Your browser doesn't support javascript.
Show: 20 | 50 | 100
Results 1 - 20 de 59
Filter
1.
BMJ Case Rep ; 15(4)2022 Apr 29.
Article in English | MEDLINE | ID: covidwho-1854260

ABSTRACT

A transgender man in his late teens presented with signs of multisystem disease, including hepatitis, mucositis and bone marrow suppression. He later developed dyspnoea, leucocytosis and bilateral pulmonary infiltrates on chest radiograph. He was treated for community-acquired pneumonia. After several days of treatment, he developed hypoxaemic respiratory failure due to bronchoscopy-confirmed diffuse alveolar haemorrhage (DAH). The differential diagnosis and workup were extensive, and he was ultimately treated with intravenous steroids and five sessions of plasmapheresis for a presumed autoimmune aetiology. Investigations were remarkable only for elevated IgM and IgG to Mycoplasma pneumoniae (MP). This case represents a rare presentation of multisystem disease secondary to MP in adults. Clinicians should consider Mycoplasma infection in cases of multisystem disease and observe for DAH even after initiation of appropriate therapy.


Subject(s)
Community-Acquired Infections , Lung Diseases , Adolescent , Adult , Bronchoscopy , Hemorrhage/etiology , Hemorrhage/therapy , Humans , Lung Diseases/diagnosis , Lung Diseases/etiology , Male , Mycoplasma pneumoniae
2.
Mayo Clin Proc ; 97(3): 579-599, 2022 03.
Article in English | MEDLINE | ID: covidwho-1720595

ABSTRACT

Coronavirus disease 2019 (COVID-19) is the third deadly coronavirus infection of the 21st century that has proven to be significantly more lethal than its predecessors, with the number of infected patients and deaths still increasing daily. From December 2019 to July 2021, this virus has infected nearly 200 million people and led to more than 4 million deaths. Our understanding of COVID-19 is constantly progressing, giving better insight into the heterogeneous nature of its acute and long-term effects. Recent literature on the long-term health consequences of COVID-19 discusses the need for a comprehensive understanding of the multisystemic pathophysiology, clinical predictors, and epidemiology to develop and inform an evidence-based, multidisciplinary management approach. A PubMed search was completed using variations on the term post-acute COVID-19. Only peer-reviewed studies in English published by July 17, 2021 were considered for inclusion. All studies discussed in this text are from adult populations unless specified (as with multisystem inflammatory syndrome in children). The preliminary evidence on the pulmonary, cardiovascular, neurological, hematological, multisystem inflammatory, renal, endocrine, gastrointestinal, and integumentary sequelae show that COVID-19 continues after acute infection. Interdisciplinary monitoring with holistic management that considers nutrition, physical therapy, psychological management, meditation, and mindfulness in addition to medication will allow for the early detection of post-acute COVID-19 sequelae symptoms and prevent long-term systemic damage. This review serves as a guideline for effective management based on current evidence, but clinicians should modify recommendations to reflect each patient's unique needs and the most up-to-date evidence. The presence of long-term effects presents another reason for vaccination against COVID-19.


Subject(s)
COVID-19/complications , Cardiovascular Diseases/etiology , Humans , Lung Diseases/etiology , Nervous System Diseases/etiology
3.
Clin Exp Pharmacol Physiol ; 49(4): 483-491, 2022 04.
Article in English | MEDLINE | ID: covidwho-1691664

ABSTRACT

Progress in the study of Covid-19 disease in rodents has been hampered by the lack of angiotensin-converting enzyme 2 (ACE2; virus entry route to the target cell) affinities for the virus spike proteins across species. Therefore, we sought to determine whether a modified protocol of lipopolysaccharide (LPS)-induced acute respiratory distress syndrome in rats can mimic both cell signalling pathways as well as severe disease phenotypes of Covid-19 disease. Rats were injected via intratracheal (IT) instillation with either 15 mg/kg of LPS (model group) or saline (control group) before being killed after 3 days. A severe acute respiratory syndrome (SARS)-like effect was observed in the model group as demonstrated by the development of a "cytokine storm" (>2.7 fold increase in blood levels of IL-6, IL-17A, GM-CSF, and TNF-α), high blood ferritin, demonstrable coagulopathy, including elevated D-dimer (approximately 10-fold increase), PAI-1, PT, and APTT (p < 0.0001). In addition, LPS increased the expression of lung angiotensin II type I receptor (AT1R)-JAK-STAT axis (>4 fold increase). Chest imaging revealed bilateral small patchy opacities of the lungs. Severe lung injury was noted by the presence of both, alveolar collapse and haemorrhage, desquamation of epithelial cells in the airway lumen, infiltration of inflammatory cells (CD45+ leukocytes), widespread thickening of the interalveolar septa, and ultrastructural alterations similar to Covid-19. Thus, these findings demonstrate that IT injection of 15 mg/kg LPS into rats, induced an AT1R/JAK/STAT-mediated cytokine storm with resultant pneumonia and coagulopathy that was commensurate with moderate and severe Covid-19 disease noted in humans.


Subject(s)
Acute Lung Injury/etiology , Blood Coagulation Disorders/etiology , COVID-19/pathology , Cytokine Release Syndrome/etiology , Hemorrhage/etiology , Lipopolysaccharides/adverse effects , Lung Diseases/etiology , Receptor, Angiotensin, Type 1/metabolism , STAT Transcription Factors/metabolism , Signal Transduction , Acute Lung Injury/pathology , Animals , Blood Coagulation Disorders/pathology , COVID-19/etiology , Cytokine Release Syndrome/pathology , Disease Models, Animal , Hemorrhage/pathology , Janus Kinases , Lung Diseases/pathology , Male , Rats , Rats, Wistar
4.
BMC Nephrol ; 23(1): 57, 2022 02 05.
Article in English | MEDLINE | ID: covidwho-1666636

ABSTRACT

BACKGROUND: Publicly available genomics datasets have grown drastically during the past decades. Although most of these datasets were initially generated to answer a pre-defined scientific question, their repurposing can be useful when new challenges such as COVID-19 arise. While the establishment and use of experimental models of COVID-19 are in progress, the potential hypotheses for mechanisms of onset and progression of COVID-19 can be generated by using in silico analysis of known molecular changes during COVID-19 and targets for SARS-CoV-2 invasion. METHODS: Selecting condition: COVID-19 infection leads to pneumonia and mechanical ventilation (PMV) and associated with acute kidney injury (AKI). There is increasing data demonstrating mechanistic links between AKI and lung injury caused by mechanical ventilation. Selecting targets: SARS-CoV-2 uses angiotensin-converting enzyme 2 (ACE2) and transmembrane protease serine 2 (TMPRSS2) for cell entry. We hypothesized that expression of ACE2 and TMPRSS2 would be affected in models of AKI and PMV. We therefore evaluated expression of ACE2 and TMPRSS2 as well as other novel molecular players of AKI and AKI-lung cross-talk in the publicly available microarray datasets GSE6730 and GSE60088, which represent gene expression of lungs and kidneys in mouse models of AKI and PMV, respectively. RESULTS: Expression of COVID-19 related genes ACE2 and TMPRSS2 was downregulated in lungs after 6 h of distant AKI effects. The expression of ACE2 decreased further after 36 h, while expression of TMPRSS2 recovered. In kidneys, both genes were downregulated by AKI, but not by distant lung injury. We also identified 53 kidney genes upregulated by PMV; and 254 lung genes upregulated by AKI, 9 genes of which were common to both organs. 3 of 9 genes were previously linked to kidney-lung cross-talk: Lcn2 (Fold Change (FC)Lung (L) = 18.6, FCKidney (K) = 6.32), Socs3 (FCL = 10.5, FCK = 10.4), Inhbb (FCL = 6.20, FCK = 6.17). This finding validates the current approach and reveals 6 new candidates, including Maff (FCL = 7.21, FCK = 5.98). CONCLUSIONS: Using our in silico approach, we identified changes in COVID-19 related genes ACE2 and TMPRSS2 in traditional mouse models of AKI and kidney-lung cross-talk. We also found changes in new candidate genes, which could be involved in the combined kidney-lung injury during COVID-19.


Subject(s)
COVID-19/complications , Computer Simulation , Kidney Diseases/etiology , Lung Diseases/etiology , SARS-CoV-2/genetics , Animals , Disease Models, Animal , Male , Mice , Mice, Inbred C57BL
5.
Can J Cardiol ; 38(3): 338-346, 2022 03.
Article in English | MEDLINE | ID: covidwho-1654182

ABSTRACT

BACKGROUND: Strict isolation precautions limit formal echocardiography use in the setting of COVID-19 infection. Information on the importance of handheld focused ultrasound for cardiac evaluation in these patients is scarce. This study investigated the utility of a handheld echocardiography device in hospitalised patients with COVID-19 in diagnosing cardiac pathologies and predicting the composite end point of in-hospital death, mechanical ventilation, shock, and acute decompensated heart failure. METHODS: From April 28 through July 27, 2020, consecutive patients diagnosed with COVID-19 underwent evaluation with the use of handheld ultrasound (Vscan Extend with Dual Probe; GE Healthcare) within 48 hours of admission. The patients were divided into 2 groups: "normal" and "abnormal" echocardiogram, as defined by biventricular systolic dysfunction/enlargement or moderate/severe valvular regurgitation/stenosis. RESULTS: Among 102 patients, 26 (25.5%) had abnormal echocardiograms. They were older with more comorbidities and more severe presenting symptoms compared with the group with normal echocardiograms. The prevalences of the composite outcome among low- and high-risk patients (oxygen saturation < 94%) were 3.1% and 27.1%, respectively. Multivariate logistic regression analysis revealed that an abnormal echocardiogram at presentation was independently associated with the composite end point (odds ratio 6.19, 95% confidence interval 1.50-25.57; P = 0.012). CONCLUSIONS: An abnormal echocardiogram in COVID-19 infection settings is associated with a higher burden of medical comorbidities and independently predicts major adverse end points. Handheld focused echocardiography can be used as an important "rule-out" tool among high-risk patients with COVID-19 and should be integrated into their routine admission evaluation. However, its routine use among low-risk patients is not recommended.


Subject(s)
COVID-19/complications , Echocardiography/instrumentation , Heart Diseases/diagnostic imaging , Lung Diseases/diagnostic imaging , Ultrasonography/instrumentation , Aged , Echocardiography/standards , Female , Heart Diseases/etiology , Hospitalization , Humans , Lung Diseases/etiology , Male , Middle Aged , Prospective Studies , SARS-CoV-2 , Ultrasonography/standards
6.
Emerg Radiol ; 29(2): 227-234, 2022 Apr.
Article in English | MEDLINE | ID: covidwho-1604573

ABSTRACT

PURPOSE: The use of lung ultrasound for diagnosis of COVID-19 has emerged during the pandemic as a beneficial diagnostic modality due to its rapid availability, bedside use, and lack of radiation. This study aimed to determine if routine ultrasound (US) imaging of the lungs of trauma patients with COVID-19 infections who undergo extended focused assessment with sonography for trauma (EFAST) correlates with computed tomography (CT) imaging and X-ray findings, as previously reported in other populations. METHODS: This was a prospective, observational feasibility study performed at two level 1 trauma centers. US, CT, and X-ray imaging were retrospectively reviewed by a surgical trainee and a board-certified radiologist to determine any correlation of imaging findings in patients with active COVID-19 infection. RESULTS: There were 53 patients with lung US images from EFAST available for evaluation and COVID-19 testing. The overall COVID-19 positivity rate was 7.5%. COVID-19 infection was accurately identified by one patient on US by the trainee, but there was a 15.1% false-positive rate for infection based on the radiologist examination. CONCLUSIONS: Evaluation of the lung during EFAST cannot be used in the trauma setting to identify patients with active COVID-19 infection or to stratify patients as high or low risk of infection. This is likely due to differences in lung imaging technique and the presence of concomitant thoracic injury.


Subject(s)
COVID-19 , Focused Assessment with Sonography for Trauma , Lung Diseases , Lung , Wounds and Injuries , COVID-19/complications , COVID-19/diagnostic imaging , COVID-19/epidemiology , False Positive Reactions , Feasibility Studies , Humans , Lung/diagnostic imaging , Lung Diseases/diagnostic imaging , Lung Diseases/etiology , Pandemics , Prospective Studies , Retrospective Studies , SARS-CoV-2 , Sensitivity and Specificity , Tomography, X-Ray Computed , Trauma Centers , Wounds and Injuries/complications , Wounds and Injuries/diagnostic imaging
7.
Ann Thorac Surg ; 113(1): e5-e8, 2022 01.
Article in English | MEDLINE | ID: covidwho-1568514

ABSTRACT

This report describes a patient with severe acute respiratory syndrome coronavirus 2 infection and irreversible lung destruction who underwent successful lung transplantation after 138 days of bridging with extracorporeal membrane oxygenation support. The case exemplifies that lung transplantation may be a possibility after very long-term coronavirus disease 2019 care, even if the patient is initially an unsuitable candidate.


Subject(s)
COVID-19/complications , Extracorporeal Membrane Oxygenation , Lung Diseases/etiology , Lung Diseases/therapy , Lung Transplantation , Humans , Long-Term Care , Male , Middle Aged
9.
Radiology ; 301(2): E383-E395, 2021 11.
Article in English | MEDLINE | ID: covidwho-1406672

ABSTRACT

The acute course of COVID-19 is variable and ranges from asymptomatic infection to fulminant respiratory failure. Patients recovering from COVID-19 can have persistent symptoms and CT abnormalities of variable severity. At 3 months after acute infection, a subset of patients will have CT abnormalities that include ground-glass opacity (GGO) and subpleural bands with concomitant pulmonary function abnormalities. At 6 months after acute infection, some patients have persistent CT changes to include the resolution of GGOs seen in the early recovery phase and the persistence or development of changes suggestive of fibrosis, such as reticulation with or without parenchymal distortion. The etiology of lung disease after COVID-19 may be a sequela of prolonged mechanical ventilation, COVID-19-induced acute respiratory distress syndrome (ARDS), or direct injury from the virus. Predictors of lung disease after COVID-19 include need for intensive care unit admission, mechanical ventilation, higher inflammatory markers, longer hospital stay, and a diagnosis of ARDS. Treatments of lung disease after COVID-19 are being investigated, including the potential of antifibrotic agents for prevention of lung fibrosis after COVID-19. Future research is needed to determine the long-term persistence of lung disease after COVID-19, its impact on patients, and methods to either prevent or treat it. © RSNA, 2021.


Subject(s)
COVID-19/complications , Lung Diseases/diagnostic imaging , Lung Diseases/etiology , Tomography, X-Ray Computed/methods , Acute Disease , Humans , Lung/diagnostic imaging , SARS-CoV-2
10.
Int J Mol Sci ; 22(5)2021 Mar 04.
Article in English | MEDLINE | ID: covidwho-1389392

ABSTRACT

Alveolar type II (ATII) cells are a key structure of the distal lung epithelium, where they exert their innate immune response and serve as progenitors of alveolar type I (ATI) cells, contributing to alveolar epithelial repair and regeneration. In the healthy lung, ATII cells coordinate the host defense mechanisms, not only generating a restrictive alveolar epithelial barrier, but also orchestrating host defense mechanisms and secreting surfactant proteins, which are important in lung protection against pathogen exposure. Moreover, surfactant proteins help to maintain homeostasis in the distal lung and reduce surface tension at the pulmonary air-liquid interface, thereby preventing atelectasis and reducing the work of breathing. ATII cells may also contribute to the fibroproliferative reaction by secreting growth factors and proinflammatory molecules after damage. Indeed, various acute and chronic diseases are associated with intensive inflammation. These include oedema, acute respiratory distress syndrome, fibrosis and numerous interstitial lung diseases, and are characterized by hyperplastic ATII cells which are considered an essential part of the epithelialization process and, consequently, wound healing. The aim of this review is that of revising the physiologic and pathologic role ATII cells play in pulmonary diseases, as, despite what has been learnt in the last few decades of research, the origin, phenotypic regulation and crosstalk of these cells still remain, in part, a mystery.


Subject(s)
Alveolar Epithelial Cells/pathology , Alveolar Epithelial Cells/physiology , Lung Diseases/physiopathology , Lung/physiology , Alveolar Epithelial Cells/cytology , Animals , COVID-19/physiopathology , Humans , Immunity, Innate , Ions/metabolism , Lung/anatomy & histology , Lung Diseases/etiology , Lung Diseases/pathology , Pulmonary Surfactant-Associated Proteins/metabolism , Regeneration
11.
Zool Res ; 42(5): 633-636, 2021 Sep 18.
Article in English | MEDLINE | ID: covidwho-1369995

ABSTRACT

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the etiologic agent responsible for the global coronavirus disease 2019 (COVID-19) pandemic. Numerous studies have demonstrated that cardiovascular disease may affect COVID-19 progression. In the present study, we investigated the effect of hypertension on viral replication and COVID-19 progression using a hypertensive mouse model infected with SARS-CoV-2. Results revealed that SARS-CoV-2 replication was delayed in hypertensive mouse lungs. In contrast, SARS-CoV-2 replication in hypertensive mice treated with the antihypertensive drug captopril demonstrated similar virus replication as SARS-CoV-2-infected normotensive mice. Furthermore, antihypertensive treatment alleviated lung inflammation induced by SARS-CoV-2 replication (interleukin (IL)-1ß up-regulation and increased immune cell infiltration). No differences in lung inflammation were observed between the SARS-CoV-2-infected normotensive mice and hypertensive mice. Our findings suggest that captopril treatment may alleviate COVID-19 progression but not affect viral replication.


Subject(s)
Antihypertensive Agents/therapeutic use , COVID-19/complications , Captopril/therapeutic use , Hypertension/complications , Lung Diseases/drug therapy , SARS-CoV-2 , Angiotensin-Converting Enzyme Inhibitors/therapeutic use , Animals , Antihypertensive Agents/pharmacology , Captopril/pharmacology , Gene Expression Regulation/drug effects , Inflammation/complications , Inflammation/drug therapy , Interleukin-1beta/genetics , Interleukin-1beta/metabolism , Lung Diseases/etiology , Lung Diseases/virology , Mice , Virus Replication/drug effects
13.
Life Sci ; 281: 119718, 2021 Sep 15.
Article in English | MEDLINE | ID: covidwho-1271709

ABSTRACT

AIMS: Hypoxia, a pathophysiological condition, is profound in several cardiopulmonary diseases (CPD). Every individual's lethality to a hypoxia state differs in terms of hypoxia exposure time, dosage units and dependent on the individual's genetic makeup. Most of the proposed markers for CPD were generally aim to distinguish disease samples from normal samples. Although, as per the 2018 GOLD guidelines, clinically useful biomarkers for several cardio pulmonary disease patients in stable condition have yet to be identified. We attempt to address these key issues through the identification of Dynamic Network Biomarkers (DNB) to detect hypoxia induced early warning signals of CPD before the catastrophic deterioration. MATERIALS AND METHODS: The human microvascular endothelial tissues microarray datasets (GSE11341) of lung and cardiac expose to hypoxia (1% O2) for 3, 24 and 48 h were retrieved from the public repository. The time dependent differentially expressed genes were subjected to tissue specificity and promoter analysis to filtrate the noise levels in the networks and to dissect the tissue specific hypoxia induced genes. These filtered out genes were used to construct the dynamic segmentation networks. The hypoxia induced dynamic differentially expressed genes were validated in the lung and heart tissues of male rats. These rats were exposed to hypobaric hypoxia (simulated altitude of 25,000 or PO2 - 282 mm of Hg) progressively for 3, 24 and 48 h. KEY FINDINGS: To identify the temporal key genes regulated in hypoxia, we ranked the dominant genes based on their consolidated topological features from tissue specific networks, time dependent networks and dynamic networks. Overall topological ranking described VEGFA as a single node dynamic hub and strongly communicated with tissue specific genes to carry forward their tissue specific information. We named this type of VEGFAcentric dynamic networks as "V-DNBs". As a proof of principle, our methodology helped us to identify the V-DNBs specific for lung and cardiac tissues namely V-DNBL and V-DNBC respectively. SIGNIFICANCE: Our experimental studies identified VEGFA, SLC2A3, ADM and ENO2 as the minimum and sufficient candidates of V-DNBL. The dynamic expression patterns could be readily exploited to capture the pre disease state of hypoxia induced pulmonary vascular remodelling. Whereas in V-DNBC the minimum and sufficient candidates are VEGFA, SCL2A3, ADM, NDRG1, ENO2 and BHLHE40. The time dependent single node expansion indicates V-DNBC could also be the pre disease state pathological hallmark for hypoxia-associated cardiovascular remodelling. The network cross-talk and expression pattern between V-DNBL and V-DNBC are completely distinct. On the other hand, the great clinical advantage of V-DNBs for pre disease predictions, a set of samples during the healthy condition should suffice. Future clinical studies might further shed light on the predictive power of V-DNBs as prognostic and diagnostic biomarkers for CPD.


Subject(s)
Heart Diseases/metabolism , Hypoxia/metabolism , Lung Diseases/metabolism , Vascular Endothelial Growth Factor A/metabolism , Animals , Biomarkers/metabolism , Clinical Deterioration , Gene Expression Regulation , Heart Diseases/etiology , Heart Diseases/pathology , Humans , Hypoxia/complications , Hypoxia/genetics , Lung Diseases/etiology , Lung Diseases/pathology , Male , Rats , Rats, Sprague-Dawley
14.
G Ital Cardiol (Rome) ; 22(7): 529-534, 2021 Jul.
Article in Italian | MEDLINE | ID: covidwho-1282350

ABSTRACT

Growing evidence about COVID-19 and its possible cardiopulmonary complications have raised concerns about a potential subclinical heart damage even in asymptomatic patients. Many countries worldwide provided recommendations for a safe return to play and sports activity for athletes with previous COVID-19 disease. Italy was among the first nations to deal with the problem of protecting athletes' health. In this regard, after an initial version released on April 2020, on December 11, 2020 the Italian Sports Medicine Federation (FMSI) updated the recommendations for the return play of non-professional athletes. The purpose of this article is to analyze and deepen the contents of the new FMSI recommendations, integrating and comparing them with the previous ones. Further updates may occur if new scientific and epidemiological evidence will rise regarding COVID-19.


Subject(s)
COVID-19 , Return to Sport/standards , COVID-19/complications , Heart Diseases/etiology , Humans , Italy , Lung Diseases/etiology , Practice Guidelines as Topic
15.
BMJ Case Rep ; 14(6)2021 Jun 21.
Article in English | MEDLINE | ID: covidwho-1280407

ABSTRACT

A 40-year-old man developed granulomatosis with polyangiitis (GPA) following a mild case of COVID-19. Initially, he experienced mild migrating joint pain for 2 months prior to testing positive for SARS-CoV-2 but dramatically worsened following resolution of his infection. The pain continued to progress until he suddenly develope haemoptysis, prompting him to present to a local hospital. The diagnosis of diffuse alveolar haemorrhage secondary to GPA was confirmed with labs, imaging and histopathology. Precipitous deterioration of GPA with concurrent COVID-19 infection indicates a possible temporal relationship. Since the onset of the pandemic, SARS-CoV-2 has been anecdotally associated with the development of various connective tissue disorders. The overlapping clinical presentations and similar appearance on lung imaging present clinicians with a diagnostic challenge. This underscores the importance of having a high index of suspicion of autoimmune diagnoses in patients who present with new or worsening findings following a COVID-19 infection.


Subject(s)
COVID-19 , Granulomatosis with Polyangiitis , Lung Diseases , Adult , Granulomatosis with Polyangiitis/complications , Granulomatosis with Polyangiitis/diagnosis , Hemorrhage/etiology , Humans , Lung Diseases/diagnostic imaging , Lung Diseases/etiology , Male , SARS-CoV-2
16.
Respir Investig ; 59(5): 614-621, 2021 Sep.
Article in English | MEDLINE | ID: covidwho-1260851

ABSTRACT

BACKGROUND: The long-term repercussions of critical COVID-19 on pulmonary function and imaging studies remains unexplored. In this study, we investigated the pulmonary function and computed tomography (CT) findings of critical COVID-19 patients approximately 100 days after symptom onset. METHODS: We retrospectively extracted data on critical COVID-19 patients who received invasive mechanical ventilation during hospitalization from April to December 2020 and evaluated their pulmonary function, residual respiratory symptoms and radiographic abnormalities on CT. RESULTS: We extracted 17 patients whose median age was 63 (interquartile range [IQR], 59-67) years. The median lengths of hospitalization and mechanical ventilation were 23 (IQR, 18-38) and 9 (IQR, 6-13) days, respectively. At 100 days after symptom onset, the following pulmonary function abnormalities were noted in 8 (47%) patients: a diffusion capacity of the lung for carbon monoxide (%DLCO) of <80% for 6 patients (35%); a percent vital capacity (%VC) of <80% for 4 patients (24%); and a forced expiratory volume in one second/forced vital capacity (FEV1%) of <70% for 1 patient (6%) who also presented with %DLCO and %VC abnormalities. Twelve (71%) patients reported residual respiratory symptoms and 16 (94%) showed abnormalities on CT. CONCLUSIONS: Over 90% of the critical COVID-19 patients who underwent invasive mechanical ventilation continued presenting with abnormal imaging studies and 47% of the patients presented with abnormal pulmonary function 100 days after symptom onset. The extent of the residual CT findings might be associated with the degree of abnormal pulmonary function in critical COVID-19 survivors.


Subject(s)
COVID-19 , Lung Diseases , Aged , COVID-19/complications , Humans , Lung/diagnostic imaging , Lung Diseases/etiology , Middle Aged , Respiratory Function Tests , Retrospective Studies , SARS-CoV-2 , Survivors
17.
Eur J Pharmacol ; 904: 174196, 2021 Aug 05.
Article in English | MEDLINE | ID: covidwho-1230461

ABSTRACT

Severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2), the responsible agent for the coronavirus disease 2019 (Covid-19), has its entry point through interaction with angiotensin converting enzyme 2 (ACE2) receptors, highly expressed in lung type II alveolar cells and other tissues, like heart, pancreas, brain, and vascular endothelium. This review aimed to elucidate the potential role of leukotrienes (LTs) in the pathogenesis and clinical presentation of SARS-CoV-2 infection, and to reveal the critical role of LT pathway receptor antagonists and inhibitors in Covid-19 management. A literature search was done in PubMed, Scopus, Web of Science and Google Scholar databases to find the potential role of montelukast and other LT inhibitors in the management of pulmonary and extra-pulmonary manifestations triggered by SARS-CoV-2. Data obtained so far underline that pulmonary and extra-pulmonary manifestations in Covid-19 are attributed to a direct effect of SARS-CoV-2 in expressed ACE2 receptors or indirectly through NF-κB dependent induction of a cytokine storm. Montelukast can ameliorate extra-pulmonary manifestations in Covid-19 either directly through blocking of Cys-LTRs in different organs or indirectly through inhibition of the NF-κB signaling pathway.


Subject(s)
Acetates/therapeutic use , COVID-19/drug therapy , Cyclopropanes/therapeutic use , Leukotriene Antagonists/therapeutic use , Leukotrienes , Lung Diseases/drug therapy , Quinolines/therapeutic use , Signal Transduction/drug effects , Sulfides/therapeutic use , COVID-19/complications , Cytokine Release Syndrome/drug therapy , Cytokine Release Syndrome/etiology , Humans , Lung Diseases/etiology , Receptors, Leukotriene/drug effects
18.
JAMA ; 325(15): 1525-1534, 2021 04 20.
Article in English | MEDLINE | ID: covidwho-1222575

ABSTRACT

Importance: Little is known about long-term sequelae of COVID-19. Objective: To describe the consequences at 4 months in patients hospitalized for COVID-19. Design, Setting, and Participants: In a prospective uncontrolled cohort study, survivors of COVID-19 who had been hospitalized in a university hospital in France between March 1 and May 29, 2020, underwent a telephone assessment 4 months after discharge, between July 15 and September 18, 2020. Patients with relevant symptoms and all patients hospitalized in an intensive care unit (ICU) were invited for further assessment at an ambulatory care visit. Exposures: Survival of hospitalization for COVID-19. Main Outcomes and Measures: Respiratory, cognitive, and functional symptoms were assessed by telephone with the Q3PC cognitive screening questionnaire and a checklist of symptoms. At the ambulatory care visit, patients underwent pulmonary function tests, lung computed tomographic scan, psychometric and cognitive tests (including the 36-Item Short-Form Health Survey and 20-item Multidimensional Fatigue Inventory), and, for patients who had been hospitalized in the ICU or reported ongoing symptoms, echocardiography. Results: Among 834 eligible patients, 478 were evaluated by telephone (mean age, 61 years [SD, 16 years]; 201 men, 277 women). During the telephone interview, 244 patients (51%) declared at least 1 symptom that did not exist before COVID-19: fatigue in 31%, cognitive symptoms in 21%, and new-onset dyspnea in 16%. There was further evaluation in 177 patients (37%), including 97 of 142 former ICU patients. The median 20-item Multidimensional Fatigue Inventory score (n = 130) was 4.5 (interquartile range, 3.0-5.0) for reduced motivation and 3.7 (interquartile range, 3.0-4.5) for mental fatigue (possible range, 1 [best] to 5 [worst]). The median 36-Item Short-Form Health Survey score (n = 145) was 25 (interquartile range, 25.0-75.0) for the subscale "role limited owing to physical problems" (possible range, 0 [best] to 100 [worst]). Computed tomographic lung-scan abnormalities were found in 108 of 171 patients (63%), mainly subtle ground-glass opacities. Fibrotic lesions were observed in 33 of 171 patients (19%), involving less than 25% of parenchyma in all but 1 patient. Fibrotic lesions were observed in 19 of 49 survivors (39%) with acute respiratory distress syndrome. Among 94 former ICU patients, anxiety, depression, and posttraumatic symptoms were observed in 23%, 18%, and 7%, respectively. The left ventricular ejection fraction was less than 50% in 8 of 83 ICU patients (10%). New-onset chronic kidney disease was observed in 2 ICU patients. Serology was positive in 172 of 177 outpatients (97%). Conclusions and Relevance: Four months after hospitalization for COVID-19, a cohort of patients frequently reported symptoms not previously present, and lung-scan abnormalities were common among those who were tested. These findings are limited by the absence of a control group and of pre-COVID assessments in this cohort. Further research is needed to understand longer-term outcomes and whether these findings reflect associations with the disease.


Subject(s)
COVID-19/complications , Hospitalization , Lung Diseases/etiology , Lung/pathology , Aged , Anxiety/etiology , COVID-19/psychology , Cognition Disorders/etiology , Cohort Studies , Depression/etiology , Dyspnea/etiology , Fatigue/etiology , Female , Follow-Up Studies , Humans , Lung/diagnostic imaging , Lung Diseases/diagnostic imaging , Lung Diseases/pathology , Male , Middle Aged , Tomography, X-Ray Computed
19.
J Thorac Imaging ; 35(6): 344-345, 2020 Nov 01.
Article in English | MEDLINE | ID: covidwho-1219915

ABSTRACT

In this hypothesis paper, we suggest that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) may induce intravascular pulmonary thrombosis, which may result in the rapid worsening of clinical conditions and, eventually, exitus. Previously published papers have demonstrated that increased levels of D-dimer at hospital admission correlate with a more severe disease (0.5 mg/L) or occurrence of death (1 mg/L). The potential prothrombotic action of the SARS-CoV-2 is supported by the topographical involvement of the lung regions with a predilection for the lower lobe with peripheral involvement. If this hypothesis is demonstrated, this could suggest the benefit of using antithrombotic/coagulation regimens for SARS-CoV-2 and, at the same time, the urgency to identify drugs that could alter the inflammatory storm, thus protecting the vessel wall.


Subject(s)
COVID-19/complications , COVID-19/physiopathology , Thrombosis/etiology , Thrombosis/physiopathology , COVID-19/blood , Fibrin Fibrinogen Degradation Products/metabolism , Humans , Lung/physiopathology , Lung Diseases/blood , Lung Diseases/etiology , Lung Diseases/physiopathology , SARS-CoV-2 , Thrombosis/blood
20.
Ann Ig ; 33(6): 615-627, 2021.
Article in English | MEDLINE | ID: covidwho-1168080

ABSTRACT

BACKGROUND: The outbreak of Coronavirus disease 2019 (COVID-19) made imperative the use of protective devices as a source control tool. As there is no definite antiviral treatment and effective vaccine, the only efficient means of protecting and mitigating infectious contagion has been the use of personal protective equipment, especially by healthcare workers. However, masks affect the humidification process of inhaled air, possibly leading to a basal inflammatory state of the upper airways. STUDY DESIGN: This is a single-center observational study conducted at the University Hospital of Catania from April 1, 2020, to June 31, 2020. METHODS: We analyzed the role of protective masks on the elimination of upper airways complaints in healthcare workers of the University Hospital of Catania. We evaluated 277 subjects through a self-administered 17 item questionnaire based on respiratory, work performance and health-related quality of life domains. RESULTS: A higher prevalence of nasal and ocular symptoms, perceived reduced work performance, difficulty in concentrating, and sleep disorders were found. After two weeks adhering to a list of good practices that we recommended, significant reversibility of the symptoms investigated and work performance enhancement were observed. CONCLUSIONS: Despite clinical complaints related to personal protective equipment, effective amelioration through usage rules is easily obtained. Given the essential use of protective masks, healthcare workers have to adhere to appropriate work and safety prevention rules.


Subject(s)
COVID-19/prevention & control , Health Personnel , Masks/adverse effects , Occupational Diseases/etiology , Quality of Life , Work Performance , Adult , COVID-19/transmission , Eye Diseases/etiology , Eye Diseases/prevention & control , Female , Guideline Adherence , Humans , Lung Diseases/etiology , Lung Diseases/prevention & control , Male , Masks/standards , Middle Aged , Nose Diseases/etiology , Nose Diseases/prevention & control , Occupational Diseases/prevention & control , Personal Protective Equipment/standards , Surveys and Questionnaires
SELECTION OF CITATIONS
SEARCH DETAIL