratory ailments, which are key elements of postacute sequelae of SARS-CoV-2 infection (PASC); however, little is known about the underlying biological factors that may direct lung recovery and the extent to which these are affected by COVID-19 severity.METHODSWe performed a prospective cohort study of individuals with persistent symptoms after acute COVID-19, collecting clinical data, pulmonary function tests, and plasma samples used for multiplex profiling of inflammatory, metabolic, angiogenic, and fibrotic factors.RESULTSSixty-one participants were enrolled across 2 academic medical centers at a median of 9 weeks (interquartile range, 6-10 weeks) after COVID-19 illness: n = 13 participants (21%) had mild COVID-19 and were not hospitalized, n = 30 participants (49%) were hospitalized but were considered noncritical, and n = 18 participants (30%) were hospitalized and in the intensive care unit (ICU). Fifty-three participants (85%) had lingering symptoms, most commonly dyspnea (69%) and cough (58%). Forced vital capacity (FVC), forced expiratory volume in 1 second (FEV1), and diffusing capacity for carbon monoxide (DLCO) declined as COVID-19 severity increased (P < 0.05) but these values did not correlate with respiratory symptoms. Partial least-squares discriminant analysis of plasma biomarker profiles clustered participants by past COVID-19 severity. Lipocalin-2 (LCN2), MMP-7, and HGF identified by our analysis were significantly higher in the ICU group (P < 0.05), inversely correlated with FVC and DLCO (P < 0.05), and were confirmed in a separate validation cohort (n = 53).CONCLUSIONSubjective respiratory symptoms are common after acute COVID-19 illness but do not correlate with COVID-19 severity or pulmonary function. Host response profiles reflecting neutrophil activation (LCN2), fibrosis signaling (MMP-7), and alveolar repair (HGF) track with lung impairment and may be novel therapeutic or prognostic targets.FundingNational Heart, Lung, and Blood Institute (K08HL130557 and R01HL142818), American Heart Association (Transformational Project Award), the DeLuca Foundation Award, a donation from Jack Levin to the Benign Hematology Program at Yale University, and Duke University.


Subject(s)
COVID-19/complications , Hepatocyte Growth Factor/analysis , Lipocalin-2/analysis , Matrix Metalloproteinase 7/analysis , Pulmonary Fibrosis , Respiratory Function Tests , COVID-19/diagnosis , COVID-19/immunology , COVID-19/physiopathology , Cough/diagnosis , Cough/etiology , Dyspnea/diagnosis , Dyspnea/etiology , Female , Humans , Lung/metabolism , Lung/pathology , Lung/physiopathology , Male , Middle Aged , Neutrophil Activation/immunology , Prognosis , Pulmonary Fibrosis/diagnosis , Pulmonary Fibrosis/etiology , Pulmonary Fibrosis/metabolism , Recovery of Function/immunology , Respiratory Function Tests/methods , Respiratory Function Tests/statistics & numerical data , SARS-CoV-2 , Severity of Illness Index
4.
Sci Rep ; 11(1): 14601, 2021 07 16.
Article in English | MEDLINE | ID: covidwho-1315612

ABSTRACT

Pulmonary fibrosis is a devastating disease, and the pathogenesis of this disease is not completely clear. Here, the medical records of 85 Covid-19 cases were collected, among which fibrosis and progression of fibrosis were analyzed in detail. Next, data independent acquisition (DIA) quantification proteomics and untargeted metabolomics were used to screen disease-related signaling pathways through clustering and enrichment analysis of the differential expression of proteins and metabolites. The main imaging features were lesions located in the bilateral lower lobes and involvement in five lobes. The closed association pathways were FcγR-mediated phagocytosis, PPAR signaling, TRP-inflammatory pathways, and the urea cycle. Our results provide evidence for the detection of serum biomarkers and targeted therapy in patients with Covid-19.


Subject(s)
COVID-19/complications , Pulmonary Fibrosis/complications , Adolescent , Adult , COVID-19/diagnosis , Female , Humans , Lung/pathology , Male , Metabolomics , Middle Aged , Proteomics , Pulmonary Fibrosis/diagnosis , Signal Transduction , Young Adult
5.
Int J Mol Sci ; 22(14)2021 Jul 13.
Article in English | MEDLINE | ID: covidwho-1314665

ABSTRACT

Lung fibrosis has specific computed tomography (CT) findings and represents a common finding in advanced COVID-19 pneumonia whose reversibility has been poorly investigated. The aim of this study was to quantify the extension of collagen deposition and aeration in postmortem cryobiopsies of critically ill COVID-19 patients and to describe the correlations with qualitative and quantitative analyses of lung CT. Postmortem transbronchial cryobiopsy samples were obtained, formalin fixed, paraffin embedded and stained with Sirius red to quantify collagen deposition, defining fibrotic samples as those with collagen deposition above 10%. Lung CT images were analyzed qualitatively with a radiographic score and quantitatively with computer-based analysis at the lobe level. Thirty samples from 10 patients with COVID-19 pneumonia deceased during invasive mechanical ventilation were included in this study. The median [interquartile range] percent collagen extension was 6.8% (4.6-16.2%). In fibrotic compared to nonfibrotic samples, the qualitative score was higher (260 (250-290) vs. 190 (120-270), p = 0.036) while the gas fraction was lower (0.46 (0.32-0.47) vs. 0.59 (0.37-0.68), p = 0.047). A radiographic score above 230 had 100% sensitivity (95% confidence interval, CI: 66.4% to 100%) and 66.7% specificity (95% CI: 41.0% to 92.3%) to detect fibrotic samples, while a gas fraction below 0.57 had 100% sensitivity (95% CI: 66.4% to 100%) and 57.1% specificity (95% CI: 26.3% to 88.0%). In COVID-19 pneumonia, qualitative and quantitative analyses of lung CT images have high sensitivity but moderate to low specificity to detect histopathological fibrosis. Pseudofibrotic CT findings do not always correspond to increased collagen deposition.


Subject(s)
COVID-19/complications , Collagen/metabolism , Pulmonary Fibrosis/diagnosis , SARS-CoV-2/isolation & purification , Tomography, X-Ray Computed/methods , Aged , Autopsy , COVID-19/epidemiology , COVID-19/virology , Female , Humans , Italy/epidemiology , Male , Middle Aged , Pulmonary Fibrosis/diagnostic imaging , Pulmonary Fibrosis/metabolism , Pulmonary Fibrosis/virology , Retrospective Studies
6.
Sci Transl Med ; 12(574)2020 12 16.
Article in English | MEDLINE | ID: covidwho-1207479

ABSTRACT

Lung transplantation can potentially be a life-saving treatment for patients with nonresolving COVID-19-associated respiratory failure. Concerns limiting lung transplantation include recurrence of SARS-CoV-2 infection in the allograft, technical challenges imposed by viral-mediated injury to the native lung, and the potential risk for allograft infection by pathogens causing ventilator-associated pneumonia in the native lung. Additionally, the native lung might recover, resulting in long-term outcomes preferable to those of transplant. Here, we report the results of lung transplantation in three patients with nonresolving COVID-19-associated respiratory failure. We performed single-molecule fluorescence in situ hybridization (smFISH) to detect both positive and negative strands of SARS-CoV-2 RNA in explanted lung tissue from the three patients and in additional control lung tissue samples. We conducted extracellular matrix imaging and single-cell RNA sequencing on explanted lung tissue from the three patients who underwent transplantation and on warm postmortem lung biopsies from two patients who had died from COVID-19-associated pneumonia. Lungs from these five patients with prolonged COVID-19 disease were free of SARS-CoV-2 as detected by smFISH, but pathology showed extensive evidence of injury and fibrosis that resembled end-stage pulmonary fibrosis. Using machine learning, we compared single-cell RNA sequencing data from the lungs of patients with late-stage COVID-19 to that from the lungs of patients with pulmonary fibrosis and identified similarities in gene expression across cell lineages. Our findings suggest that some patients with severe COVID-19 develop fibrotic lung disease for which lung transplantation is their only option for survival.


Subject(s)
COVID-19/surgery , Lung Transplantation , Lung/surgery , Pulmonary Fibrosis/surgery , Adult , Aged, 80 and over , COVID-19/diagnosis , COVID-19/physiopathology , COVID-19/virology , COVID-19 Nucleic Acid Testing , Databases, Factual , Disease Progression , Female , Humans , In Situ Hybridization, Fluorescence , Lung/physiopathology , Lung/virology , Male , Middle Aged , Pulmonary Fibrosis/diagnosis , Pulmonary Fibrosis/physiopathology , Pulmonary Fibrosis/virology , RNA-Seq , Recovery of Function , Retrospective Studies , Severity of Illness Index , Single-Cell Analysis , Treatment Outcome
7.
High Blood Press Cardiovasc Prev ; 28(4): 373-381, 2021 Jul.
Article in English | MEDLINE | ID: covidwho-1205023

ABSTRACT

The aim of the study was to assess the short-term consequences of SARS-CoV-2-related pneumonia, also in relation to radiologic/laboratory/clinical indices of risk at baseline. This prospective follow-up cohort study included 94 patients with confirmed COVID-19 admitted to a medical ward at the Montichiari Hospital, Brescia, Italy from February 28th to April 30th, 2020. Patients had COVID-19 related pneumonia with respiratory failure. Ninety-four patients out of 193 survivors accepted to be re-evaluated after discharge, on average after 4 months. In » of the patients an evidence of pulmonary fibrosis was detected, as indicated by an altered diffusing capacity of the lung for carbon monoxide (DLCO); in 6-7% of patients the alteration was classified as of moderate/severe degree. We also evaluated quality of life thorough a structured questionnaire: 52% of the patients still lamented fatigue, 36% effort dyspnea, 10% anorexia, 14% dysgeusia or anosmia, 31% insomnia and 21% anxiety. Finally, we evaluated three prognostic indices (the Brixia radiologic score, the Charlson Comorbidity Index and the 4C mortality score) in terms of prediction of the clinical consequences of the disease. All of them significantly predicted the extent of short-term lung involvement. In conclusion, our study demonstrated that SARS-CoV-2-related pneumonia is associated to relevant short-term clinical consequences, both in terms of persistence of symptoms and in terms of impairment of DLCO (indicator of a possible development of pulmonary fibrosis); some severity indices of the disease may predict short-term clinical outcome. Further studies are needed to ascertain whether such manifestations may persist long-term.


Subject(s)
COVID-19/virology , Lung Diseases, Interstitial/virology , Lung/virology , Pulmonary Fibrosis/virology , SARS-CoV-2/pathogenicity , COVID-19/complications , COVID-19/diagnosis , Follow-Up Studies , Host-Pathogen Interactions , Humans , Italy , Lung/pathology , Lung/physiopathology , Lung Diseases, Interstitial/diagnosis , Lung Diseases, Interstitial/physiopathology , Prognosis , Prospective Studies , Pulmonary Diffusing Capacity , Pulmonary Fibrosis/diagnosis , Pulmonary Fibrosis/physiopathology , Quality of Life , Time Factors
8.
Expert Rev Respir Med ; 15(6): 791-803, 2021 06.
Article in English | MEDLINE | ID: covidwho-1203511

ABSTRACT

Introduction: Coronavirus disease 2019 (COVID-19) is still increasing worldwide, and as a result, the number of patients with pulmonary fibrosis secondary to COVID-19 will expand over time. Risk factors, histopathological characterization, pathophysiology, prevalence, and management of post-COVID-19 pulmonary fibrosis are poorly understood, and few studies have addressed these issues.Areas covered:This article reviews the current evidence regarding post-COVID-19 pulmonary fibrosis, with an emphasis on the potential risk factors, histopathology, pathophysiology, functional and tomographic features, and potential therapeutic modalities. A search on the issue was performed in the MEDLINE, Embase, and SciELO databases and the Cochrane library between 1 December 2019, and 25 January 2021. Studies were reviewed and relevant topics were incorporated into this narrative review. Expert opinion: Pulmonary sequelae may occur secondary to COVID-19, which needs to be included as a potential etiology in the current differential diagnosis of pulmonary fibrosis. Therefore, serial clinical, tomographic, and functional screening for pulmonary fibrosis is recommended after COVID-19, mainly in patients with pulmonary involvement in the acute phase of the disease. Further studies are necessary to determine the risk factors, markers, pathophysiology, and appropriate management of post-COVID-19 pulmonary fibrosis.


Subject(s)
COVID-19/complications , Pulmonary Fibrosis/etiology , COVID-19/diagnosis , COVID-19/pathology , COVID-19/therapy , Databases, Factual , Diagnosis, Differential , Disease Progression , Humans , Lung/pathology , Lung/virology , Pulmonary Fibrosis/diagnosis , Pulmonary Fibrosis/pathology , Pulmonary Fibrosis/therapy , Risk Factors , SARS-CoV-2/physiology , Severity of Illness Index , Tomography, X-Ray Computed/methods
9.
PLoS One ; 16(3): e0248957, 2021.
Article in English | MEDLINE | ID: covidwho-1146198

ABSTRACT

The characteristics and evolution of pulmonary fibrosis in patients with coronavirus disease 2019 (COVID-19) have not been adequately studied. AI-assisted chest high-resolution computed tomography (HRCT) was used to investigate the proportion of COVID-19 patients with pulmonary fibrosis, the relationship between the degree of fibrosis and the clinical classification of COVID-19, the characteristics of and risk factors for pulmonary fibrosis, and the evolution of pulmonary fibrosis after discharge. The incidence of pulmonary fibrosis in patients with severe or critical COVID-19 was significantly higher than that in patients with moderate COVID-19. There were significant differences in the degree of pulmonary inflammation and the extent of the affected area among patients with mild, moderate and severe pulmonary fibrosis. The IL-6 level in the acute stage and albumin level were independent risk factors for pulmonary fibrosis. Ground-glass opacities, linear opacities, interlobular septal thickening, reticulation, honeycombing, bronchiectasis and the extent of the affected area were significantly improved 30, 60 and 90 days after discharge compared with at discharge. The more severe the clinical classification of COVID-19, the more severe the residual pulmonary fibrosis was; however, in most patients, pulmonary fibrosis was improved or even resolved within 90 days after discharge.


Subject(s)
Artificial Intelligence , COVID-19/pathology , Pulmonary Fibrosis/diagnosis , Thorax/diagnostic imaging , COVID-19/complications , COVID-19/virology , Female , Humans , Image Processing, Computer-Assisted , Interleukin-6/metabolism , Male , Middle Aged , Patient Discharge , Pulmonary Fibrosis/etiology , Risk Factors , SARS-CoV-2/isolation & purification , Severity of Illness Index , Tomography, X-Ray Computed
10.
Infect Dis Poverty ; 10(1): 31, 2021 Mar 18.
Article in English | MEDLINE | ID: covidwho-1140517

ABSTRACT

BACKGROUND: The coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) has led to a significant number of mortalities worldwide. COVID-19 poses a serious threat to human life. The clinical manifestations of COVID-19 are diverse and severe and 20% of infected patients are reported to be in a critical condition. A loss in lung function and pulmonary fibrosis are the main manifestations of patients with the severe form of the disease. The lung function is affected, even after recovery, thereby greatly affecting the psychology and well-being of patients, and significantly reducing their quality of life. METHODS: Participants must meet the following simultaneous inclusion criteria: over 18 years of age, should have recovered from severe or critical COVID-19 cases, should exhibit pulmonary fibrosis after recovery, and should exhibit Qi-Yin deficiency syndrome as indicated in the system of traditional Chinese medicine (TCM). The eligible candidates will be randomized into treatment or control groups. The treatment group will receive modern medicine (pirfenidone) plus TCM whereas the control group will be administered modern medicine plus TCM placebo. The lung function index will be continuously surveyed and recorded. By comparing the treatment effect between the two groups, the study intend to explore whether TCM can improve the effectiveness of modern medicine in patients with pulmonary fibrosis arising as a sequelae after SARS-CoV-2 infection. DISCUSSION: Pulmonary fibrosis is one of fatal sequelae for some severe or critical COVID-19 cases, some studies reveal that pirfenidone lead to a delay in the decline of forced expiratory vital capacity, thereby reducing the mortality partly. Additionally, although TCM has been proven to be efficacious in treating pulmonary fibrosis, its role in treating pulmonary fibrosis related COVID-19 has not been explored. Hence, a multicenter, parallel-group, randomized controlled, interventional, prospective clinical trial has been designed and will be conducted to determine if a new comprehensive treatment for pulmonary fibrosis related to COVID-19 is feasible and if it can improve the quality of life of patients. TRIAL REGISTRATION: This multicenter, parallel-group, randomized controlled, interventional, prospective trial was registered at the Chinese Clinical Trial Registry (ChiCTR2000033284) on 26th May 2020 (prospective registered).


Subject(s)
COVID-19/complications , COVID-19/virology , Pulmonary Fibrosis/etiology , Pulmonary Fibrosis/therapy , SARS-CoV-2 , Antiviral Agents/therapeutic use , Combined Modality Therapy , Data Analysis , Medicine, Chinese Traditional , Pulmonary Fibrosis/diagnosis , Quality of Life , Treatment Outcome
11.
Clin Chim Acta ; 517: 48-53, 2021 Jun.
Article in English | MEDLINE | ID: covidwho-1101132

ABSTRACT

OBJECTIVE: Coronavirus Disease 2019 (COVID-19) caused by a novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is still spreading worldwide, which may progress to pulmonary fibrosis (PF), leading to the worsen outcome. As the markers of lung injury, the correlation of Krebs von den Lungen-6 (KL-6) and fibronectin (Fn) with pulmonary fibrosis in COVID-19 was still unclear. METHODS: 113 patients diagnosed as COVID-19 were enrolled in this retrospective study, and divided into three categories as mild, moderate and severe cases. The concentrations of serum KL-6 and Fn at hospital admission were tested using the method of latex agglutination assay and immunoturbidimetic assay, respectively. RESULTS: Compared with that in the non-severe COVID-19 cases and normal control subjects, serum KL-6 concentration on admission was significantly higher in the severe group, which was positively correlated with C-reactive protein, and negatively correlated with lymphocytes count. Whereas, no obvious elevation in serum Fn concentration was investigated in COVID-19 patients with the different phenotypes. The severe cases displayed the higher incident rate of pulmonary fibrosis at hospital discharge. Compared with non-PF patients, the COVID-19 cases with PF had the higher serum KL-6 values. CONCLUSION: Serum KL-6 concentration was significantly elevated in severe COVID-19 patients, which may be useful for evaluating the disease severity. For early prevention of the development of pulmonary fibrosis, high concentrations of serum KL-6 in the early stage of COVID-19 should be paid close attention.


Subject(s)
COVID-19 , Fibronectins/blood , Mucin-1/blood , Pulmonary Fibrosis , Adolescent , Adult , Aged , Aged, 80 and over , Biomarkers , COVID-19/diagnosis , Female , Humans , Male , Middle Aged , Pulmonary Fibrosis/blood , Pulmonary Fibrosis/diagnosis , Retrospective Studies , Young Adult
12.
J Gene Med ; 23(3): e3318, 2021 03.
Article in English | MEDLINE | ID: covidwho-1084739

ABSTRACT

Pulmonary fibrosis is characterized by progressive and irreversible scarring in the lungs with poor prognosis and treatment. It is caused by various factors, including environmental and occupational exposures, and some rheumatic immune diseases. Even the rapid global spread of the COVID-19 pandemic can also cause pulmonary fibrosis with a high probability. Functions attributed to long non-coding RNAs (lncRNAs) make them highly attractive diagnostic and therapeutic targets in fibroproliferative diseases. Therefore, an understanding of the specific mechanisms by which lncRNAs regulate pulmonary fibrotic pathogenesis is urgently needed to identify new possibilities for therapy. In this review, we focus on the molecular mechanisms and implications of lncRNAs targeted protein-coding and non-coding genes during pulmonary fibrogenesis, and systematically analyze the communication of lncRNAs with various types of RNAs, including microRNA, circular RNA and mRNA. Finally, we propose the potential approach of lncRNA-based diagnosis and therapy for pulmonary fibrosis. We hope that understanding these interactions between protein-coding and non-coding genes will contribute to the development of lncRNA-based clinical applications for pulmonary fibrosis.


Subject(s)
Genetic Markers/genetics , Pulmonary Fibrosis/genetics , RNA, Long Noncoding/genetics , Gene Expression Regulation , Genetic Therapy/methods , Humans , MicroRNAs/genetics , Proteins/genetics , Pulmonary Fibrosis/diagnosis , Pulmonary Fibrosis/pathology , Pulmonary Fibrosis/therapy , RNA, Circular/genetics
13.
Respir Res ; 22(1): 38, 2021 Feb 05.
Article in English | MEDLINE | ID: covidwho-1067230

ABSTRACT

Pulmonary fibrosis has been identified as a main factor leading to pulmonary dysfunction and poor quality of life in post-recovery Severe Acute Respiratory Syndrome (SARS) survivor's consequent to SARS-Cov-2 infection. Thus there is an urgent medical need for identification of readily available biomarkers that in patients with SARS-Cov-2 infection are able to; (1) identify patients in most need of medical care prior to admittance to an intensive care unit (ICU), and; (2) identify patients post-infection at risk of developing persistent fibrosis of lungs with subsequent impaired quality of life and increased morbidity and mortality. An intense amount of research have focused on wound healing and Extracellular Matrix (ECM) remodelling of the lungs related to lung function decline in pulmonary fibrosis (PF). A range of non-invasive serological biomarkers, reflecting tissue remodelling, and fibrosis have been shown to predict risk of acute exacerbations, lung function decline and mortality in PF and other interstitial lung diseases (Sand et al. in Respir Res 19:82, 2018). We suggest that lessons learned from such PF studies of the pathological processes leading to lung function decline could be used to better identify patients infected with SARS-Co-V2 at most risk of acute deterioration or persistent fibrotic damage of the lung and could consequently be used to guide treatment decisions.


Subject(s)
COVID-19/metabolism , Extracellular Matrix/metabolism , Pulmonary Fibrosis/metabolism , Wound Healing/physiology , Animals , Biomarkers/metabolism , COVID-19/diagnosis , Humans , Lung/metabolism , Pulmonary Fibrosis/diagnosis
15.
Am J Case Rep ; 21: e926921, 2020 Nov 21.
Article in English | MEDLINE | ID: covidwho-940353

ABSTRACT

BACKGROUND Since December 2019, an outbreak caused by a novel coronavirus infection (severe acute respiratory syndrome coronavirus 2, SARS-CoV-2) occurred in Wuhan, China, and it rapidly spread all over the world. The clinical spectrum of coronavirus disease 2019 (COVID-19) is wide, with acute respiratory distress syndrome (ARDS) occurring in 15% of patients affected, requiring high oxygen support. Currently, there is no clearly effective antiviral therapy. Steroids and immunomodulators are under investigation for potential activity. Little is known about middle and long-term sequelae on respiratory function. According to some authors, COVID-19 could cause pulmonary fibrosis. We report 3 cases of pulmonary fibrosis detected on follow-up computed tomography (CT) imaging in 3 female patients who recovered from COVID-19 pneumonia in Italy (L'Aquila, Abruzzo). CASE REPORT All patients were female and had no significant previous respiratory disease or history of smoke exposure, and none had received high-flow oxygen support during treatment of the disease. In all cases, late onset of mild dyspnea, slow and incomplete respiratory recovery, and early evidence of fibrous signs on chest CT scan were characteristic of the clinical course. CONCLUSIONS This report focuses on a possible scenario of long-term lung damage in COVID-19 pneumonia survivors. Limitations are lack of long-term follow-up and functional data in the very early phase. It is advantageous that all COVID-19 pneumonia patients undergo serial chest CT and spirometry long-term follow-up for at least 1 year to assess residual damage. This is particularly relevant in those with slow respiratory recovery and long hospitalization.


Subject(s)
COVID-19/diagnosis , Lung/diagnostic imaging , Pulmonary Fibrosis/diagnosis , SARS-CoV-2 , Tomography, X-Ray Computed/methods , Aged , Aged, 80 and over , COVID-19/complications , COVID-19/epidemiology , Female , Humans , Middle Aged , Pandemics , Pulmonary Fibrosis/complications , Radiography, Thoracic
16.
Med Sci Monit ; 26: e928996, 2020 Nov 01.
Article in English | MEDLINE | ID: covidwho-921300

ABSTRACT

Since the initial reports of coronavirus disease 2019 (COVID-19) in China in late 2019, infections from severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) have spread rapidly, resulting in a global pandemic that has caused millions of deaths. Initially, the large number of infected people required the direction of global healthcare resources to provide supportive care for the acutely ill population in an attempt to reduce mortality. While clinical trials for safe and effective antiviral agents are ongoing, and vaccine development programs are being accelerated, long-term sequelae of SARS-CoV-2 infection have become increasingly recognized and concerning. Although the upper and lower respiratory tracts are the main sites of entry of SARS-CoV-2 into the body, resulting in COVID-19 pneumonia as the most common presentation, acute lung damage may be followed by pulmonary fibrosis and chronic impairment of lung function, with impaired quality of life. Also, increasing reports have shown that SARS-CoV-2 infection involves the central nervous system (CNS) and the peripheral nervous system (PNS) and directly or indirectly damages neurons, leading to long-term neurological sequelae. This review aims to provide an update on the mechanisms involved in the development of the long-term sequelae of SARS-CoV-2 infection in the 3 main areas of lung injury, neuronal injury, and neurodegenerative diseases, including Alzheimer disease, Parkinson disease, and multiple sclerosis, and highlights the need for patient monitoring following the acute stage of infection with SARS-CoV-2 to provide a rationale for the prevention, diagnosis, and management of these potential long-term sequelae.


Subject(s)
COVID-19/complications , Lung Injury/epidemiology , Neurodegenerative Diseases/epidemiology , Pulmonary Fibrosis/epidemiology , SARS-CoV-2/pathogenicity , COVID-19/epidemiology , COVID-19/immunology , COVID-19/virology , Disease Progression , Humans , Lung Injury/diagnosis , Lung Injury/immunology , Lung Injury/prevention & control , Neurodegenerative Diseases/diagnosis , Neurodegenerative Diseases/immunology , Neurodegenerative Diseases/prevention & control , Pandemics , Pulmonary Fibrosis/diagnosis , Pulmonary Fibrosis/immunology , Pulmonary Fibrosis/prevention & control , Quality of Life , SARS-CoV-2/immunology , Time Factors
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