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1.
EuropePMC; 2020.
Preprint in English | EuropePMC | ID: ppcovidwho-325094

ABSTRACT

Background: Coronavirus Disease-2019 (COVID-19) has caused considerable morbidity and mortality. Hence, there is an urgency to find effective treatment. Tocilizumab, an inhibitor of IL-6, has been widely proposed as a treatment of severely ill patients without robust evidence supporting its use. Methods: In this multicentre, retrospective, cohort study, we included 5,235 adult patients who were admitted to 3 hospitals in Wuhan, China with confirmed COVID-19 from January 20 to March 18, 2020 . 65 patients in tocilizumab group and 130 patients in non-tocilizumab group were propensity score matched at a ratio of 2:1 based on age, sex, and comorbidities. Detailed demographic data, comorbidities, radiological and laboratory parameters, complications and treatments were compared between tocilizumab group and non-tocilizumab group. Furthermore, univariable and multivariable Logistic and Cox regression models were used to explore the risk of complications and in-hospital death associated with tocilizumab. Findings: During the follow-up, patients in non-tocilizumab group were more likely to develop into death (42 [32·31%] vs 14 [21·54%]). After adjusting for confounding, the detected risk for in-hospital death was lower in the tocilizumab group versus the non-tocilizumab group (HR=0·47;95% CI=0·25-0·90;p=0·023). In the multivariable logistic regression model, use of tocilizumab was associated with a lower risk of ARDS (OR=0 · 23;95% CI=0·11-0·45;p<0·0001). Before treatment the patients had heightened inflammation and more dysregulated immune cells, which might aggravate disease progression. However, abnormally elevated IL-6, CRP, fibrinogen and APTT decreased in COVID-19 patients after treatment. And the counts of lymphocytes and immune cells subset in peripheral blood, which decreased in patients, returned to normal after treatment. No obvious complications were observed. Interpretation: Tocilizumab may be of value in improving outcomes in severe patients of COVID-19, which provided a novel strategy for COVID-19-induced cytokine release syndrome (CRS). Our preliminary data could inform bedside decisions until more data from randomized, controlled clinical trials becomes available.Funding Statement: SARS-CoV-2 Pneumonia Emergency Technology Public Relations Project of Tongji Medical College, Huazhong University of Science and Technology (No. 2020kfyXGYJ043) and National Key Research and Development Plan for the Emergency Management of Novel Coronavi rus Pneumonia, China (No. 2020YFC0845100).Declaration of Interests: The authors report no conflicts of interest.Ethics Approval Statement: This study was approved by the Ethics Committee of Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology (TJ-C20200108) and granted a waiver of informed consent from study participants.

2.
EuropePMC; 2021.
Preprint in English | EuropePMC | ID: ppcovidwho-323601

ABSTRACT

Background: The COVID-19 pandemic has been considered a great threat to global public health. We aimed to clarify the risk factors associated with the development of acute respiratory distress syndrome (ARDS) and progression from ARDS to death and construct a risk prediction model. Methods: : In this single-centered, retrospective, and observational study, 796 COVID-19 patients developed ARDS and 735 COVID-19 patients without ARDS were matched by propensity score at an approximate ratio of 1:1 based on age, sex and comorbidities. Demographic data, symptoms, radiological findings, laboratory examinations, and clinical outcomes were compared between those with or without ARDS. Univariable and multivariable logistic regression models were applied to explore the risk factors for development of ARDS and progression from ARDS to death and establish a comprehensive risk model. Results: : Higher SOFA, qSOFA, APACHE II and SIRS scores, elevated inflammatory cytokines, dysregulated multi-organ damage biomarkers, decreased immune cell subsets were associated with higher proportion of death (34.17% vs 1.22%;P <0.001) and increased risk odds of death (OR=57.216, 95%CI=28.373-115.378;P <0.001) in COVID-19 patients with ARDS. In addition to previous reported risk factors related to ARDS development and death, such as neutrophils, IL-6, D-Dimer, leukocytes and platelet, we identified elevated TNF-α (OR=1.146, 95%CI=1.100-1.194;P <0.001), CK-MB (OR=1.350, 95%CI=1.180-1.545;P <0.001), declined ALB (OR=0.834, 95%CI=0.799-0.872;P <0.001), CD8 + T cells (OR=0.983, 95%CI=0.976-0.990;P <0.001) and CD3 - CD19 + B cells (OR=0.992, 95%CI=0.988-0.997;P =0.003) as novel risk factors. Most importantly, the predictive accuracy of the combined model integrating four score systems and these risk factors demonstrated highest among all models for the development of ARDS (AUC= 0.904) and the progression from ARDS to death (AUC= 0.959). Conclusion: COVID-19 patients with ARDS were more likely to develop into death. The potential risk factors and the comprehensive prediction model could be helpful to identify patients that are at risk of developing ARDS with poor prognosis at an early stage, which might help physicians to formulate a timely therapeutic strategy.

3.
EuropePMC; 2021.
Preprint in English | EuropePMC | ID: ppcovidwho-315604

ABSTRACT

Human activities are hugely restricted by COVID-19, recently. Robots that can conduct inter-floor navigation attract much public attention, since they can substitute human workers to conduct the service work. However, current robots either depend on human assistance or elevator retrofitting, and fully autonomous inter-floor navigation is still not available. As the very first step of inter-floor navigation, elevator button segmentation and recognition hold an important position. Therefore, we release the first large-scale publicly available elevator panel dataset in this work, containing 3,718 panel images with 35,100 button labels, to facilitate more powerful algorithms on autonomous elevator operation. Together with the dataset, a number of deep learning based implementations for button segmentation and recognition are also released to benchmark future methods in the community. The dataset will be available at \url{https://github.com/zhudelong/elevator_button_recognition

4.
EuropePMC; 2020.
Preprint in English | EuropePMC | ID: ppcovidwho-313437

ABSTRACT

Background: Coronavirus disease 2019 (COVID-19) has spread globally. However, the association between COVID-19 and disseminated intravascular coagulation (DIC) has been scarcely addressed. We aimed to systematically characterize the clinical features and examine risk factors for DIC development in COVID-19 patients. Methods: : In this single-centered, retrospective, and observational study, all patients with DIC (N=59) and 270 patients without DIC were matched by propensity score matching based on age, sex, and comorbidities. Demographic data, symptoms, radiological, laboratory examinations, and clinical outcomes were compared between patients with and without DIC. Furthermore, univariable and multivariable logistic regression were used to explore the risk factors associated with DIC development in COVID-19 patients. Results: : Higher proportion of patients with DIC and COVID-19 (54 of 59 [91·53%]) developed into death than non DIC patients (58 of 270 [21·48%]). Patients with DIC presented aggravated inflammation responses, liver damage, and especially coagulation dysfunction. Moreover, in addition to previously reported coagulation-related markers, such as FDP, D-dimer, and platelet, we also identified several novel risk factors associated with DIC development, including decreased fibrinogen (OR=0·476, 95%CI=0·380-0·596, P <0·0001) and ALB (0·901, 0·845- 0·961, P =0·0015), and elevated IL-6 (1·010, 1·005-1·015, P =0·00017) and TNF-α (1·053, 1·016-1·091, P =0·0045). Conclusions: : Patients with DIC and COVID-19 were predisposed to poor clinical outcomes. These risk factors identified may be helpful for early surveillance of disease progression and making standardized treatment strategies.

5.
EuropePMC; 2020.
Preprint in English | EuropePMC | ID: ppcovidwho-313435

ABSTRACT

Background: The coronavirus disease 2019 (COVID-19) has caused global pandemic, resulting in considerable mortality. The risk factors, clinical treatments and especially comprehensive risk models for COVID-19 death are urgently warranted. Methods In this retrospective study, 281 non-survivors and 712 survivors with propensity score matching by age, sex and comorbidities were enrolled from January 13, 2020 to March 31, 2020. Results Higher SOFA, qSOFA, APACHE II and SIRS scores, hypoxia, elevated inflammatory cytokines, multi-organ dysfunction, decreased immune cells subsets and complications were significantly associated with the higher COVID-19 death risk. In addition to traditional predictors for death risk, including APACHE II (AUC = 0.83), SIRS (AUC = 0.75), SOFA (AUC = 0.70) and qSOFA scores (AUC = 0.61), another four prediction models that included immune cells subsets (AUC = 0.90), multiple organ damage biomarkers (AUC = 0.89), complications (AUC = 0.88) and inflammatory-related indexes (AUC = 0.75) were established. Additionally, the predictive accuracy of combining these risk factors (AUC = 0.950) was also significantly higher than that of each risk group alone, outperforming previous risk models, which was significant for early clinical management for COVID-19. Conclusions The potential risk factors could help to predict the clinical prognosis of COVID-19 patients at an early stage. The combined model might be more suitable for the death risk evaluation of COVID-19.

6.
Journal of Organizational and End User Computing ; 33(6):1-18, 2021.
Article in English | ProQuest Central | ID: covidwho-1444400

ABSTRACT

The coronavirus disease 2019 (COVID-19) epidemic that began in early 2020 quickly formed a global trend, bringing unprecedented shocks to many countries’ and even the global trade economy. Big data is the main feature of the Internet era, which has transformed the industrial development pattern of modern society and has now flourished in the field of trade economy;therefore, it is of great significance to apply the big data analysis technology to study the impact of the COVID-19 epidemic on the global trade economy. On the basis of summarizing and analyzing previous research works, this paper, expounded the research status and significance of the impact of the COVID-19 epidemic on the global trade economy, elaborated the development background, The study results of this paper provide a reference for further researches on the impact of the impact of the COVID-19 epidemic on the global trade economy based on big data analysis.

7.
BMC Infect Dis ; 21(1): 951, 2021 Sep 14.
Article in English | MEDLINE | ID: covidwho-1412707

ABSTRACT

BACKGROUND: The coronavirus disease 2019 (COVID-19) has caused a global pandemic, resulting in considerable mortality. The risk factors, clinical treatments, especially comprehensive risk models for COVID-19 death are urgently warranted. METHODS: In this retrospective study, 281 non-survivors and 712 survivors with propensity score matching by age, sex, and comorbidities were enrolled from January 13, 2020 to March 31, 2020. RESULTS: Higher SOFA, qSOFA, APACHE II and SIRS scores, hypoxia, elevated inflammatory cytokines, multi-organ dysfunction, decreased immune cell subsets, and complications were significantly associated with the higher COVID-19 death risk. In addition to traditional predictors for death risk, including APACHE II (AUC = 0.83), SIRS (AUC = 0.75), SOFA (AUC = 0.70) and qSOFA scores (AUC = 0.61), another four prediction models that included immune cells subsets (AUC = 0.90), multiple organ damage biomarkers (AUC = 0.89), complications (AUC = 0.88) and inflammatory-related indexes (AUC = 0.75) were established. Additionally, the predictive accuracy of combining these risk factors (AUC = 0.950) was also significantly higher than that of each risk group alone, which was significant for early clinical management for COVID-19. CONCLUSIONS: The potential risk factors could help to predict the clinical prognosis of COVID-19 patients at an early stage. The combined model might be more suitable for the death risk evaluation of COVID-19.


Subject(s)
COVID-19 , Sepsis , Humans , Intensive Care Units , Organ Dysfunction Scores , Prognosis , ROC Curve , Retrospective Studies , Risk Factors , SARS-CoV-2
8.
BMC Infect Dis ; 21(1): 951, 2021 Sep 14.
Article in English | MEDLINE | ID: covidwho-1406708

ABSTRACT

BACKGROUND: The coronavirus disease 2019 (COVID-19) has caused a global pandemic, resulting in considerable mortality. The risk factors, clinical treatments, especially comprehensive risk models for COVID-19 death are urgently warranted. METHODS: In this retrospective study, 281 non-survivors and 712 survivors with propensity score matching by age, sex, and comorbidities were enrolled from January 13, 2020 to March 31, 2020. RESULTS: Higher SOFA, qSOFA, APACHE II and SIRS scores, hypoxia, elevated inflammatory cytokines, multi-organ dysfunction, decreased immune cell subsets, and complications were significantly associated with the higher COVID-19 death risk. In addition to traditional predictors for death risk, including APACHE II (AUC = 0.83), SIRS (AUC = 0.75), SOFA (AUC = 0.70) and qSOFA scores (AUC = 0.61), another four prediction models that included immune cells subsets (AUC = 0.90), multiple organ damage biomarkers (AUC = 0.89), complications (AUC = 0.88) and inflammatory-related indexes (AUC = 0.75) were established. Additionally, the predictive accuracy of combining these risk factors (AUC = 0.950) was also significantly higher than that of each risk group alone, which was significant for early clinical management for COVID-19. CONCLUSIONS: The potential risk factors could help to predict the clinical prognosis of COVID-19 patients at an early stage. The combined model might be more suitable for the death risk evaluation of COVID-19.


Subject(s)
COVID-19 , Sepsis , Humans , Intensive Care Units , Organ Dysfunction Scores , Prognosis , ROC Curve , Retrospective Studies , Risk Factors , SARS-CoV-2
9.
Front Med ; 16(1): 111-125, 2022 Feb.
Article in English | MEDLINE | ID: covidwho-1356049

ABSTRACT

The Coronavirus disease 2019 (COVID-19) has spread globally. Although mixed liver impairment has been reported in COVID-19 patients, the association of liver injury caused by specific subtype especially chronic hepatitis B (CHB) with COVID-19 has not been elucidated. In this multi-center, retrospective, and observational cohort study, 109 CHB and 327 non-CHB patients with COVID-19 were propensity score matched at an approximate ratio of 3:1 on the basis of age, sex, and comorbidities. Demographic characteristics, laboratory examinations, disease severity, and clinical outcomes were compared. Furthermore, univariable and multivariable logistic and Cox regression models were used to explore the risk factors for disease severity and mortality, respectively. A higher proportion of CHB patients (30 of 109 (27.52%)) developed into severe status than non-CHB patients (17 of 327 (5.20%)). In addition to previously reported liver impairment markers, such as alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, and total bilirubin, we identified several novel risk factors including elevated lactate dehydrogenase (⩾ 245 U/L, hazard ratio (HR) = 8.639, 95% confidence interval (CI) = 2.528-29.523; P < 0.001) and coagulation-related biomarker D-dimer (⩾ 0.5 µg/mL, HR = 4.321, 95% CI = 1.443-12.939; P = 0.009) and decreased albumin (< 35 g/L, HR = 0.131, 95% CI = 0.048-0.361; P < 0.001) and albumin/globulin ratio (< 1.5, HR = 0.123, 95% CI = 0.017-0.918; P = 0.041). In conclusion, COVID-19 patients with CHB were more likely to develop into severe illness and die. The risk factors that we identified may be helpful for early clinical surveillance of critical progression.


Subject(s)
COVID-19 , Hepatitis B, Chronic , Cohort Studies , Hepatitis B, Chronic/complications , Hepatitis B, Chronic/epidemiology , Humans , Retrospective Studies , Risk Factors
10.
Food Funct ; 12(8): 3393-3404, 2021 Apr 26.
Article in English | MEDLINE | ID: covidwho-1201666

ABSTRACT

The global health emergency generated by coronavirus disease-2019 has prompted the search for immunomodulatory agents. There are many potential natural products for drug discovery and development to tackle this disease. One of these candidates is the Ganoderma lucidum fungal immunomodulatory protein (FIP-glu). In the present study, we clarify the influences of N-linked glycans on the improvement of anti-inflammatory activity and the potential mechanisms of action. Four proteins, including FIP-glu (WT) and its mutants N31S, T36N and N31S/T36N, were successfully expressed in P. pastoris, of which T36N and N31S/T36N were glycoproteins. After treatment with peptide-N-glycosidase F, the results of SDS-PAGE and Western blot showed that the glycan moiety was removed completely, indicating that the glycan moiety was N-linked. This was also demonstrated by UPLC-qTOF-MS. The cytotoxicity assay showed that N-linked glycans decreased the cytotoxicity of WT; while, the RT-qPCR assay showed that N-glycosylated WT regulated the mRNA expression of IL-6 and TGF-ß1. The Western blot results showed that N-glycosylated WT reduced the phosphorylation level of p38 MAPK. In conclusion, our findings revealed a novel mechanism by which N-glycosylation of FIP-glu improved its anti-inflammatory activity through the regulation of the expression of inflammatory cytokines in RAW264.7 via inhibition of p38 MAPK phosphorylation. It was proved that N-glycosylation significantly improved the functional properties of FIP-glu, providing theoretical and technical support for expanding the application of FIPs in the food and pharmaceutical industries.


Subject(s)
Fungal Proteins/pharmacology , Immunologic Factors/pharmacology , Immunomodulation/drug effects , Reishi , p38 Mitogen-Activated Protein Kinases/metabolism , Animals , Blotting, Western , Chromatography, High Pressure Liquid , Cytokines , Electrophoresis, Polyacrylamide Gel , Glycoproteins/metabolism , Glycosylation , Mass Spectrometry , Mice , Peptide-N4-(N-acetyl-beta-glucosaminyl) Asparagine Amidase , RAW 264.7 Cells , Real-Time Polymerase Chain Reaction , Saccharomycetales
11.
J Glob Health ; 11: 05006, 2021 Mar 27.
Article in English | MEDLINE | ID: covidwho-1173056

ABSTRACT

BACKGROUND: In December 2019, coronavirus disease 2019 (COVID-19) emerged in Wuhan city and rapidly spread throughout China. So far, it has caused ~ 4000 deaths in this country. We aimed to systematically characterize clinical features and determine risk factors of sudden death for COVID-19 patients. METHODS: Deceased patients with COVID-19 in Tongji hospital from January 22 to March 23, 2020 were extracted. Patients who died within 24 hours after admission were identified as sudden deaths, and the others formed non-sudden deaths. The differences in clinical characteristics between the two groups were estimated. Risk factors associated with sudden deaths were explored by logistic regression. RESULTS: 281 deceased patients were enrolled in this study. Sudden death occurred in 28 (10.0%) patients, including 4 (14.3%) admitted to the intensive care unit. Fatigue was more common in sudden deaths (11, 47.8%) than in non-sudden deaths (40, 17.2%). Both the count and percentage of eosinophils were lower in sudden deaths than that in non-sudden deaths (P = 0.006 and P = 0.004). Compared with non-sudden deaths, sudden deaths had higher plasma levels of procalcitonin, C-reactive protein, D-dimer, alanine aminotransferase, aspartate aminotransferase, gamma-glutamyl transferase, lactate dehydrogenase, alkaline phosphatase and N-terminal pro-brain natriuretic peptide. There were not significant differences in gender, age, chest CT image features and comorbidities observed. CONCLUSIONS: The differences between the two groups suggested more severe systemic inflammation, multi-organ dysfunction, especially impaired liver and heart function in COVID-19 patients who died suddenly after admission. More researches are needed to verify these points.


Subject(s)
COVID-19/mortality , Death, Sudden/epidemiology , Patient Admission/statistics & numerical data , SARS-CoV-2 , Aged , Cause of Death , China/epidemiology , Death, Sudden/etiology , Female , Hospital Mortality , Humans , Male , Middle Aged , Retrospective Studies , Risk Factors
12.
Preprint in English | bioRxiv | ID: ppbiorxiv-435497

ABSTRACT

As the coronavirus disease 2019 (COVID-19) pandemic rages on, it is important to explore new evolution-resistant vaccine antigens and new vaccine platforms that can produce readily scalable, inexpensive vaccines with easier storage and transport. We report here a synthetic biology-based vaccine platform that employs an expression vector with an inducible Gram-negative autotransporter to express vaccine antigens on surface of genome-reduced bacteria to enhance interaction of vaccine antigen with immune system. As a proof of principle, we utilized genome-reduced E. coli to express SARS-CoV-2 and porcine epidemic diarrhea virus (PEDV) fusion peptide (FP) on the cell surface, and evaluated their use as a killed whole cell vaccine. The FP sequence is highly conserved across coronaviruses; the 6 FP core amino acid residues along with the 4 adjacent residues upstream and the 3 residues downstream the core are identical between SARS-CoV-2 and PEDV. We tested the efficacy of PEDV FP and SARS-CoV-2 FP vaccines in a PEDV challenge pig model. We demonstrated that both vaccines induced potent anamnestic responses upon virus challenge, potentiated IFN-{gamma} responses, reduced viral RNA loads in jejunum tissue, and provided significant protection against clinical disease. However, neither vaccines elicited sterilizing immunity. Since SARS-CoV-2 FP and PEDV FP vaccines provided similar clinical protection, the coronavirus FP could be a target for a broadly-protective vaccine using any platform. Importantly, the genome-reduced bacterial surface-expressed vaccine platform, when using a vaccine appropriate bacterial vector, has potential utility as an inexpensive, readily manufactured, and rapid vaccine platform for other pathogens. Significance StatementWe report a new vaccine platform to express vaccine antigens on surface of genome-reduced bacteria to enhance vaccine immunogenicity. We demonstrated the utility of this vaccine platform by expressing the highly conserved fusion peptide (FP) of SARS-CoV-2 and porcine epidemic diarrhea virus on the surface of E.coli to produce killed whole cell bacterial vaccines. The vaccine primes a potent anamnestic response, potentiates IFN-{gamma} responses, and provides significant protection in pigs against disease following virus challenge. The FP could be a target for a broadly-protective coronavirus vaccine since a Betacoronavirus SARS-CoV-2 FP vaccine provided cross-protection against Alphacoronavirus PEDV. When using a vaccine appropriate bacteria vector, this inexpensive new vaccine platform offers the potential for use in developing countries.

14.
J Immunol ; 206(3): 599-606, 2021 02 01.
Article in English | MEDLINE | ID: covidwho-969665

ABSTRACT

The coronavirus disease 2019 (COVID-19) has caused a global pandemic, resulting in considerable morbidity and mortality. Tocilizumab, an inhibitor of IL-6, has been widely repurposed as a treatment of severely ill patients without robust evidence supporting its use. In this study, we aimed to systematically describe the effectiveness of treatment and prevention of the cytokine storms in COVID-19 patients with tocilizumab. In this multicentered retrospective and observational cohort study, 65 patients with COVID-19 receiving tocilizumab and 130 not receiving tocilizumab were propensity score matched at a ratio of 2:1 based on age, sex, and comorbidities from January 20, 2020 to March 18, 2020 in Wuhan, China. After adjusting for confounding, the detected risk for in-hospital death was lower in the tocilizumab group versus nontocilizumab group (hazard ratio = 0.47; 95% confidence interval = 0.25-0.90; p = 0.023). Moreover, use of tocilizumab was associated with a lower risk of acute respiratory distress syndrome (odds ratio = 0.23; 95% confidence interval = 0.11-0.45; p < 0.0001). Furthermore, patients had heightened inflammation and more dysregulated immune cells before treatment, which might aggravate disease progression. After tocilizumab administration, abnormally elevated IL-6, C-reactive protein, fibrinogen, and activated partial thromboplastin time decreased. Tocilizumab may be of value in prolonging survival in patients with severe COVID-19, which provided a novel strategy for COVID-19-induced cytokine release syndrome. Our findings could inform bedside decisions until data from randomized, controlled clinical trials become available.


Subject(s)
Antibodies, Monoclonal, Humanized/therapeutic use , COVID-19/complications , COVID-19/drug therapy , Cytokine Release Syndrome/complications , Cytokine Release Syndrome/drug therapy , Drug Repositioning , Respiratory Distress Syndrome/complications , Respiratory Distress Syndrome/drug therapy , Aged , COVID-19/immunology , Cohort Studies , Cytokine Release Syndrome/immunology , Female , Humans , Interleukin-6/immunology , Male , Middle Aged , Respiratory Distress Syndrome/immunology , Retrospective Studies , SARS-CoV-2 , Severity of Illness Index
15.
J Asthma ; 59(2): 230-238, 2022 02.
Article in English | MEDLINE | ID: covidwho-922319

ABSTRACT

OBJECTIVE: Although it is reported that patients with coronavirus disease 2019 (COVID-19) disease who have comorbidities are at higher risk to suffer adverse clinical outcomes, there are inadequate evidence to clarify the association between COVID-19 and asthma. On this ground, this study aims to systematically analyze the clinical characteristics of COVID-19 patients with asthma. METHODS: In this single-center, retrospective and observational cohort study, 21 COVID-19 patients with asthma and 100 non-asthma COVID-19 patients were statistically matched by propensity score based on age, sex and comorbidities. Meanwhile, a collection and comparison concerning demographic indicators, clinical and laboratory examinations, treatments and outcomes were conducted between two groups to specify their differences. RESULTS: Statistically, the COVID-19 patients with asthma had a higher proportion of ICU admission (14.3% [3/21] vs. 2.1% [2/96] p = 0.040) than those who do not have. On top this, a higher level of inflammatory responses, such as interleukin 6, interleukin 8, procalcitonin, leukocytes, neutrophils and CD4+ T cells was presented in asthma patients. Moreover, the increase of organ damage indices like D-dimer, lactate dehydrogenase and high-sensitivity cardiac troponin I, were more pronounced in COVID-19 patients with asthma. CONCLUSIONS: Exacerbated inflammatory responses and multiple organ damages were triggered in COVID-19 patients with asthma, which highlights more intensive surveillance and supportive treatment.


Subject(s)
Asthma/epidemiology , COVID-19/epidemiology , COVID-19/physiopathology , Adult , Age Factors , Aged , China/epidemiology , Comorbidity , Female , Humans , Inflammation Mediators/metabolism , Intensive Care Units , Male , Middle Aged , Organ Dysfunction Scores , Retrospective Studies , SARS-CoV-2 , Sex Factors
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