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2.
J Renin Angiotensin Aldosterone Syst ; 21(4): 1470320320972018, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-33169644

RESUMO

In the wake of the COVID-19 pandemic it has become clear that there is a need for therapies that are capable of reducing damage caused to patients from infections. Infections that induce Acute Respiratory Distress Syndrome (ARDS) are especially devastating because lung damage is so critical and difficult to manage. Angiotensin (1-7) [A(1-7)] has already been shown to protect pulmonary health and architecture in various models of disease. There is also evidence that A(1-7) can modulate immune function and protect various organs (lung, kidney, and heart) from oxidative damage and inflammation. Here we focus on making a case for the development of novel therapies that target the protective arm of the Renin Angiotensin System (RAS).


Assuntos
Angiotensina I/uso terapêutico , Betacoronavirus/fisiologia , Infecções por Coronavirus/complicações , Fragmentos de Peptídeos/uso terapêutico , Pneumonia Viral/complicações , Síndrome do Desconforto Respiratório do Adulto/tratamento farmacológico , Síndrome do Desconforto Respiratório do Adulto/virologia , Angiotensina I/fisiologia , Animais , Infecções por Coronavirus/mortalidade , Humanos , Pandemias , Fragmentos de Peptídeos/fisiologia , Peptidil Dipeptidase A/metabolismo , Pneumonia Viral/mortalidade , Sistema Renina-Angiotensina/efeitos dos fármacos , Sistema Renina-Angiotensina/fisiologia
3.
ASAIO J ; 66(10): 1069-1072, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-33136589

RESUMO

Extracorporeal membrane oxygenation (ECMO) is recognized as organ support for potentially reversible acute respiratory distress syndrome (ARDS). However, limited resource during the outbreak and the coagulopathy associated with coronavirus disease 2019 (COVID-19) make the utilization of venovenous (VV) ECMO highly challenging. We herein report specific considerations for cannulation configurations and ECMO management during the pandemic. High blood flow and anticoagulation at higher levels than usual practice for VV ECMO may be required because of thrombotic hematologic profile of COVID-19. Among our first 24 cases (48.8 ± 8.9 years), 17 patients were weaned from ECMO after a mean duration of 19.0 ± 10.1 days and 16 of them have been discharged from ICU.


Assuntos
Infecções por Coronavirus/terapia , Oxigenação por Membrana Extracorpórea/métodos , Pneumonia Viral/terapia , Anticoagulantes/uso terapêutico , Betacoronavirus , Infecções por Coronavirus/complicações , Oxigenação por Membrana Extracorpórea/efeitos adversos , Feminino , Heparina/uso terapêutico , Humanos , Masculino , Pessoa de Meia-Idade , Pandemias , Pneumonia Viral/complicações , Síndrome do Desconforto Respiratório do Adulto/virologia , Trombose/etiologia , Trombose/prevenção & controle
4.
ASAIO J ; 66(10): 1079-1083, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-33136592

RESUMO

Observational evidence suggests that excessive inflammation with cytokine storm may play a critical role in development of acute respiratory distress syndrome (ARDS) in COVID-19. We report the emergency use of immunomodulatory therapy utilizing an extracorporeal selective cytopheretic device (SCD) in two patients with elevated serum interleukin (IL)-6 levels and refractory COVID-19 ARDS requiring extracorporeal membrane oxygenation (ECMO). The two patients were selected based on clinical criteria and elevated levels of IL-6 (>100 pg/ml) as a biomarker of inflammation. Once identified, emergency/expanded use permission for SCD treatment was obtained and patient consented. Six COVID-19 patients (four on ECMO) with severe ARDS were also screened with IL-6 levels less than 100 pg/ml and were not treated with SCD. The two enrolled patients' PaO2/FiO2 ratios increased from 55 and 58 to 200 and 192 at 52 and 50 hours, respectively. Inflammatory indices also declined with IL-6 falling from 231 and 598 pg/ml to 3.32 and 116 pg/ml, respectively. IL-6/IL-10 ratios also decreased from 11.8 and 18 to 0.7 and 0.62, respectively. The two patients were successfully weaned off ECMO after 17 and 16 days of SCD therapy, respectively. The results observed with SCD therapy on these two critically ill COVID-19 patients with severe ARDS and elevated IL-6 is encouraging. A multicenter clinical trial is underway with an FDA-approved investigational device exemption to evaluate the potential of SCD therapy to effectively treat COVID-19 intensive care unit patients.


Assuntos
Infecções por Coronavirus/imunologia , Infecções por Coronavirus/terapia , Estado Terminal/terapia , Citaferese/métodos , Interleucina-6/sangue , Pneumonia Viral/imunologia , Pneumonia Viral/terapia , Adulto , Betacoronavirus , Infecções por Coronavirus/sangue , Cuidados Críticos/métodos , Oxigenação por Membrana Extracorpórea/métodos , Humanos , Imunomodulação , Masculino , Pessoa de Meia-Idade , Pandemias , Pneumonia Viral/sangue , Síndrome do Desconforto Respiratório do Adulto/terapia , Síndrome do Desconforto Respiratório do Adulto/virologia
6.
Int J Occup Environ Med ; 11(4): 157-178, 2020 10.
Artigo em Inglês | MEDLINE | ID: mdl-33098401

RESUMO

The novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes coronavirus disease 2019 (COVID-19) and has created a worldwide pandemic. Many patients with this infection have an asymptomatic or mild illness, but a small percentage of patients require hospitalization and intensive care. Patients with respiratory tract involvement have a spectrum of presentations that range from scattered ground-glass infiltrates to diffuse infiltrates with consolidation. Patients with the latter radiographic presentation have severe hypoxemia and usually require mechanical ventilation. In addition, some patients develop multiorgan failure, deep venous thrombi with pulmonary emboli, and cytokine storm syndrome. The respiratory management of these patients should focus on using low tidal volume ventilation with low intrathoracic pressures. Some patients have significant recruitable lung and may benefit from higher positive end-expiratory pressure (PEEP) levels and/or prone positioning. There is no well-established anti-viral treatment for this infection; the United States Food and Drug Administration (FDA) has provided emergency use authorization for convalescent plasma and remdesivir for the treatment of patients with COVID-19. In addition, randomized trials have demonstrated that dexamethasone improves outcomes in patients on mechanical ventilators or on oxygen. There are ongoing trials of other drugs which have the potential to moderate the acute inflammatory state seen in some of these patients. These patients often need prolonged high-level intensive care. Hospitals are confronted with significant challenges in patient management, supply management, health care worker safety, and health care worker burnout.


Assuntos
Betacoronavirus , Infecções por Coronavirus/complicações , Pneumonia Viral/complicações , Síndrome do Desconforto Respiratório do Adulto/virologia , Monofosfato de Adenosina/análogos & derivados , Monofosfato de Adenosina/uso terapêutico , Alanina/análogos & derivados , Alanina/uso terapêutico , Antivirais/uso terapêutico , Infecções por Coronavirus/terapia , Infecções por Coronavirus/virologia , Humanos , Imunização Passiva/métodos , Pulmão/virologia , Pandemias , Pneumonia Viral/terapia , Pneumonia Viral/virologia , Respiração com Pressão Positiva/métodos , Síndrome do Desconforto Respiratório do Adulto/terapia , Estados Unidos
7.
Rev Bras Ter Intensiva ; 32(3): 354-362, 2020.
Artigo em Português, Inglês | MEDLINE | ID: mdl-33053024

RESUMO

OBJECTIVE: The infection caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) spreads worldwide and is considered a pandemic. The most common manifestation of SARS-CoV-2 infection (coronavirus disease 2019 - COVID-19) is viral pneumonia with varying degrees of respiratory compromise and up to 40% of hospitalized patients might develop acute respiratory distress syndrome. Several clinical trials evaluated the role of corticosteroids in non-COVID-19 acute respiratory distress syndrome with conflicting results. We designed a trial to evaluate the effectiveness of early intravenous dexamethasone administration on the number of days alive and free of mechanical ventilation within 28 days after randomization in adult patients with moderate or severe acute respiratory distress syndrome due to confirmed or probable COVID-19. METHODS: This is a pragmatic, prospective, randomized, stratified, multicenter, open-label, controlled trial including 350 patients with early-onset (less than 48 hours before randomization) moderate or severe acute respiratory distress syndrome, defined by the Berlin criteria, due to COVID-19. Eligible patients will be randomly allocated to either standard treatment plus dexamethasone (Intervention Group) or standard treatment without dexamethasone (Control Group). Patients in the intervention group will receive dexamethasone 20mg intravenous once daily for 5 days, followed by dexamethasone 10mg IV once daily for additional 5 days or until intensive care unit discharge, whichever occurs first. The primary outcome is ventilator-free days within 28 days after randomization, defined as days alive and free from invasive mechanical ventilation. Secondary outcomes are all-cause mortality rates at day 28, evaluation of the clinical status at day 15 assessed with a 6-level ordinal scale, mechanical ventilation duration from randomization to day 28, Sequential Organ Failure Assessment Score evaluation at 48 hours, 72 hours and 7 days and intensive care unit -free days within 28.


Assuntos
Infecções por Coronavirus/tratamento farmacológico , Dexametasona/administração & dosagem , Glucocorticoides/administração & dosagem , Pneumonia Viral/tratamento farmacológico , Síndrome do Desconforto Respiratório do Adulto/tratamento farmacológico , Adulto , Infecções por Coronavirus/fisiopatologia , Humanos , Unidades de Terapia Intensiva , Escores de Disfunção Orgânica , Pandemias , Pneumonia Viral/fisiopatologia , Estudos Prospectivos , Respiração Artificial , Síndrome do Desconforto Respiratório do Adulto/virologia , Fatores de Tempo
11.
Front Immunol ; 11: 558898, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-33072097

RESUMO

The dysregulated release of cytokines has been identified as one of the key factors behind poorer outcomes in COVID-19. This "cytokine storm" produces an excessive inflammatory and immune response, especially in the lungs, leading to acute respiratory distress (ARDS), pulmonary edema and multi-organ failure. Alleviating this inflammatory state is crucial to improve prognosis. Pro-inflammatory factors play a central role in COVID-19 severity, especially in patients with comorbidities. In these situations, an overactive, untreated immune response can be deadly, suggesting that mortality in COVID-19 cases is likely due to this virally driven hyperinflammation. Administering immunomodulators has not yielded conclusive improvements in other pathologies characterized by dysregulated inflammation such as sepsis, SARS-CoV-1, and MERS. The success of these drugs at reducing COVID-19-driven inflammation is still anecdotal and comes with serious risks. It is also imperative to screen the elderly for risk factors that predispose them to severe COVID-19. Immunosenescence and comorbidities should be taken into consideration. In this review, we summarize the latest data available about the role of the cytokine storm in COVID-19 disease severity as well as potential therapeutic approaches to ameliorate it. We also examine the role of inflammation in other diseases and conditions often comorbid with COVID-19, such as aging, sepsis, and pulmonary disorders. Finally, we identify gaps in our knowledge and suggest priorities for future research aimed at stratifying patients according to risk as well as personalizing therapies in the context of COVID19-driven hyperinflammation.


Assuntos
Betacoronavirus/imunologia , Infecções por Coronavirus/imunologia , Citocinas/imunologia , Pneumonia Viral/imunologia , Síndrome do Desconforto Respiratório do Adulto/imunologia , Infecções por Coronavirus/mortalidade , Humanos , Fatores Imunológicos/imunologia , Fatores Imunológicos/uso terapêutico , Inflamação/tratamento farmacológico , Inflamação/imunologia , Inflamação/mortalidade , Pandemias , Pneumonia Viral/mortalidade , Síndrome do Desconforto Respiratório do Adulto/mortalidade , Síndrome do Desconforto Respiratório do Adulto/patologia , Síndrome do Desconforto Respiratório do Adulto/virologia
12.
Biochemistry (Mosc) ; 85(7): 833-837, 2020 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-33040727

RESUMO

Nrf2 is a key transcription factor responsible for antioxidant defense in many tissues and cells, including alveolar epithelium, endothelium, and macrophages. Furthermore, Nrf2 functions as a transcriptional repressor that inhibits expression of the inflammatory cytokines in macrophages. Critically ill patients with COVID-19 infection often present signs of high oxidative stress and systemic inflammation - the leading causes of mortality. This article suggests rationale for the use of Nrf2 inducers to prevent development of an excessive inflammatory response in COVID-19 patients.


Assuntos
Betacoronavirus , Infecções por Coronavirus/tratamento farmacológico , Infecções por Coronavirus/metabolismo , Citocinas/antagonistas & inibidores , Citocinas/metabolismo , Terapia de Alvo Molecular/métodos , Fator 2 Relacionado a NF-E2/metabolismo , Pneumonia Viral/tratamento farmacológico , Pneumonia Viral/metabolismo , Animais , Antioxidantes/farmacologia , Antioxidantes/uso terapêutico , Catequina/análogos & derivados , Catequina/farmacologia , Catequina/uso terapêutico , Infecções por Coronavirus/virologia , Fumarato de Dimetilo/farmacologia , Fumarato de Dimetilo/uso terapêutico , Feminino , Humanos , Imunossupressores/farmacologia , Imunossupressores/uso terapêutico , Inflamação/metabolismo , Isotiocianatos/farmacologia , Isotiocianatos/uso terapêutico , Masculino , Camundongos , Estresse Oxidativo/efeitos dos fármacos , Pandemias , Pneumonia Viral/virologia , Síndrome do Desconforto Respiratório do Adulto/tratamento farmacológico , Síndrome do Desconforto Respiratório do Adulto/metabolismo , Síndrome do Desconforto Respiratório do Adulto/virologia , Resveratrol/farmacologia , Resveratrol/uso terapêutico , Transdução de Sinais/efeitos dos fármacos , Tiossulfatos/farmacologia , Tiossulfatos/uso terapêutico
13.
Crit Care ; 24(1): 610, 2020 10 16.
Artigo em Inglês | MEDLINE | ID: mdl-33066801

RESUMO

BACKGROUND: Data on SARS-CoV-2 load in lower respiratory tract (LRT) are scarce. Our objectives were to describe the viral shedding and the viral load in LRT and to determine their association with mortality in critically ill COVID-19 patients. METHODS: We conducted a binational study merging prospectively collected data from two COVID-19 reference centers in France and Switzerland. First, we described the viral shedding duration (i.e., time to negativity) in LRT samples. Second, we analyzed viral load in LRT samples. Third, we assessed the association between viral presence in LRT and mortality using mixed-effect logistic models for clustered data adjusting for the time between symptoms' onset and date of sampling. RESULTS: From March to May 2020, 267 LRT samples were performed in 90 patients from both centers. The median time to negativity was 29 (IQR 23; 34) days. Prolonged viral shedding was not associated with age, gender, cardiac comorbidities, diabetes, immunosuppression, corticosteroids use, or antiviral therapy. The LRT viral load tended to be higher in non-survivors. This difference was statistically significant after adjusting for the time interval between onset of symptoms and date of sampling (OR 3.78, 95% CI 1.13-12.64, p = 0.03). CONCLUSIONS: The viral shedding in LRT lasted almost 30 days in median in critically ill patients, and the viral load in the LRT was associated with the 6-week mortality.


Assuntos
Betacoronavirus/isolamento & purificação , Infecções por Coronavirus/diagnóstico , Pneumonia Viral/diagnóstico , Síndrome do Desconforto Respiratório do Adulto/terapia , Síndrome do Desconforto Respiratório do Adulto/virologia , Sistema Respiratório/virologia , Idoso , Infecções por Coronavirus/mortalidade , Estado Terminal/mortalidade , Feminino , França/epidemiologia , Humanos , Masculino , Pessoa de Meia-Idade , Pandemias , Pneumonia Viral/mortalidade , Estudos Prospectivos , Respiração Artificial , Suíça/epidemiologia , Carga Viral , Eliminação de Partículas Virais
15.
Front Immunol ; 11: 2167, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-33013911

RESUMO

The inflammatory response to and the subsequent development of Adult Respiratory Distress Syndrome (ARDS) is considered to underpin COVID-19 pathogenesis. With a developing world catastrophe, we need to examine our known therapeutic stocks, to assess suitability for prevention and/or treatment of this pro-inflammatory virus. Analyzing commonly available and inexpensive immunomodulatory and anti-inflammatory medications to assess their possible effectiveness in improving the host response to COVID-19, this paper recommends the following: (1) optimize current health-cease (reduce) smoking, ensure adequate hypertension and diabetes control, continue exercising; (2) start on an HMG CoA reductase inhibitor "statin" for its immunomodulatory and anti-inflammatory properties, which may reduce the mortality associated with ARDS; and (3) consider using Diclofenac (or other COX-2 inhibition medications) for its anti-inflammatory and virus toxicity properties. For purposes of effectiveness, this needs to be in the early course of the disease (post infection and/or symptom presentation) and given in a high dose. The downsides to these recommended interventions are considered manageable at this stage of the pandemic.


Assuntos
Betacoronavirus , Infecções por Coronavirus/complicações , Infecções por Coronavirus/tratamento farmacológico , Inibidores de Ciclo-Oxigenase 2/uso terapêutico , Inibidores de Hidroximetilglutaril-CoA Redutases/uso terapêutico , Pneumonia Viral/complicações , Pneumonia Viral/tratamento farmacológico , Síndrome do Desconforto Respiratório do Adulto/complicações , Síndrome do Desconforto Respiratório do Adulto/tratamento farmacológico , Corticosteroides/uso terapêutico , Animais , Anti-Inflamatórios não Esteroides/efeitos adversos , Anti-Inflamatórios não Esteroides/uso terapêutico , Antivirais/efeitos adversos , Antivirais/uso terapêutico , Infecções por Coronavirus/prevenção & controle , Infecções por Coronavirus/virologia , Inibidores de Ciclo-Oxigenase 2/efeitos adversos , Diclofenaco/efeitos adversos , Diclofenaco/uso terapêutico , Interações Hospedeiro-Patógeno/efeitos dos fármacos , Humanos , Inibidores de Hidroximetilglutaril-CoA Redutases/efeitos adversos , Pandemias/prevenção & controle , Pneumonia Viral/prevenção & controle , Pneumonia Viral/virologia , Síndrome do Desconforto Respiratório do Adulto/prevenção & controle , Síndrome do Desconforto Respiratório do Adulto/virologia , Internalização do Vírus/efeitos dos fármacos
16.
BMJ Open ; 10(10): e043651, 2020 10 10.
Artigo em Inglês | MEDLINE | ID: mdl-33040020

RESUMO

OBJECTIVES: COVID-19 causes lung parenchymal and endothelial damage that lead to hypoxic acute respiratory failure (hARF). The influence of hARF severity on patients' outcomes is still poorly understood. DESIGN: Observational, prospective, multicentre study. SETTING: Three academic hospitals in Milan (Italy) involving three respiratory high dependency units and three general wards. PARTICIPANTS: Consecutive adult hospitalised patients with a virologically confirmed diagnosis of COVID-19. Patients aged <18 years or unable to provide informed consent were excluded. INTERVENTIONS: Anthropometrical, clinical characteristics and blood biomarkers were assessed within the first 24 hours from admission. hARF was graded as follows: severe (partial pressure of oxygen to fraction of inspired oxygen ratio (PaO2/FiO2) <100 mm Hg); moderate (PaO2/FiO2 101-200 mm Hg); mild (PaO2/FiO2 201-300 mm Hg) and normal (PaO2/FiO2 >300 mm Hg). PRIMARY AND SECONDARY OUTCOME MEASURES: The primary outcome was the assessment of clinical characteristics and in-hospital mortality based on the severity of respiratory failure. Secondary outcomes were intubation rate and application of continuous positive airway pressure during hospital stay. RESULTS: 412 patients were enrolled (280 males, 68%). Median (IQR) age was 66 (55-76) years with a PaO2/FiO2 at admission of 262 (140-343) mm Hg. 50.2% had a cardiovascular disease. Prevalence of mild, moderate and severe hARF was 24.4%, 21.9% and 15.5%, respectively. In-hospital mortality proportionally increased with increasing impairment of gas exchange (p<0.001). The only independent risk factors for mortality were age ≥65 years (HR 3.41; 95% CI 2.00 to 5.78, p<0.0001), PaO2/FiO2 ratio ≤200 mm Hg (HR 3.57; 95% CI 2.20 to 5.77, p<0.0001) and respiratory failure at admission (HR 3.58; 95% CI 1.05 to 12.18, p=0.04). CONCLUSIONS: A moderate-to-severe impairment in PaO2/FiO2 was independently associated with a threefold increase in risk of in-hospital mortality. Severity of respiratory failure is useful to identify patients at higher risk of mortality. TRIAL REGISTRATION NUMBER: NCT04307459.


Assuntos
Infecções por Coronavirus/patologia , Mortalidade Hospitalar , Hospitalização , Oxigênio/sangue , Pneumonia Viral/patologia , Síndrome do Desconforto Respiratório do Adulto/etiologia , Síndrome Respiratória Aguda Grave/etiologia , Índice de Gravidade de Doença , Idoso , Betacoronavirus , Gasometria , Infecções por Coronavirus/metabolismo , Infecções por Coronavirus/mortalidade , Infecções por Coronavirus/virologia , Feminino , Hospitais , Humanos , Hipóxia , Unidades de Terapia Intensiva , Itália/epidemiologia , Pulmão/metabolismo , Pulmão/patologia , Pulmão/virologia , Masculino , Pessoa de Meia-Idade , Pandemias , Pressão Parcial , Pneumonia Viral/metabolismo , Pneumonia Viral/mortalidade , Pneumonia Viral/virologia , Estudos Prospectivos , Síndrome do Desconforto Respiratório do Adulto/mortalidade , Síndrome do Desconforto Respiratório do Adulto/terapia , Síndrome do Desconforto Respiratório do Adulto/virologia , Insuficiência Respiratória/etiologia , Insuficiência Respiratória/mortalidade , Insuficiência Respiratória/terapia , Insuficiência Respiratória/virologia , Fatores de Risco , Síndrome Respiratória Aguda Grave/mortalidade , Síndrome Respiratória Aguda Grave/terapia , Síndrome Respiratória Aguda Grave/virologia
17.
Front Immunol ; 11: 588724, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-33117402

RESUMO

SARS-CoV-2 infection is a new threat to global public health in the 21st century (2020), which has now rapidly spread around the globe causing severe pneumonia often linked to Acute Respiratory Distress Syndrome (ARDS) and hyperinflammatory syndrome. SARS-CoV-2 is highly contagious through saliva droplets. The structural analysis suggests that the virus enters human cells through the ligation of the spike protein to angiotensin-converting enzyme 2 (ACE2). The progression of Covid-19 has been divided into three main stages: stage I-viral response, stage II-pulmonary phase, and stage III-hyperinflammation phase. Once the patients enter stage III, it will likely need ventilation and it becomes difficult to manage. Thus, it will be of paramount importance to find therapies to prevent or slow down the progression of the disease toward stage III. The key event leading to hyperinflammation seems to be the activation of Th-17 immunity response and Cytokine storm. B2-adrenergic receptors (B2ARs) are expressed on airways and on all the immune cells such as macrophages, dendritic cells, B and T lymphocytes. Blocking (B2AR) has been proven, also in clinical settings, to reduce Th-17 response and negatively modulate inflammatory cytokines including IL-6 while increasing IFNγ. Non-selective beta-blockers are currently used to treat several diseases and have been proven to reduce stress-induced inflammation and reduce anxiety. For these reasons, we speculate that targeting B2AR in the early phase of Covid-19 might be beneficial to prevent hyperinflammation.


Assuntos
Antagonistas de Receptores Adrenérgicos beta 2/uso terapêutico , Infecções por Coronavirus/tratamento farmacológico , Infecções por Coronavirus/patologia , Síndrome da Liberação de Citocina/tratamento farmacológico , Pneumonia Viral/tratamento farmacológico , Pneumonia Viral/patologia , Receptores Adrenérgicos beta 2/efeitos dos fármacos , Síndrome do Desconforto Respiratório do Adulto/tratamento farmacológico , Betacoronavirus/efeitos dos fármacos , Síndrome da Liberação de Citocina/patologia , Humanos , Inflamação/tratamento farmacológico , Inflamação/imunologia , Inflamação/patologia , Neoplasias/tratamento farmacológico , Neoplasias/patologia , Pandemias , Síndrome do Desconforto Respiratório do Adulto/patologia , Síndrome do Desconforto Respiratório do Adulto/virologia , Células Th17/imunologia
18.
Physiol Rep ; 8(20): e14619, 2020 10.
Artigo em Inglês | MEDLINE | ID: mdl-33112512

RESUMO

Coronavirus Disease 2019 (COVID-19) is a public health emergency of international concern with increasing cases globally, including in Indonesia. COVID-19 clinical manifestations ranging from asymptomatic, acute respiratory illness, respiratory failure that necessitate mechanical ventilation and support in an intensive care unit (ICU), to multiple organ dysfunction syndromes. Some patients might present with happy hypoxia, a condition where patients have low oxygen saturations (SpO2  < 90%), but are not in significant respiratory distress and often appear clinically well, which is confusing for the doctors and treatment strategies. Most infections are mild in nature and have a relatively low case fatality rate (CFR); however, critical COVID-19 patients who need support in ICU have high CFR. We would like to report a case of happy hypoxia in a critical COVID-19-positive ICU hospitalized patient who survived from Indonesia.


Assuntos
Infecções por Coronavirus/complicações , Hipóxia/virologia , Pneumonia Viral/complicações , Betacoronavirus , Infecções por Coronavirus/patologia , Humanos , Indonésia , Masculino , Pessoa de Meia-Idade , Pandemias , Pneumonia Viral/patologia , Síndrome do Desconforto Respiratório do Adulto/virologia
20.
J Exp Med ; 217(12)2020 12 07.
Artigo em Inglês | MEDLINE | ID: mdl-32886755

RESUMO

COVID-19 includes lung infection ranging from mild pneumonia to life-threatening acute respiratory distress syndrome (ARDS). Dysregulated host immune response in the lung is a key feature in ARDS pathophysiology. However, cellular actors involved in COVID-19-driven ARDS are poorly understood. Here, in blood and airways of severe COVID-19 patients, we serially analyzed unconventional T cells, a heterogeneous class of T lymphocytes (MAIT, γδT, and iNKT cells) with potent antimicrobial and regulatory functions. Circulating unconventional T cells of COVID-19 patients presented with a profound and persistent phenotypic alteration. In the airways, highly activated unconventional T cells were detected, suggesting a potential contribution in the regulation of local inflammation. Finally, expression of the CD69 activation marker on blood iNKT and MAIT cells of COVID-19 patients on admission was predictive of clinical course and disease severity. Thus, COVID-19 patients present with an altered unconventional T cell biology, and further investigations will be required to precisely assess their functions during SARS-CoV-2-driven ARDS.


Assuntos
Betacoronavirus/genética , Infecções por Coronavirus/imunologia , Células T Invariáveis Associadas à Mucosa/metabolismo , Células T Matadoras Naturais/metabolismo , Fenótipo , Pneumonia Viral/imunologia , Receptores de Antígenos de Linfócitos T gama-delta/metabolismo , Síndrome do Desconforto Respiratório do Adulto/imunologia , Idoso , Antígenos CD/sangue , Antígenos de Diferenciação de Linfócitos T/sangue , Células Cultivadas , Infecções por Coronavirus/virologia , Citocinas/metabolismo , Feminino , Humanos , Inflamação/imunologia , Inflamação/metabolismo , Lectinas Tipo C/sangue , Masculino , Pessoa de Meia-Idade , Células T Invariáveis Associadas à Mucosa/imunologia , Células T Matadoras Naturais/imunologia , Pandemias , Pneumonia Viral/virologia , Prognóstico , Estudos Prospectivos , Síndrome do Desconforto Respiratório do Adulto/virologia , Índice de Gravidade de Doença
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