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3.
Am J Physiol Lung Cell Mol Physiol ; 321(3): L595-L599, 2021 09 01.
Article in English | MEDLINE | ID: covidwho-1413174
4.
Am J Physiol Lung Cell Mol Physiol ; 319(3): L513-L517, 2020 09 01.
Article in English | MEDLINE | ID: covidwho-1093882
5.
Front Med (Lausanne) ; 7: 598379, 2020.
Article in English | MEDLINE | ID: covidwho-954188

ABSTRACT

Coronavirus disease 2019 (COVID-19)-associated acute respiratory distress syndrome (ARDS) is associated with high mortality. Lung-protective ventilation is the current standard of care in patients with ARDS, but it might lead to hypercapnia, which is independently associated with worse outcomes. Extracorporeal carbon dioxide removal (ECCO2R) has been proposed as an adjuvant therapy to avoid progression of clinical severity and limit further ventilator-induced lung injury, but its use in COVID-19 has not been described yet. Acute kidney injury requiring renal replacement therapy (RRT) is common among critically ill COVID-19 patients. In centers with available dialysis, low-flow ECCO2R (<500 mL/min) using RRT platforms could be carried out by dialysis specialists and might be an option to efficiently allocate resources during the COVID-19 pandemic for patients with hypercapnia as the main indication. Here, we report the feasibility, safety, and efficacy of ECCO2R using an RRT platform to provide either standalone ECCO2R or ECCO2R combined with RRT in four hypercapnic patients with moderate ARDS. A randomized clinical trial is required to assess the overall benefit and harm. Clinical Trial Registration: ClinicalTrials.gov. Unique identifier: NCT04351906.

6.
Am J Physiol Lung Cell Mol Physiol ; 320(4): L590-L599, 2021 04 01.
Article in English | MEDLINE | ID: covidwho-945036

ABSTRACT

Despite the pandemic status of COVID-19, there is limited information about host risk factors and treatment beyond supportive care. Immunoglobulin G (IgG) could be a potential treatment target. Our aim was to determine the incidence of IgG deficiency and associated risk factors in a cohort of 62 critically ill patients with COVID-19 admitted to two German ICUs (72.6% male, median age: 61 yr). Thirteen (21.0%) of the patients displayed IgG deficiency (IgG < 7 g/L) at baseline (predominant for the IgG1, IgG2, and IgG4 subclasses). Patients who were IgG-deficient had worse measures of clinical disease severity than those with normal IgG levels (shorter duration from disease onset to ICU admission, lower ratio of [Formula: see text] to [Formula: see text], higher Sequential Organ Failure Assessment score, and higher levels of ferritin, neutrophil-to-lymphocyte ratio, and serum creatinine). Patients who were IgG-deficient were also more likely to have sustained lower levels of lymphocyte counts and higher levels of ferritin throughout the hospital stay. Furthermore, patients who were IgG-deficient compared with those with normal IgG levels displayed higher rates of acute kidney injury (76.9% vs. 26.5%; P = 0.001) and death (46.2% vs. 14.3%; P = 0.012), longer ICU [28 (6-48) vs. 12 (3-18) days; P = 0.012] and hospital length of stay [30 (22-50) vs. 18 (9-24) days; P = 0.004]. Univariable logistic regression showed increasing odds of 90-day overall mortality associated with IgG-deficiency (odds ratio 5.14, 95% confidence interval 1.3-19.9; P = 0.018). IgG deficiency might be common in patients with COVID-19 who are critically ill, and warrants investigation as both a marker of disease severity as well as a potential therapeutic target.


Subject(s)
COVID-19/virology , Immunoglobulins/deficiency , SARS-CoV-2/pathogenicity , Severity of Illness Index , Cohort Studies , Female , Humans , Intensive Care Units , Male , Middle Aged , Risk Factors
7.
Thorax ; 76(2): 201-204, 2021 02.
Article in English | MEDLINE | ID: covidwho-920934

ABSTRACT

Various forms of diffuse parenchymal lung disease have been proposed as potential consequences of severe COVID­19. We describe the clinical, radiological and histological findings of patients with COVID­19-associated acute respiratory distress syndrome who later developed severe organising pneumonia including longitudinal follow-up. Our findings may have important implications for the therapeutic modalities in the late-phase of severe COVID­19 and might partially explain why a subgroup of COVID­19 patients benefits from systemic corticosteroids.


Subject(s)
COVID-19/complications , Lung/diagnostic imaging , Pneumonia/etiology , SARS-CoV-2 , Aged , Biopsy , COVID-19/diagnosis , COVID-19/epidemiology , Humans , Male , Middle Aged , Pneumonia/diagnosis , Tomography, X-Ray Computed
8.
Am J Physiol Lung Cell Mol Physiol ; 319(4): L670-L674, 2020 10 01.
Article in English | MEDLINE | ID: covidwho-798131

ABSTRACT

The severity of coronavirus disease 2019 (COVID-19) is linked to an increasing number of risk factors, including exogenous (environmental) stimuli such as air pollution, nicotine, and cigarette smoke. These three factors increase the expression of angiotensin I converting enzyme 2 (ACE2), a key receptor involved in the entry of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)-the etiological agent of COVID-19-into respiratory tract epithelial cells. Patients with severe COVID-19 are managed with oxygen support, as are at-risk individuals with chronic lung disease. To date, no study has examined whether an increased fraction of inspired oxygen (FiO2) may affect the expression of SARS-CoV-2 entry receptors and co-receptors, including ACE2 and the transmembrane serine proteases TMPRSS1, TMPRSS2, and TMPRSS11D. To address this, steady-state mRNA levels for genes encoding these SARS-CoV-2 receptors were assessed in the lungs of mouse pups chronically exposed to elevated FiO2, and in the lungs of preterm-born human infants chronically managed with an elevated FiO2. These two scenarios served as models of chronic elevated FiO2 exposure. Additionally, SARS-CoV-2 receptor expression was assessed in primary human nasal, tracheal, esophageal, bronchial, and alveolar epithelial cells, as well as primary mouse alveolar type II cells exposed to elevated oxygen concentrations. While gene expression of ACE2 was unaffected, gene and protein expression of TMPRSS11D was consistently upregulated by exposure to an elevated FiO2. These data highlight the need for further studies that examine the relative contribution of the various viral co-receptors on the infection cycle, and point to oxygen supplementation as a potential risk factor for COVID-19.


Subject(s)
Coronavirus Infections/pathology , Membrane Proteins/metabolism , Peptidyl-Dipeptidase A/metabolism , Pneumonia, Viral/pathology , Respiratory Mucosa/metabolism , Serine Endopeptidases/metabolism , Serine Proteases/metabolism , Alveolar Epithelial Cells/metabolism , Angiotensin-Converting Enzyme 2 , Animals , Betacoronavirus , COVID-19 , Cells, Cultured , Female , Humans , Male , Membrane Proteins/genetics , Mice , Mice, Inbred C57BL , Oxygen/administration & dosage , Oxygen/analysis , Pandemics , Receptors, Virus/metabolism , Risk Factors , SARS-CoV-2 , Serine Endopeptidases/genetics , Serine Proteases/genetics , Severity of Illness Index
9.
Am J Physiol Lung Cell Mol Physiol ; 318(5): L1010-L1015, 2020 05 01.
Article in English | MEDLINE | ID: covidwho-700924
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