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Frontiers in molecular biosciences ; 7:157-157, 2020.
Article | WHO COVID | ID: covidwho-689155


Introduction: A recently emerging respiratory disease named coronavirus disease 2019 (COVID-19) has quickly spread across the world This disease is initiated by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) and uncontrolled cytokine storm, but it remains unknown as to whether a robust antibody response is related to clinical deterioration and poor outcome in COVID-19 patients Methods: Anti-SARS-CoV-2 IgG and IgM antibodies were determined by chemiluminescence analysis (CLIA) in COVID-19 patients at a single center in Wuhan Median IgG and IgM levels in acute and convalescent-phase sera (within 35 days) for all included patients were calculated and compared between severe and non-severe patients Immune response phenotyping based on the late IgG levels and neutrophil-to-lymphocyte ratio (NLR) was characterized to stratified patients into different disease severities and outcomes Results: A total of 222 patients were included in this study IgG was first detected on day 4 of illness, and its peak levels occurred in the fourth week Severe cases were more frequently found in patients with high IgG levels, compared to those with low IgG levels (51 8 vs 32 3%;p = 0 008) Severity rates for patients with NLR(hi)IgG(hi), NLR(hi)IgG(lo), NLR(lo)IgG(hi), and NLR(lo)IgG(lo) phenotype were 72 3, 48 5, 33 3, and 15 6%, respectively (p < 0 0001) Furthermore, severe patients with NLR(hi)IgG(hi), NLR(hi)IgG(lo) had higher inflammatory cytokines levels including IL-2, IL-6 and IL-10, and decreased CD4+ T cell count compared to those with NLR(lo)IgG(lo) phenotype (p < 0 05) Recovery rates for severe patients with NLR(hi)IgG(hi), NLR(hi)IgG(lo), NLR(lo)IgG(hi), and NLR(lo)IgG(lo) phenotype were 58 8% (20/34), 68 8% (11/16), 80 0% (4/5), and 100% (12/12), respectively (p = 0 0592) Dead cases only occurred in NLR(hi)IgG(hi) and NLR(hi)IgG(lo) phenotypes Conclusions: COVID-19 severity is associated with increased IgG response, and an immune response phenotyping based on the late IgG response and NLR could act as a simple complementary tool to discriminate between severe and non-severe COVID-19 patients, and further predict their clinical outcome

PLoS One ; 15(7): e0235458, 2020.
Article in English | MEDLINE | ID: covidwho-638588


A recently developed pneumonia caused by SARS-CoV-2 bursting in Wuhan, China, has quickly spread across the world. We report the clinical characteristics of 82 cases of death from COVID-19 in a single center. Clinical data on 82 death cases laboratory-confirmed as SARS-CoV-2 infection were obtained from a Wuhan local hospital's electronic medical records according to previously designed standardized data collection forms. All patients were local residents of Wuhan, and a large proportion of them were diagnosed with severe illness when admitted. Due to the overwhelming of our system, a total of 14 patients (17.1%) were treated in the ICU, 83% of deaths never received Critical Care Support, only 40% had mechanical ventilation support despite 100% needing oxygen and the leading cause of death being pulmonary. Most of the patients who died were male (65.9%). More than half of the patients who died were older than 60 years (80.5%), and the median age was 72.5 years. The bulk of the patients who died had comorbidities (76.8%), including hypertension (56.1%), heart disease (20.7%), diabetes (18.3%), cerebrovascular disease (12.2%), and cancer (7.3%). Respiratory failure remained the leading cause of death (69.5%), followed by sepsis/MOF (28.0%), cardiac failure (14.6%), hemorrhage (6.1%), and renal failure (3.7%). Furthermore, respiratory, cardiac, hemorrhagic, hepatic, and renal damage were found in 100%, 89%, 80.5%, 78.0%, and 31.7% of patients, respectively. On admission, lymphopenia (89.2%), neutrophilia (74.3%), and thrombocytopenia (24.3%) were usually observed. Most patients had a high neutrophil-to-lymphocyte ratio of >5 (94.5%), high systemic immune-inflammation index of >500 (89.2%), and increased C-reactive protein (100%), lactate dehydrogenase (93.2%), and D-dimer (97.1%) levels. A high level of IL-6 (>10 pg/ml) was observed in all detected patients. The median time from initial symptoms to death was 15 days (IQR 11-20), and a significant association between aspartate aminotransferase (p = 0.002), alanine aminotransferase (p = 0.037) and time from initial symptoms to death was remarkably observed. Older males with comorbidities are more likely to develop severe disease and even die from SARS-CoV-2 infection. Respiratory failure is the main cause of COVID-19, but the virus itself and cytokine release syndrome-mediated damage to other organs, including cardiac, renal, hepatic, and hemorrhagic damage, should be taken seriously as well.

Coronavirus Infections/mortality , Coronavirus Infections/pathology , Pneumonia, Viral/mortality , Pneumonia, Viral/pathology , Adult , Age Factors , Aged , Betacoronavirus , Cause of Death , China/epidemiology , Comorbidity , Coronavirus Infections/epidemiology , Coronavirus Infections/therapy , Female , Humans , Male , Middle Aged , Pandemics , Pneumonia, Viral/epidemiology , Pneumonia, Viral/therapy , Respiratory Insufficiency/pathology , Retrospective Studies
Int J Cardiol ; 311: 116-121, 2020 07 15.
Article in English | MEDLINE | ID: covidwho-38503


BACKGROUND: A novel coronavirus disease (COVID-19) in Wuhan has caused an outbreak and become a major public health issue in China and great concern from international community. Myocarditis and myocardial injury were suspected and may even be considered as one of the leading causes for death of COVID-19 patients. Therefore, we focused on the condition of the heart, and sought to provide firsthand evidence for whether myocarditis and myocardial injury were caused by COVID-19. METHODS: We enrolled patients with confirmed diagnosis of COVID-19 retrospectively and collected heart-related clinical data, mainly including cardiac imaging findings, laboratory results and clinical outcomes. Serial tests of cardiac markers were traced for the analysis of potential myocardial injury/myocarditis. RESULTS: 112 COVID-19 patients were enrolled in our study. There was evidence of myocardial injury in COVID-19 patients and 14 (12.5%) patients had presented abnormalities similar to myocarditis. Most of patients had normal levels of troponin at admission, that in 42 (37.5%) patients increased during hospitalization, especially in those that died. Troponin levels were significantly increased in the week preceding the death. 15 (13.4%) patients have presented signs of pulmonary hypertension. Typical signs of myocarditis were absent on echocardiography and electrocardiogram. CONCLUSIONS: The clinical evidence in our study suggested that myocardial injury is more likely related to systemic consequences rather than direct damage by the 2019 novel coronavirus. The elevation in cardiac markers was probably due to secondary and systemic consequences and can be considered as the warning sign for recent adverse clinical outcomes of the patients.

Cause of Death , Coronavirus Infections/diagnosis , Coronavirus Infections/epidemiology , Hospitalization/statistics & numerical data , Myocardial Infarction/epidemiology , Myocarditis/epidemiology , Pneumonia, Viral/diagnosis , Pneumonia, Viral/epidemiology , Adult , Biomarkers/blood , China , Cohort Studies , Comorbidity , Coronary Angiography/methods , Echocardiography, Doppler/methods , Female , Hospitals, University , Humans , Male , Middle Aged , Myocardial Infarction/diagnosis , Myocardial Infarction/therapy , Myocarditis/diagnosis , Myocarditis/therapy , Pandemics , Prognosis , Retrospective Studies , Risk Assessment , Severity of Illness Index , Survival Analysis , Treatment Outcome