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1.
Medicine (Baltimore) ; 101(35): e30146, 2022 Sep 02.
Статья в английский | MEDLINE | ID: covidwho-2008664

Реферат

BACKGROUND: There is currently no objective computed tomography (CT)-defined grading system for coronavirus disease (COVID-19)-related pulmonary fibrosis. We propose a CT-based radiological scale that adapts the histological fibrosis scale to pulmonary fibrosis CT findings, to evaluate possible predictive factors for the degree of fibrosis in these patients. METHODS: A new radiological fibrosis grading system was created based on existing histological fibrosis scales. One hundred forty-seven COVID-19 patients with any degree of fibrosis on CT were evaluated. Smoking status, the presence of hypertension, the duration of hospital stays, the presence of comorbid diseases, and the levels of prognostic and predictive factors for COVID-19 were evaluated, and how these parameters affected the fibrosis scores was examined. RESULTS: Of 147 patients, 17.7% had grade 1, 17% had grade 2, 51.7% had grade 3, and 13.6% had grade 4 fibrosis. ANOVA revealed statistically significant relationships between the fibrosis scores and lactate dehydrogenase values, lymphocyte count, C-reactive protein level, and length of hospital stay. Smoking, advanced age, hypertension, and male sex showed significantly higher scores for fibrosis. CONCLUSIONS: Using our CT-defined lung fibrosis grading system, we could predict the severity of fibrosis as well as the resultant lung pathology in COVID-19 patients. Thus, disease exacerbation and development of permanent severe fibrosis can be prevented using the appropriate treatment methods in high-risk patients.


Тема - темы
COVID-19 , Hypertension , Pulmonary Fibrosis , C-Reactive Protein , COVID-19/diagnostic imaging , Fibrosis , Humans , Lactate Dehydrogenases , Male , Pulmonary Fibrosis/diagnostic imaging , Pulmonary Fibrosis/etiology , Tomography, X-Ray Computed/methods
2.
Tuberk Toraks ; 70(2): 203-205, 2022 06.
Статья в английский | MEDLINE | ID: covidwho-1934520
3.
Tuberk Toraks ; 70(2): 179-186, 2022 Jun.
Статья в английский | MEDLINE | ID: covidwho-1934519

Реферат

Introduction: Although the epidemiological and clinical characteristics of COVID-19 patients have been described; the pathogenesis of the disease and its long-term consequences are still unclear. Pulmonary fibrosis is one of these late outcomes. In this study we evaluated Interleukin-17 (IL-17), vascular endothelial growth factor (VEGF), and immunoglobulin G4 (IgG4) levels of COVID-19 infected patients with different clinical course and their effect on pulmonary fibrosis in post-COVID period. Materials and Methods: In total, 90 patients were evaluated. Among the patients who presented for a control visit between 3-12 weeks after acute infection; patients with signs of pulmonary sequelae radiologically (traction bronchiectasis, interseptal thickening, disorders in parenchyma architecture) were classified as Group I (n= 32), patients who recovered without sequelae radiologically as Group II (n= 32). The Control group included healthy individuals who did not have COVID-19, and was classified as Group III (n= 26). Result: The mean age in Group I was significantly higher than Group II and III (p<0.001). There was a statistically significant difference between the VEGF and IL-17 values based on the patient group they are in (p<0.05). Vascular endothelial growth factor values of Group I and III were significantly lower than the patients in Group II (p<0.001). IL-17 values of Group I and II were found to be significantly lower than Group III (p= 0.005). There was no statistically significant relationship between groups in terms of IgG4 values. Conclusions: In our study, it was observed that the profibrotic effects of VEGF, IL-17, and IgG4 were not dominant in patients who recovered with pulmonary sequelae after COVID; therefore, it is thought that different mechanisms mentioned or not yet revealed may cause this outcome.


Тема - темы
COVID-19 , Pulmonary Fibrosis , Disease Progression , Humans , Immunoglobulin G , Interleukin-17 , Lung/diagnostic imaging , Pulmonary Fibrosis/etiology , Vascular Endothelial Growth Factor A , Vascular Endothelial Growth Factors
4.
Molecules ; 27(9)2022 Apr 24.
Статья в английский | MEDLINE | ID: covidwho-1810048

Реферат

Cepharanthine (CEP) has excellent anti-SARS-CoV-2 properties, indicating its favorable potential for COVID-19 treatment. However, its application is challenged by its poor dissolubility and oral bioavailability. The present study aimed to improve the bioavailability of CEP by optimizing its solubility and through a pulmonary delivery method, which improved its bioavailability by five times when compared to that through the oral delivery method (68.07% vs. 13.15%). An ultra-performance liquid chromatography tandem-mass spectrometry (UPLC-MS/MS) method for quantification of CEP in rat plasma was developed and validated to support the bioavailability and pharmacokinetic studies. In addition, pulmonary fibrosis was recognized as a sequela of COVID-19 infection, warranting further evaluation of the therapeutic potential of CEP on a rat lung fibrosis model. The antifibrotic effect was assessed by analysis of lung index and histopathological examination, detection of transforming growth factor (TGF)-ß1, interleukin-6 (IL-6), α-smooth muscle actin (α-SMA), and hydroxyproline level in serum or lung tissues. Our data demonstrated that CEP could significantly alleviate bleomycin (BLM)-induced collagen accumulation and inflammation, thereby exerting protective effects against pulmonary fibrosis. Our results provide evidence supporting the hypothesis that pulmonary delivery CEP may be a promising therapy for pulmonary fibrosis associated with COVID-19 infection.


Тема - темы
COVID-19 , Pulmonary Fibrosis , Animals , Benzylisoquinolines , Biological Availability , Bleomycin/pharmacology , COVID-19/complications , COVID-19/drug therapy , Chromatography, Liquid , Humans , Lung , Pulmonary Fibrosis/chemically induced , Pulmonary Fibrosis/etiology , Rats , Tandem Mass Spectrometry , Transforming Growth Factor beta1/metabolism
5.
Arch Bronconeumol ; 58 Suppl 1: 6-7, 2022 04.
Статья в английский, испанский | MEDLINE | ID: covidwho-1797170
6.
Indian J Pediatr ; 89(7): 728, 2022 07.
Статья в английский | MEDLINE | ID: covidwho-1739429
8.
Am J Case Rep ; 23: e934830, 2022 Feb 13.
Статья в английский | MEDLINE | ID: covidwho-1687480

Реферат

BACKGROUND Physicians worldwide have been reporting many cases of COVID-19-induced pulmonary fibrosis. We report the case of a 51-year-old Filipino asthmatic woman who developed post-COVID-19 pulmonary fibrosis subsequently treated with Nintedanib. CASE REPORT The patient presented with a 4-day history of flu-like symptoms in September 2020 and was eventually diagnosed with severe COVID-19 pneumonia. Despite receiving Dexamethasone, Tocilizumab, Remdesivir, and multiple antibiotics, there was increasing oxygen requirement, necessitating ICU admission and high-flow nasal cannula (HFNC). An additional course of hydrocortisone was given due to asthma exacerbation, gradually liberating her from the HFNC. A chest CT scan showed extensive parenchymal changes, for which she received methylprednisolone and physical rehabilitation with persistence of respiratory symptoms. After 40 days of hospitalization, she was sent home on oxygen support and Nintedanib. The patient initially had severe dyspnea (Borg Scale 7) with 6-minute walk distance (6MWD) of 295 meters. Pulmonary function showed moderately severe restrictive lung defect at 52% predicted total lung capacity (TLC) and severely reduced DLCO (28% predicted). Chest CT scoring indicated severe lung involvement. One month after Nintedanib treatment, her Borg Scale improved to 4. Her 6MWD, TLC, and DLCO increased to 434 meters, 64% predicted, and 36% predicted, respectively. A chest CT scan showed regressing fibrosis. After 6 months of treatment, her pulmonary function normalized. DLCO remained moderately reduced (59% predicted) but her 6MWD (457 meters) and CT scan results continued to improve. CONCLUSIONS Nintedanib, along with other interventions, may have potentially improved pulmonary function and CT scan findings in a COVID-19 survivor with pulmonary fibrosis 6 months after treatment.


Тема - темы
COVID-19 , Pulmonary Fibrosis , Female , Humans , Lung , Middle Aged , Pulmonary Fibrosis/diagnostic imaging , Pulmonary Fibrosis/etiology , SARS-CoV-2 , Tomography, X-Ray Computed
9.
Medicine (Baltimore) ; 101(3): e28639, 2022 Jan 21.
Статья в английский | MEDLINE | ID: covidwho-1642427

Реферат

ABSTRACT: The development of pulmonary fibrosis is a rare complication of the novel coronavirus disease 2019 (COVID-19). Limited information is available in the literature about that, and the present study aimed to address this gap.This case-control study included 64 patients with post-COVID-19 pulmonary fibrosis who were hospitalized for COVID-19.The percentage of patients aged ≥65 years (44%) who demised was higher than those who survived (25%). Male patients (62%) had higher mortality than female patients (37%). The most frequently reported clinical symptoms were shortness of breath (98%), cough (91%), and fever (70%). Most COVID-19 patients with pulmonary fibrosis (81%) were admitted to an intensive care unit (ICU), and 63% required mechanical ventilation. Bilateral lung infiltrates (94%), "ground glass" opacity (91%), "honeycomb" lung (25%), and pulmonary consolidation (9%) were commonly identified in COVID-19 patients with pulmonary fibrosis who survived. The findings for computed tomography and dyspnea scale were significantly higher in severe cases admitted to the ICU who required mechanical ventilation. A higher computerized tomography score also correlated significantly with a longer duration of stay in hospital and a higher degree of dyspnea. Half of the COVID-19 patients with pulmonary fibrosis (50%) who survived required oxygen therapy, and those with "honeycomb" lung required long-term oxygen therapy to a far greater extent than others. Cox regression revealed that smoking and asthma were significantly associated with ICU admission and the risk of mortality.Post-COVID-19 pulmonary fibrosis is a severe complication that leads to permanent lung damage or death.


Тема - темы
COVID-19/complications , Lung/diagnostic imaging , Adrenal Cortex Hormones/therapeutic use , Anticoagulants/therapeutic use , COVID-19/epidemiology , Case-Control Studies , Cough/etiology , Dyspnea/etiology , Female , Fever/etiology , Humans , Intensive Care Units , Male , Oxygen , Prednisolone/therapeutic use , Pulmonary Fibrosis/etiology , Pulmonary Fibrosis/therapy , Retrospective Studies , SARS-CoV-2 , Saudi Arabia/epidemiology , Tomography, X-Ray Computed , Vitamins/therapeutic use
10.
Medicine (Baltimore) ; 100(47): e27980, 2021 Nov 24.
Статья в английский | MEDLINE | ID: covidwho-1604285

Реферат

RATIONALE: Pulmonary fibrosis is an infamous sequela of coronavirus disease 2019 (COVID-19) pneumonia leading to long-lasting respiratory problems and activity limitations. Pulmonary rehabilitation is beneficial to improve the symptoms of lung fibrosis. We experienced a post-COVID-19 pulmonary fibrosis patient who received a structured exercise-based pulmonary rehabilitation program. PATIENT CONCERNS: This article presents a case of successful pulmonary rehabilitation of a patient with post-COVID-19 pulmonary fibrosis. The patient could not cut off the oxygen supplement even after a successful recovery from COVID-19. DIAGNOSIS: Diagnosis of COVID-19 was based on the reverse transcription-polymerase chain reaction (RT-PCR). Pulmonary fibrosis was diagnosed by patient's complaint, clinical appearance, and computed tomography (CT) on chest. INTERVENTION: The patient underwent ten sessions of exercise-based rehabilitation program according to Consensus Document on Pulmonary Rehabilitation in Korea, 2015. OUTCOME: On the 8th day, he could cut off the oxygen supplementation and complete the one-hour exercise without oxygen. He was discharged after completing the 10-session program without any activity limitations. LESSONS: Exercise-based pulmonary rehabilitation will help the post-COVID-19 pulmonary fibrosis patients. This case suggested the importance of pulmonary rehabilitation program to the post-COVID-19 pulmonary fibrosis patient.


Тема - темы
COVID-19/complications , Lung/diagnostic imaging , Pulmonary Fibrosis/rehabilitation , COVID-19/diagnosis , COVID-19 Testing , Humans , Lung/pathology , Male , Middle Aged , Oxygen , Pulmonary Fibrosis/diagnostic imaging , Pulmonary Fibrosis/etiology , Reverse Transcriptase Polymerase Chain Reaction , SARS-CoV-2 , Tomography, X-Ray Computed
11.
Am J Chin Med ; 50(1): 33-51, 2022.
Статья в английский | MEDLINE | ID: covidwho-1608685

Реферат

Qingfei Paidu decoction (QFPD) has been repeatedly recommended for the clinical treatment of novel coronavirus disease 2019 (COVID-19) in multiple provinces throughout China. A possible complication of COVID-19 lung involvement is pulmonary fibrosis, which causes chronic breathing difficulties and affects the patient's quality of life. Therefore, there is an important question regarding whether QFPD can alleviate the process of pulmonary fibrosis and its potential mechanisms. To explore this issue, this study demonstrated the anti-pulmonary fibrosis activity and mode of action of QFPD in vivo and in vitro pulmonary fibrosis models and network pharmacology. The results showed that QFPD effectively ameliorated the bleomycin-induced inflammation and collagen deposition in mice and significantly improved the epithelial-mesenchymal transition in pulmonary fibrosis in mice. In addition, QFPD inhibited bleomycin-induced M2 polarization of macrophages in pulmonary tissues. An in-depth study of the mechanism of QFPD in the treatment of pulmonary fibrosis based on network pharmacology and molecular simulation revealed that SRC was the main target of QFPD and sitosterol (a key compound in QFPD). QFPD and sitosterol regulate the EMT process and M2 polarization of macrophages by inhibiting the activation of SRC, thereby alleviating pulmonary fibrosis in mice. COVID-19 infection might produce severe fibrosis, and antifibrotic therapy with QFPD may be valuable in preventing severe neocoronavirus disease in patients with IPF, which could be a key factor explaining the role of QFPD in the treatment of COVID-19.


Тема - темы
COVID-19 , Pulmonary Fibrosis , Animals , Drugs, Chinese Herbal , Epithelial-Mesenchymal Transition , Humans , Mice , Mice, Inbred C57BL , Pulmonary Fibrosis/drug therapy , Pulmonary Fibrosis/etiology , Quality of Life , SARS-CoV-2
12.
Pan Afr Med J ; 40: 169, 2021.
Статья в английский | MEDLINE | ID: covidwho-1566818

Реферат

Twenty months into the COVID-19 pandemic, we are still learning about the various long-term consequences of COVID-19 infection. While many patients do recover with minimal long-term consequences, some patients develop irreversible parenchymal and interstitial lung damage leading to diffuse pulmonary fibrosis. Unfortunately, these are some of the consequences of post-SARS-CoV-2 infection which thousands more people around the world will experience and which will outlast the pandemic for a long time to come. It is now being observed at various leading medical centres around the world that lung transplantation may be the only meaningful treatment available to a select group of patients experiencing serious lung damage and non-resolving COVID-19-associated respiratory failure, resulting from the triad of coronavirus infection, a hyper-inflammatory immune response to it and the inability of the human body to repair that injury.


Тема - темы
COVID-19 , Lung Transplantation , Pulmonary Fibrosis , Humans , Incidence , Lung/pathology , Pandemics , Pulmonary Fibrosis/epidemiology , Pulmonary Fibrosis/etiology , Pulmonary Fibrosis/pathology , SARS-CoV-2
13.
J Transl Med ; 19(1): 496, 2021 12 07.
Статья в английский | MEDLINE | ID: covidwho-1561217

Реферат

Pulmonary fibrosis is the end stage of a broad range of heterogeneous interstitial lung diseases and more than 200 factors contribute to it. In recent years, the relationship between virus infection and pulmonary fibrosis is getting more and more attention, especially after the outbreak of SARS-CoV-2 in 2019, however, the mechanisms underlying the virus-induced pulmonary fibrosis are not fully understood. Here, we review the relationship between pulmonary fibrosis and several viruses such as Human T-cell leukemia virus (HTLV), Human immunodeficiency virus (HIV), Cytomegalovirus (CMV), Epstein-Barr virus (EBV), Murine γ-herpesvirus 68 (MHV-68), Influenza virus, Avian influenza virus, Middle East Respiratory Syndrome (MERS)-CoV, Severe acute respiratory syndrome (SARS)-CoV and SARS-CoV-2 as well as the mechanisms underlying the virus infection induced pulmonary fibrosis. This may shed new light on the potential targets for anti-fibrotic therapy to treat pulmonary fibrosis induced by viruses including SARS-CoV-2.


Тема - темы
COVID-19 , Epstein-Barr Virus Infections , Pulmonary Fibrosis , SARS Virus , Virus Diseases , Animals , Herpesvirus 4, Human , Humans , Mice , Pulmonary Fibrosis/etiology , SARS-CoV-2
14.
Am J Case Rep ; 22: e933458, 2021 Dec 01.
Статья в английский | MEDLINE | ID: covidwho-1547795

Реферат

BACKGROUND The COVID-19 global pandemic is ongoing, and despite vaccination efforts, SARS-CoV-2 continues to circulate worldwide. The spectrum of COVID-19 illness is broad, from asymptomatic infection to respiratory failure and acute respiratory distress syndrome (ARDS), and the long-term sequelae of infection are unclear. COVID-19-related pulmonary fibrosis has been previously described in the setting of critical illness and ARDS but has not been well described in cases requiring minimal supplemental oxygen. CASE REPORT We present the case of a 42-year-old man hospitalized with coronavirus disease 2019 (COVID-19) who initially required minimal supplemental oxygen but weeks later developed progressive pulmonary fibrosis requiring high-flow nasal cannula and ICU admission. Using novel computed tomography (CT) imaging processing techniques, we demonstrate progression from initial ground-glass opacities to pulmonary fibrosis and traction bronchiectasis over several months. Additionally, we describe clinical responsiveness to an extended course of corticosteroids. CONCLUSIONS Although pulmonary fibrosis is a known complication of severe COVID-19-related ARDS requiring mechanical ventilation, our report suggests that patients with milder forms of COVID-19 infection may develop post-acute pulmonary fibrosis.


Тема - темы
COVID-19 , Pulmonary Fibrosis , Respiratory Distress Syndrome , Adult , Humans , Male , Pandemics , Pulmonary Fibrosis/etiology , Respiratory Distress Syndrome/etiology , SARS-CoV-2
15.
J Postgrad Med ; 67(4): 224-227, 2021.
Статья в английский | MEDLINE | ID: covidwho-1542882

Реферат

One of the common long-term consequences observed in survivors of COVID-19 pneumonia is the persistence of respiratory symptoms and/or radiological lung abnormalities. The exact prevalence of these post-COVID pulmonary changes is yet unclear. Few authors, based on their early observations, have labeled these persistent computed tomography (CT) abnormalities as post-COVID lung fibrosis, which appears to be an overstatement. Lately, it is being observed that many of the changes seen in post-COVID lungs are temporary and tend to show resolution on follow-up, with only a few developing into lung fibrosis. Thus, based on the presumptive diagnosis of lung fibrosis, these patients should not be blindly started on anti-fibrotic drugs. One must not forget that these drugs can do more harm than good, if used injudiciously. It is better to use the term "post-COVID interstitial lung changes", which covers a broader spectrum of pulmonary changes seen in patients who have recovered from COVID-19 pneumonia. At the same time, it is essential to identify the sub-set of COVID-19 survivors who are at an increased risk of developing lung fibrosis and to carefully chalk out management strategies so as to modify the course of the disease and prevent irreversible damage. Meticulous and systematic longitudinal follow-up studies consisting of clinical, laboratory, imaging, and pulmonary function tests are needed for the exact estimation of the burden of lung fibrosis, to understand the nature of residual pulmonary changes, and to predict the likelihood of development of lung fibrosis in COVID-19 survivors.


Тема - темы
COVID-19 , Lung Diseases, Interstitial , Pulmonary Fibrosis , Humans , Lung/diagnostic imaging , Pulmonary Fibrosis/diagnosis , Pulmonary Fibrosis/etiology , SARS-CoV-2
16.
Expert Opin Investig Drugs ; 30(12): 1183-1195, 2021 Dec.
Статья в английский | MEDLINE | ID: covidwho-1541410

Реферат

INTRODUCTION: Lung injury in severe COVID-19 pneumonia can rapidly evolve to established pulmonary fibrosis, with prognostic implications in the acute phase of the disease and long-lasting impact on the quality of life of COVID-19 survivors. This is an emerging medical need, and it has been hypothesized that antifibrotic treatments could have a role in ameliorating the fibrotic process in the lungs of these patients. AREAS COVERED: The safety and efficacy of available antifibrotic drugs (nintedanib and pirfenidone) and novel promising agents are being assessed in several ongoing clinical trials that were performed either in critically ill patients admitted to intensive care, or in discharged patients presenting fibrotic sequalae from COVID-19. Literature search was performed using Medline and Clinicaltrials.org databases (2001-2021). EXPERT OPINION: Despite the strong rationale support the use of antifibrotic therapies in COVID-related fibrosis, there are several uncertainties regarding the timing for their introduction and the real risks/benefits ratio of antifibrotic treatment in the acute and the chronic phases of the disease. The findings of ongoing clinical trials and the long-term observation of longitudinal cohorts will eventually clarify the best management approach for these patients.


Тема - темы
/therapeutic use , COVID-19/complications , Pulmonary Fibrosis/drug therapy , Pulmonary Fibrosis/etiology , Animals , Critical Illness , Humans , Indoles/therapeutic use , Pyridones
17.
Lancet Respir Med ; 9(5): 487-497, 2021 05.
Статья в английский | MEDLINE | ID: covidwho-1537196

Реферат

BACKGROUND: Lung transplantation is a life-saving treatment for patients with end-stage lung disease; however, it is infrequently considered for patients with acute respiratory distress syndrome (ARDS) attributable to infectious causes. We aimed to describe the course of disease and early post-transplantation outcomes in critically ill patients with COVID-19 who failed to show lung recovery despite optimal medical management and were deemed to be at imminent risk of dying due to pulmonary complications. METHODS: We established a multi-institutional case series that included the first consecutive transplants for severe COVID-19-associated ARDS known to us in the USA, Italy, Austria, and India. De-identified data from participating centres-including information relating to patient demographics and pre-COVID-19 characteristics, pretransplantation disease course, perioperative challenges, pathology of explanted lungs, and post-transplantation outcomes-were collected by Northwestern University (Chicago, IL, USA) and analysed. FINDINGS: Between May 1 and Sept 30, 2020, 12 patients with COVID-19-associated ARDS underwent bilateral lung transplantation at six high-volume transplant centres in the USA (eight recipients at three centres), Italy (two recipients at one centre), Austria (one recipient), and India (one recipient). The median age of recipients was 48 years (IQR 41-51); three of the 12 patients were female. Chest imaging before transplantation showed severe lung damage that did not improve despite prolonged mechanical ventilation and extracorporeal membrane oxygenation. The lung transplant procedure was technically challenging, with severe pleural adhesions, hilar lymphadenopathy, and increased intraoperative transfusion requirements. Pathology of the explanted lungs showed extensive, ongoing acute lung injury with features of lung fibrosis. There was no recurrence of SARS-CoV-2 in the allografts. All patients with COVID-19 could be weaned off extracorporeal support and showed short-term survival similar to that of transplant recipients without COVID-19. INTERPRETATION: The findings from our report show that lung transplantation is the only option for survival in some patients with severe, unresolving COVID-19-associated ARDS, and that the procedure can be done successfully, with good early post-transplantation outcomes, in carefully selected patients. FUNDING: National Institutes of Health. VIDEO ABSTRACT.


Тема - темы
COVID-19 , Critical Illness/therapy , Lung Transplantation/methods , Lung , Respiratory Distress Syndrome , Blood Transfusion/methods , COVID-19/complications , COVID-19/diagnosis , COVID-19/physiopathology , COVID-19/surgery , Critical Care/methods , Extracorporeal Membrane Oxygenation/methods , Female , Humans , Intraoperative Care/methods , Lung/diagnostic imaging , Lung/pathology , Male , Middle Aged , Outcome and Process Assessment, Health Care , Pulmonary Fibrosis/etiology , Pulmonary Fibrosis/pathology , Respiration, Artificial/methods , Respiratory Distress Syndrome/etiology , Respiratory Distress Syndrome/surgery , SARS-CoV-2/pathogenicity
18.
Ann Thorac Surg ; 114(1): e17-e19, 2022 07.
Статья в английский | MEDLINE | ID: covidwho-1499633

Реферат

Lung transplantation has been well described for patients with coronavirus disease 2019 (COVID-19) in the acute setting, but less so for the resulting pulmonary sequelae. This report describes a case of lung transplantation for post-COVID-19 pulmonary fibrosis. A 52-year-old woman contracted COVID-19 in July 2020 and mounted a partial recovery, but she went on to have declining function over the ensuing 3 months, with development of fibrocystic lung changes. She underwent bilateral lung transplantation and recovered rapidly, was discharged home on postoperative day 14, and has done well in follow-up. This case report demonstrates that lung transplantation is an acceptable therapy for post-COVID-19 pulmonary fibrosis.


Тема - темы
COVID-19 , Lung Transplantation , Pulmonary Fibrosis , Female , Humans , Lung , Middle Aged , Pulmonary Fibrosis/etiology , Pulmonary Fibrosis/surgery
19.
Biochem Pharmacol ; 193: 114812, 2021 11.
Статья в английский | MEDLINE | ID: covidwho-1474355

Реферат

Pulmonary fibrosis (PF) is characterised by several grades of chronic inflammation and collagen deposition in the interalveolar space and is a hallmark of interstitial lung diseases (ILDs). Recently, infectious agents have emerged as driving causes for PF development; however, the role of viral/bacterial infections in the initiation and propagation of PF is still debated. In this context, the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the virus responsible for the current coronavirus disease 2019 (COVID-19) pandemic, has been associated with acute respiratory distress syndrome (ARDS) and PF development. Although the infection by SARS-CoV-2 can be eradicated in most cases, the development of fibrotic lesions cannot be precluded; furthermore, whether these lesions are stable or progressive fibrotic events is still unknown. Herein, an overview of the main molecular mechanisms driving the fibrotic process together with the currently approved and newly proposed therapeutic solutions was given. Then, the most recent data that emerged from post-COVID-19 patients was discussed, in order to compare PF and COVID-19-dependent PF, highlighting shared and specific mechanisms. A better understanding of PF aetiology is certainly needed, also to develop effective therapeutic strategies and COVID-19 pathology is offering one more chance to do it. Overall, the work reported here could help to define new approaches for therapeutic intervention in the diversity of the ILD spectrum.


Тема - темы
COVID-19/complications , Pulmonary Fibrosis/immunology , Pulmonary Fibrosis/metabolism , Animals , COVID-19/etiology , COVID-19/immunology , COVID-19/metabolism , Humans , Inflammation Mediators/immunology , Inflammation Mediators/metabolism , Neutrophils/immunology , Neutrophils/metabolism , Pulmonary Fibrosis/etiology
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