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Article ; Online: Inclusion in the Pulmonary, Critical Care, and Sleep Medicine Physician-Scientist Workforce. Building with Intention.

Suber, Tomeka L / Neptune, Enid R / Lee, Janet S

ATS scholar

2020 Volume 1, Issue 4, Page(s) 353–363

Abstract: Physician-scientists comprise an exceedingly small fraction of the physician workforce. As the fields of pulmonary, critical care, and sleep medicine continue to invest in the development of the physician-scientist workforce, recruitment and retention ... ...

Abstract	Physician-scientists comprise an exceedingly small fraction of the physician workforce. As the fields of pulmonary, critical care, and sleep medicine continue to invest in the development of the physician-scientist workforce, recruitment and retention strategies need to consider the temporal trend in the decline in numbers of trainees pursuing basic research, the challenges of trainees from underrepresented groups in medicine, and opportunities for career and scientific advancement of women physician-scientists. In this perspective article, we examine the headwinds in the training and education of physician-scientists and highlight potential solutions to reverse these trends.
Language	English
Publishing date	2020-08-12
Publishing country	United States
Document type	Journal Article
ISSN	2690-7097
ISSN (online)	2690-7097
DOI	10.34197/ats-scholar.2020-0026PS
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Article: Glucocorticoid use in acute respiratory failure from pulmonary causes and association with early changes in the systemic host immune response.

Al-Yousif, Nameer / Nouraie, Seyed M / Broerman, Matthew J / Zhang, Yingze / Suber, Tomeka L / Evankovich, John / Bain, William G / Kitsios, Georgios D / McVerry, Bryan J / Shah, Faraaz A

Intensive care medicine experimental

2024 Volume 12, Issue 1, Page(s) 24

Abstract: Background: Glucocorticoids are commonly used in patients with or at-risk for acute respiratory distress syndrome (ARDS), but optimal use remains unclear despite well-conducted clinical trials. We performed a secondary analysis in patients previously ... ...

Abstract	Background: Glucocorticoids are commonly used in patients with or at-risk for acute respiratory distress syndrome (ARDS), but optimal use remains unclear despite well-conducted clinical trials. We performed a secondary analysis in patients previously enrolled in the Acute Lung Injury and Biospecimen Repository at the University of Pittsburgh. The primary aim of our study was to investigate early changes in host response biomarkers in response to real-world use of glucocorticoids in patients with acute respiratory failure due to ARDS or at-risk due to a pulmonary insult. Participants had baseline plasma samples obtained on study enrollment and on follow-up 3 to 5 days later to measure markers of innate immunity (IL-6, IL-8, IL-10, TNFr1, ST2, fractalkine), epithelial injury (sRAGE), endothelial injury (angiopoietin-2), and host response to bacterial infections (procalcitonin, pentraxin-3). In our primary analyses, we investigated the effect of receiving glucocorticoids between baseline and follow-up samples on host response biomarkers measured at follow-up by doubly robust inverse probability weighting analysis. In exploratory analyses, we examined associations between glucocorticoid use and previously characterized host response subphenotypes (hyperinflammatory and hypoinflammatory). Results: 67 of 148 participants (45%) received glucocorticoids between baseline and follow-up samples. Dose and type of glucocorticoids varied. Regimens that used hydrocortisone alone were most common (37%), and median daily dose was equivalent to 40 mg methylprednisolone (interquartile range: 21, 67). Participants who received glucocorticoids were more likely to be female, to be on immunosuppressive therapy at baseline, and to have higher baseline levels of ST-2, fractalkine, IL-10, pentraxin-3, sRAGE, and TNFr1. Glucocorticoid use was associated with decreases in IL-6 and increases in fractalkine. In exploratory analyses, glucocorticoid use was more frequent in participants in the hyperinflammatory subphenotype (58% vs 40%, p = 0.05), and was not associated with subphenotype classification at the follow-up time point (p = 0.16). Conclusions: Glucocorticoid use varied in a cohort of patients with or at-risk for ARDS and was associated with early changes in the systemic host immune response.
Language	English
Publishing date	2024-03-05
Publishing country	Germany
Document type	Journal Article
ZDB-ID	2740385-3
ISSN	2197-425X
ISSN	2197-425X
DOI	10.1186/s40635-024-00605-y
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Article ; Online: Serum metabolomic signatures of fatty acid oxidation defects differentiate host-response subphenotypes of acute respiratory distress syndrome.

Suber, Tomeka L / Wendell, Stacy G / Mullett, Steven J / Zuchelkowski, Benjamin / Bain, William / Kitsios, Georgios D / McVerry, Bryan J / Ray, Prabir / Ray, Anuradha / Mallampalli, Rama K / Zhang, Yingze / Shah, Faraaz / Nouraie, Seyed Mehdi / Lee, Janet S

Respiratory research

2023 Volume 24, Issue 1, Page(s) 136

Abstract: Background: Fatty acid oxidation (FAO) defects have been implicated in experimental models of acute lung injury and associated with poor outcomes in critical illness. In this study, we examined acylcarnitine profiles and 3-methylhistidine as markers of ... ...

Abstract	Background: Fatty acid oxidation (FAO) defects have been implicated in experimental models of acute lung injury and associated with poor outcomes in critical illness. In this study, we examined acylcarnitine profiles and 3-methylhistidine as markers of FAO defects and skeletal muscle catabolism, respectively, in patients with acute respiratory failure. We determined whether these metabolites were associated with host-response ARDS subphenotypes, inflammatory biomarkers, and clinical outcomes in acute respiratory failure. Methods: In a nested case-control cohort study, we performed targeted analysis of serum metabolites of patients intubated for airway protection (airway controls), Class 1 (hypoinflammatory), and Class 2 (hyperinflammatory) ARDS patients (N = 50 per group) during early initiation of mechanical ventilation. Relative amounts were quantified by liquid chromatography high resolution mass spectrometry using isotope-labeled standards and analyzed with plasma biomarkers and clinical data. Results: Of the acylcarnitines analyzed, octanoylcarnitine levels were twofold increased in Class 2 ARDS relative to Class 1 ARDS or airway controls (P = 0.0004 and < 0.0001, respectively) and was positively associated with Class 2 by quantile g-computation analysis (P = 0.004). In addition, acetylcarnitine and 3-methylhistidine were increased in Class 2 relative to Class 1 and positively correlated with inflammatory biomarkers. In all patients within the study with acute respiratory failure, increased 3-methylhistidine was observed in non-survivors at 30 days (P = 0.0018), while octanoylcarnitine was increased in patients requiring vasopressor support but not in non-survivors (P = 0.0001 and P = 0.28, respectively). Conclusions: This study demonstrates that increased levels of acetylcarnitine, octanoylcarnitine, and 3-methylhistidine distinguish Class 2 from Class 1 ARDS patients and airway controls. Octanoylcarnitine and 3-methylhistidine were associated with poor outcomes in patients with acute respiratory failure across the cohort independent of etiology or host-response subphenotype. These findings suggest a role for serum metabolites as biomarkers in ARDS and poor outcomes in critically ill patients early in the clinical course.
MeSH term(s)	Humans ; Acetylcarnitine ; Case-Control Studies ; Biomarkers ; Respiratory Distress Syndrome/diagnosis ; Respiratory Insufficiency/diagnosis ; Respiratory Insufficiency/complications ; Fatty Acids
Chemical Substances	octanoylcarnitine (S1HB7P0O16) ; Acetylcarnitine (6DH1W9VH8Q) ; Biomarkers ; Fatty Acids
Language	English
Publishing date	2023-05-20
Publishing country	England
Document type	Journal Article
ZDB-ID	2041675-1
ISSN	1465-993X ; 1465-993X
ISSN (online)	1465-993X
ISSN	1465-993X
DOI	10.1186/s12931-023-02447-w
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Article ; Online: IL-37-induced activation of glycogen synthase kinase 3β promotes IL-1R8/Sigirr phosphorylation, internalization, and degradation in lung epithelial cells.

Li, Lian / Wei, Jianxin / Suber, Tomeka L / Ye, Qinmao / Miao, Jiaxing / Li, Shuang / Taleb, Sarah J / Tran, Kevin C / Tamaskar, Arya S / Zhao, Jing / Zhao, Yutong

Journal of cellular physiology

2021 Volume 236, Issue 8, Page(s) 5676–5685

Abstract: Interleukin (IL)-37 diminishes a variety of inflammatory responses through ligation to its receptor IL-1R8/Sigirr. Sigirr is a Toll like receptor/IL-1R family member. We have shown that Sigirr is not stable in response to IL-37 treatment. IL-37-induced ... ...

Abstract	Interleukin (IL)-37 diminishes a variety of inflammatory responses through ligation to its receptor IL-1R8/Sigirr. Sigirr is a Toll like receptor/IL-1R family member. We have shown that Sigirr is not stable in response to IL-37 treatment. IL-37-induced Sigirr degradation is mediated by the ubiquitin-proteasome system, and the process is reversed by a deubiquitinase, USP13. However, the molecular mechanisms by which USP13 regulates Sigirr stability have not been revealed. In this study, we investigate the roles of glycogen synthesis kinase 3β (GSK3β) in Sigirr phosphorylation and stability. IL-37 stimulation induced Sigirr phosphorylation and degradation, as well as activation of GSK3β. Inhibition of GSK3β attenuated IL-37-induced Sigirr phosphorylation, while exogenous expressed GSK3β promoted Sigirr phosphorylation at threonine (T)372 residue. Sigirr association with GSK3β was detected. Amino acid residues 51-101 in GSK3β were identified as the Sigirr binding domain. These data indicate that GSK3β mediates IL-37-induced threonine phosphorylation of Sigirr. Further, we investigated the role of GSK3β-mediated phosphorylation of Sigirr in Sigirr degradation. Inhibition of GSK3β attenuated IL-37-induced Sigirr degradation, while T372 mutant of Sigirr was resistant to IL-37-mediated degradation. Furthermore, inhibition of Sigirr phosphorylation prevented Sigirr internalization and association with USP13, suggesting GSK3β promotes Sigirr degradation through disrupting Sigirr association with USP13.
MeSH term(s)	Animals ; Cells, Cultured ; Epithelial Cells/drug effects ; Epithelial Cells/metabolism ; Glycogen Synthase Kinase 3 beta/drug effects ; Glycogen Synthase Kinase 3 beta/metabolism ; Humans ; Interleukin-1/pharmacology ; Lung/drug effects ; Lung/metabolism ; Mice ; Phosphorylation/drug effects ; Proteasome Endopeptidase Complex/metabolism ; Receptors, Interleukin-1/drug effects ; Receptors, Interleukin-1/metabolism ; Signal Transduction ; Toll-Like Receptors/metabolism
Chemical Substances	IL37 protein, human ; Interleukin-1 ; Receptors, Interleukin-1 ; SIGIRR protein, human ; Toll-Like Receptors ; Glycogen Synthase Kinase 3 beta (EC 2.7.11.1) ; Proteasome Endopeptidase Complex (EC 3.4.25.1)
Language	English
Publishing date	2021-01-05
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	3116-1
ISSN	1097-4652 ; 0021-9541
ISSN (online)	1097-4652
ISSN	0021-9541
DOI	10.1002/jcp.30253
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Article ; Online: Considerations for Racial Diversity in the Cardiology Workforce in the United States of America.

Johnson, Amber E / Birru Talabi, Mehret / Bonifacino, Eliana / Culyba, Alison J / Jonassaint, Naudia L / Nance, Melonie A / Napoé, G Sarah / Olafiranye, Oladipupo / Owusu-Ansah, Sylvia / Suber, Tomeka L

Journal of the American College of Cardiology

2021 Volume 77, Issue 15, Page(s) 1934–1937

MeSH term(s)	Cardiology/statistics & numerical data ; Cardiovascular Diseases/epidemiology ; Cardiovascular Diseases/ethnology ; Cardiovascular Diseases/therapy ; Continental Population Groups/statistics & numerical data ; Cultural Competency ; Cultural Diversity ; Ethnic Groups/statistics & numerical data ; Health Workforce/statistics & numerical data ; Humans ; Population Groups/statistics & numerical data ; United States/epidemiology
Language	English
Publishing date	2021-04-20
Publishing country	United States
Document type	Journal Article
ZDB-ID	605507-2
ISSN	1558-3597 ; 0735-1097
ISSN (online)	1558-3597
ISSN	0735-1097
DOI	10.1016/j.jacc.2021.02.043
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Zs.A 1846: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Lung Epithelium Releases Growth Differentiation Factor 15 in Response to Pathogen-mediated Injury.

Shah, Faraaz A / Bahudhanapati, Harinath / Jiang, Mao / Tabary, Mohammadreza / van der Geest, Rick / Tolman, Nathanial J / Kochin, Megan / Xiong, Zeyu / Al-Yousif, Nameer / Sayed, Khaled / Benos, Panayiotis V / Raffensperger, Kristen / Evankovich, John / Neal, Matthew D / Snyder, Mark E / Eickelberg, Oliver / Ray, Prabir / Dela Cruz, Charles / Bon, Jessica /

McVerry, Bryan J / Straub, Adam C / Jurczak, Michael J / Suber, Tomeka L / Zhang, Yingze / Chen, Kong / Kitsios, Georgios D / Lee, Janet S / Alder, Jonathan K / Bain, William G

American journal of respiratory cell and molecular biology

2024 Volume 70, Issue 5, Page(s) 379–391

Abstract: GDF15 (growth differentiation factor 15) is a stress cytokine with several proposed roles, including support of stress erythropoiesis. Higher circulating GDF15 levels are prognostic of mortality during acute respiratory distress syndrome, but the ... ...

Abstract	GDF15 (growth differentiation factor 15) is a stress cytokine with several proposed roles, including support of stress erythropoiesis. Higher circulating GDF15 levels are prognostic of mortality during acute respiratory distress syndrome, but the cellular sources and downstream effects of GDF15 during pathogen-mediated lung injury are unclear. We quantified GDF15 in lower respiratory tract biospecimens and plasma from patients with acute respiratory failure. Publicly available data from severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection were reanalyzed. We used mouse models of hemorrhagic acute lung injury mediated by
MeSH term(s)	Growth Differentiation Factor 15/genetics ; Growth Differentiation Factor 15/metabolism ; Animals ; COVID-19/metabolism ; COVID-19/virology ; Humans ; Mice ; SARS-CoV-2 ; Pseudomonas aeruginosa ; Lung/metabolism ; Lung/pathology ; Lung/virology ; Male ; Pseudomonas Infections/metabolism ; Acute Lung Injury/pathology ; Acute Lung Injury/metabolism ; Female ; Mice, Inbred C57BL ; Mice, Knockout ; Respiratory Mucosa/metabolism ; Respiratory Mucosa/pathology ; Disease Models, Animal
Chemical Substances	Growth Differentiation Factor 15 ; GDF15 protein, human ; Gdf15 protein, mouse
Language	English
Publishing date	2024-01-31
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1025960-0
ISSN	1535-4989 ; 1044-1549
ISSN (online)	1535-4989
ISSN	1044-1549
DOI	10.1165/rcmb.2023-0429OC
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Article ; Online: FBXO17 promotes cell proliferation through activation of Akt in lung adenocarcinoma cells.

Suber, Tomeka L / Nikolli, Ina / O'Brien, Michael E / Londino, James / Zhao, Jing / Chen, Kong / Mallampalli, Rama K / Zhao, Yutong

Respiratory research

2018 Volume 19, Issue 1, Page(s) 206

Abstract: Background: The ubiquitin-proteasome pathway, mediated in part, by ubiquitin E3 ligases, is critical in regulating cellular processes such as cell proliferation, apoptosis, and migration. FBXO17 was recently identified as an F-box protein that targets ... ...

Abstract	Background: The ubiquitin-proteasome pathway, mediated in part, by ubiquitin E3 ligases, is critical in regulating cellular processes such as cell proliferation, apoptosis, and migration. FBXO17 was recently identified as an F-box protein that targets glycogen synthase kinase-3β to the E3 ubiquitin ligase protein complex for polyubiquitination and proteasomal degradation. Here, we identified that in several lung adenocarcinoma cell lines, FBXO17 cellular protein was detected at relatively high levels, as was expression in a subset of lung cancers. Hence, we investigated the effects of FBXO17 on cell proliferation. Methods: Single cell RNA sequencing analysis was performed on a resection of a non-small cell lung carcinoma tumor to examine FBXO17 expression. Multiple lung cancer cell lines were immunoblotted, and The Cancer Genome Atlas was analyzed to determine if FBXO17 expression was amplified in a subset of lung cancers. A549 cells were transfected with empty vector or FBXO17-V5 plasmid and immunoblotted for Akt pathway mediators including PDK1, ERK1/2, ribosomal protein S6, and CREB. Cell proliferation and viability were analyzed by trypan blue exclusion, BrdU incorporation and an MTS-based fluorometric assay. Studies were also performed after transfecting with sifbxo17. Samples were used in an RNA microarray analysis to evaluate pathways affected by reduced FBXO17 gene expression. Results: We observed that overexpression of FBXO17 increased A549 cell proliferation coupled with Akt activation. Ectopically expressed FBXO17 also increased ERK1/2 kinase activation and increased phosphorylation of RPS6, a downstream target of mTOR. We also observed an increased number of cells in S-phase and increased metabolic activity of lung epithelial cells expressing FBXO17. FBXO17 knockdown reduced Akt Ser 473 phosphorylation approaching statistical significance with no effect on Thr 308. However, ERK1/2 phosphorylation, cellular metabolic activity, and overall cell numbers were reduced. When we analyzed RNA profiles of A549 cells with reduced FBXO17 expression, we observed downregulation of several genes associated with cell proliferation and metabolism. Conclusions: These data support a role for FBXO17 abundance, when left unchecked, in regulating cell proliferation and survival through modulation of Akt and ERK kinase activation. The data raise a potential role for the F-box subunit in modulating tumorigenesis.
MeSH term(s)	A549 Cells ; Adenocarcinoma of Lung/metabolism ; Adenocarcinoma of Lung/pathology ; Cell Proliferation/physiology ; F-Box Proteins/biosynthesis ; Humans ; Lung Neoplasms/metabolism ; Lung Neoplasms/pathology ; Proto-Oncogene Proteins c-akt/metabolism
Chemical Substances	F-Box Proteins ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1)
Language	English
Publishing date	2018-10-25
Publishing country	England
Document type	Journal Article
ZDB-ID	2041675-1
ISSN	1465-993X ; 1465-9921
ISSN (online)	1465-993X
ISSN	1465-9921
DOI	10.1186/s12931-018-0910-0
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Article ; Online: Trajectories of Host-Response Subphenotypes in Patients With COVID-19 Across the Spectrum of Respiratory Support.

Lu, Michael / Drohan, Callie / Bain, William / Shah, Faraaz A / Bittner, Matthew / Evankovich, John / Prendergast, Niall T / Hensley, Matthew / Suber, Tomeka L / Fitzpatrick, Meghan / Ramanan, Raj / Murray, Holt / Schaefer, Caitlin / Qin, Shulin / Wang, Xiaohong / Zhang, Yingze / Nouraie, Seyed M / Gentry, Heather / Murray, Cathy /

Patel, Asha / Macatangay, Bernard J / Jacobs, Jana / Mellors, John W / Lee, Janet S / Ray, Prabir / Ray, Anuradha / Methé, Barbara / Morris, Alison / McVerry, Bryan J / Kitsios, Georgios D

CHEST critical care

2023 Volume 1, Issue 3

Abstract: Background: Hospitalized patients with severe COVID-19 follow heterogeneous clinical trajectories, requiring different levels of respiratory support and experiencing diverse clinical outcomes. Differences in host immune responses to SARS-CoV-2 infection ...

Abstract	Background: Hospitalized patients with severe COVID-19 follow heterogeneous clinical trajectories, requiring different levels of respiratory support and experiencing diverse clinical outcomes. Differences in host immune responses to SARS-CoV-2 infection may account for the heterogeneous clinical course, but we have limited data on the dynamic evolution of systemic biomarkers and related subphenotypes. Improved understanding of the dynamic transitions of host subphenotypes in COVID-19 may allow for improved patient selection for targeted therapies. Research question: We examined the trajectories of host-response profiles in severe COVID-19 and evaluated their prognostic impact on clinical outcomes. Study design and methods: In this prospective observational study, we enrolled 323 inpatients with COVID-19 receiving different levels of baseline respiratory support: (1) low-flow oxygen (37%), (2) noninvasive ventilation (NIV) or high-flow oxygen (HFO; 29%), (3) invasive mechanical ventilation (27%), and (4) extracorporeal membrane oxygenation (7%). We collected plasma samples on enrollment and at days 5 and 10 to measure host-response biomarkers. We classified patients by inflammatory subphenotypes using two validated predictive models. We examined clinical, biomarker, and subphenotype trajectories and outcomes during hospitalization. Results: IL-6, procalcitonin, and angiopoietin 2 persistently were elevated in patients receiving higher levels of respiratory support, whereas soluble receptor of advanced glycation end products (sRAGE) levels displayed the inverse pattern. Patients receiving NIV or HFO at baseline showed the most dynamic clinical trajectory, with 24% eventually requiring intubation and exhibiting worse 60-day mortality than patients receiving invasive mechanical ventilation at baseline (67% vs 35%; Interpretation: Longitudinal study of the systemic host response in COVID-19 revealed substantial and predictive interindividual variability influenced by baseline levels of respiratory support.
Language	English
Publishing date	2023-09-14
Publishing country	United States
Document type	Journal Article
ISSN	2949-7884
ISSN (online)	2949-7884
DOI	10.1016/j.chstcc.2023.100018
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Article ; Online: Post-translational modification of the interferon-gamma receptor alters its stability and signaling.

Londino, James D / Gulick, Dexter L / Lear, Travis B / Suber, Tomeka L / Weathington, Nathaniel M / Masa, Luke S / Chen, Bill B / Mallampalli, Rama K

The Biochemical journal

2017 Volume 474, Issue 20, Page(s) 3543–3557

Abstract: The IFN gamma receptor 1 (IFNGR1) binds IFN-γ and activates gene transcription pathways crucial for controlling bacterial and viral infections. Although decreases in IFNGR1 surface levels have been demonstrated to inhibit IFN-γ signaling, little is known ...

Abstract	The IFN gamma receptor 1 (IFNGR1) binds IFN-γ and activates gene transcription pathways crucial for controlling bacterial and viral infections. Although decreases in IFNGR1 surface levels have been demonstrated to inhibit IFN-γ signaling, little is known regarding the molecular mechanisms controlling receptor stability. Here, we show in epithelial and monocytic cell lines that IFNGR1 displays K48 polyubiquitination, is proteasomally degraded, and harbors three ubiquitin acceptor sites at K277, K279, and K285. Inhibition of glycogen synthase kinase 3 beta (GSK3β) destabilized IFNGR1 while overexpression of
MeSH term(s)	CRISPR-Cas Systems/genetics ; HEK293 Cells ; Humans ; Interferon-gamma/pharmacology ; Protein Processing, Post-Translational/drug effects ; Protein Processing, Post-Translational/physiology ; Protein Stability/drug effects ; Receptors, Interferon/chemistry ; Receptors, Interferon/genetics ; Receptors, Interferon/metabolism ; Signal Transduction/drug effects ; Signal Transduction/physiology ; Interferon gamma Receptor
Chemical Substances	Receptors, Interferon ; Interferon-gamma (82115-62-6)
Language	English
Publishing date	2017-10-10
Publishing country	England
Document type	Journal Article
ZDB-ID	2969-5
ISSN	1470-8728 ; 0006-2936 ; 0306-3275 ; 0264-6021
ISSN (online)	1470-8728
ISSN	0006-2936 ; 0306-3275 ; 0264-6021
DOI	10.1042/BCJ20170548
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Article ; Online: Longitudinal changes in age and race of patients with SARS-CoV-2 in a multi-hospital health system

Barbash, Ian J / Harrison, Lee / Jacobs, Jana L / Shah, Faraaz Ali / Suber, Tomeka L / Quinn, Kevin L / Marroquin, Oscar C / Gladwin, Mark T / Sackrowitz, Rachel E / Morris, Alison

medRxiv

Abstract: Background: The COVID-19 pandemic continues to affect the United States and the world. Media reports have suggested that the wave of the alpha variant in the Spring of 2021 in the US caused more cases among younger patients and racial and ethnic ... ...

Abstract	Background: The COVID-19 pandemic continues to affect the United States and the world. Media reports have suggested that the wave of the alpha variant in the Spring of 2021 in the US caused more cases among younger patients and racial and ethnic subgroups. Approach: We analyzed electronic health record data from a multihospital health system to test whether younger patients accounted for more cases and more severe disease, and whether racial disparities are widening. We compared demographics, patient characteristics, and hospitalization variables for patients admitted from November 2020 through January 2021 to those admitted in March and April 2021. Results: We analyzed data for 37, 502 unique inpatients and outpatients at 21 hospitals from November 1, 2020 to April 30, 2021. Compared to patients from November through January, those with positive tests in March and April were younger and less likely to die. Among patients under age 50, those with positive tests in March and April were three times as likely to be hospitalized and twice as likely to require ICU admission or mechanical ventilation. Individuals identified as Black represented a greater proportion of cases and hospitalizations in March and April as compared to November through January. Conclusions: We found that relative COVID-19 hospitalization rates for younger individuals and individuals identified as Black were rising over time. These findings have important implications for ongoing public health measures to mitigate the impact of the pandemic.
Keywords	covid19
Language	English
Publishing date	2021-08-18
Publisher	Cold Spring Harbor Laboratory Press
Document type	Article ; Online
DOI	10.1101/2021.08.16.21262016
Database	COVID19

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