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1.
Eur Heart J Cardiovasc Pharmacother ; 8(4): 392-401, 2022 Jun 08.
Article in English | MEDLINE | ID: covidwho-1746904

ABSTRACT

AIMS: The aim of this study was to investigate the effects of Neuraminidase inhibitors (NI) on COVID-19 in a retrospective study. METHODS AND RESULTS: The study included an overall COVID-19 patients (n = 3267) and a 1:1 propensity score-matched patients (n = 972). The levels of plasma N-acetylneuraminic acid and neuraminidase expression were further evaluated in a panel of hospitalized and 1-month post-infection recovered COVID-19 subjects. The mortality rate in the overall patients was 9.6% (313/3267) and 9.2% (89/972) in the propensity-score matched patients. The NI treatment lowered the mortality rate (5.7% vs. 10.3%) and the critically ill conversion rate (14.1% vs. 19.7%) compare to those in the non-NI group in the overall patients and evaluated in the propensity score-matched patients when applying the multivariate Cox model for adjusting imbalanced confounding factors. Furthermore, NI treatment was associated with attenuated cytokine storm levels and acute heart injury but not liver or kidney injuries. Further analysis in a small panel of patients found the levels of N-acetylneuraminic acid and neuraminidase (dominantly the NEU3 isoform) were elevated in the hospitalized COVID-19 subjects and recovered at the 1-month post-infection stage, suggesting increasing desialylation in COVID-19 patients. CONCLUSION: These results suggest that NI treatment is associated with decreased mortality in COVID-19 subjects, especially for those subjects with acute heart injury.


Subject(s)
Antiviral Agents , COVID-19 , Neuraminidase , Antiviral Agents/therapeutic use , COVID-19/drug therapy , COVID-19/mortality , Cardiovascular Diseases/virology , Humans , N-Acetylneuraminic Acid , Neuraminidase/antagonists & inhibitors , Retrospective Studies
2.
EuropePMC; 2020.
Preprint in English | EuropePMC | ID: ppcovidwho-324760

ABSTRACT

Background: COVID-19 epidemic continues to spread rapidly around the world, causing severe multi-organ injury and high mortality in a subset of patients. Individuals with diabetes mellitus are at a higher risk of SARS-CoV-2 infection and worse outcomes than the general population without diabetes. While glucose control was observed to be associated with attenuated mortality, limited evidence is available to determine whether glucose control by insulin was beneficial for COVID-19 patients with diabetes.Methods: This retrospective study focused on a cohort of 689 COVID-19 patients from Wuhan, China, diagnosed with diabetes, and assessed the clinical outcomes associated with insulin treatment. Kaplan-Meier survival analysis and proportional Cox regression were employed to analyze the influence of insulin treatment on all cause death.Results: Among the 689 diabetic patients infected with COVID-19, 106 patients died (fatality was 15.4%). The fatality of COVID-19 patients with diabetes treated with insulin was significantly higher than those without insulin treatment (27.2% vs. 3.5%, p < 0.001). The HR was 6.57 (95% CI 3.09 to 13.99;p < 0.001) after adjustment for age, gender, coronary heart disease, COPD, chronic kidney disease, pulse, respiratory rate, SpO2, lymphocyte count, albumin, NT-proBNP and glucose. Further survival analysis in several subgroups and critically ill group showed the similar effect of insulin on adverse outcome in COVID-19 patients with diabetes.Conclusion: According to this retrospective study, insulin treatment increases the mortality in COVID-19 patients with diabetes. Thus, close observation especially glucose and vital signs monitoring are very important when COVID-19 patients with diabetes treated with insulin.Funding: This work was supported in part by projects from Ministry of Science and Technology of China (No. 2020YFC0844500), Nature Science Foundation of China (Nos. 31130031), Emergency project fund of Chinese Academy of Sciences (No. 2020YJFK0105) and Chinese Academy of Engineering and Ma Yun Foundation (No. 2020-CMKYGG-05). Conflict of Interest: The authors have declared that no competing interests exist.Ethical Approval: This study was approved by the institutional review board of Tongji Hospital (IRBID: TJ-IRB20200229). The written informed consent was waived by the Ethics Committee because of the retrospective and anonymous nature of the data.

3.
J Transl Int Med ; 9(3): 152-160, 2021 Sep.
Article in English | MEDLINE | ID: covidwho-1472377

ABSTRACT

2019 novel coronavirus disease (COVID-19) is caused by the infection of severe acute respiratory syndrome novel coronavirus (SARS-CoV-2). It is characterized by substantial respiratory symptoms and complicated with widespread other organ injuries. Cardiovascular impairment is one of the notable extrapulmonary manifestations, in terms of the deterioration of pre-existing cardiovascular diseases and newly onset acute events. We hereby review the high-quality reports about cardiovascular involvement in COVID-19 and summarize the main clinical characteristics of cardiac relevance for the all the first line clinical physicians. Additionally, the possible underlying mechanisms and the rationale for the application of specific medications, such as renin-angiotensin-aldosterone system inhibitors and hydroxychloroquine are also discussed.

4.
Front Cardiovasc Med ; 8: 654405, 2021.
Article in English | MEDLINE | ID: covidwho-1247849

ABSTRACT

Background: Accumulating evidence has revealed that coronavirus disease 2019 (COVID-19) patients may be complicated with myocardial injury during hospitalization. However, data regarding persistent cardiac involvement in patients who recovered from COVID-19 are limited. Our goal is to further explore the sustained impact of COVID-19 during follow-up, focusing on the cardiac involvement in the recovered patients. Methods: In this prospective observational follow-up study, we enrolled a total of 40 COVID-19 patients (20 with and 20 without cardiac injury during hospitalization) who were discharged from Zhongnan Hospital of Wuhan University for more than 6 months, and 27 patients (13 with and 14 without cardiac injury during hospitalization) were finally included in the analysis. Clinical information including self-reported symptoms, medications, laboratory findings, Short Form 36-item scores, 6-min walk test, clinical events, electrocardiogram assessment, echocardiography measurement, and cardiac magnetic resonance imaging was collected and analyzed. Results: Among 27 patients finally included, none of patients reported any obvious cardiopulmonary symptoms at the 6-month follow-up. There were no statistically significant differences in terms of the quality of life and exercise capacity between the patients with and without cardiac injury. No significant abnormalities were detected in electrocardiogram manifestations in both groups, except for nonspecific ST-T changes, premature beats, sinus tachycardia/bradycardia, PR interval prolongation, and bundle-branch block. All patients showed normal cardiac structure and function, without any statistical differences between patients with and without cardiac injury by echocardiography. Compared with patients without cardiac injury, patients with cardiac injury exhibited a significantly higher positive proportion in late gadolinium enhancement sequences [7/13 (53.8%) vs. 1/14 (7.1%), p = 0.013], accompanied by the elevation of circulating ST2 level [median (interquartile range) = 16.6 (12.1, 22.5) vs. 12.5 (9.5, 16.7); p = 0.044]. Patients with cardiac injury presented higher levels of aspartate aminotransferase, creatinine, high-sensitivity troponin I, lactate dehydrogenase, and N-terminal pro-B-type natriuretic peptide than those without cardiac injury, although these indexes were within the normal range for all recovered patients at the 6-month follow-up. Among patients with cardiac injury, patients with positive late gadolinium enhancement presented higher cardiac biomarker (high-sensitivity troponin I) and inflammatory factor (high-sensitivity C-reactive protein) on admission than the late gadolinium enhancement-negative subgroup. Conclusions: Our preliminary 6-month follow-up study with a limited number of patients revealed persistent cardiac involvement in 29.6% (8/27) of recovered patients from COVID-19 after discharge. Patients with cardiac injury during hospitalization were more prone to develop cardiac fibrosis during their recovery. Among patients with cardiac injury, those with relatively higher cardiac biomarkers and inflammatory factors on admission appeared more likely to have cardiac involvement in the convalescence phase.

5.
Biosci Rep ; 41(3)2021 03 26.
Article in English | MEDLINE | ID: covidwho-1180288

ABSTRACT

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has induced an ongoing global health crisis. Here we utilized a combination of targeted amino acids (AAs) and clinical biochemical profiling to analyze the plasma of coronavirus disease 2019 (COVID-19) subjects at the hospitalization stage and 1-month post-infection convalescent stage, respectively, to investigate the systematic injury during COVID-19 disease progress. We found the virus-induced inflammatory status and reduced liver synthesis capacity in hospitalized patients, which manifested with increased branched-chain AAs (BCAAs), aromatic AAs (AAAs), one-carbon related metabolites, and decreased methionine. Most of these disturbances during infection recover except for the increased levels of medium-chain acylcarnitines (ACs) in the convalescent subjects, implying the existence of incomplete fatty acids oxidation during recovery periods. Our results suggested that the imbalance of the AA profiling in COVID-19 patients. The majority of disturbed AAs recovered in 1 month. The incomplete fatty acid oxidation products suggested it might take longer time for convalescent patients to get complete recovery.


Subject(s)
Amino Acids/metabolism , COVID-19/metabolism , COVID-19/virology , SARS-CoV-2/physiology , Adult , Aged , Aged, 80 and over , Amino Acids/blood , Biomarkers , COVID-19/diagnosis , COVID-19/epidemiology , Comorbidity , Female , Hospitalization , Host-Pathogen Interactions , Humans , Male , Metabolomics/methods , Middle Aged , Severity of Illness Index
6.
Acta Pharmacol Sin ; 42(10): 1567-1574, 2021 Oct.
Article in English | MEDLINE | ID: covidwho-1054010

ABSTRACT

COVID-19 is a multiorgan systemic inflammatory disease caused by SARS-CoV-2 virus. Patients with COVID-19 often exhibit cardiac dysfunction and myocardial injury, but imaging evidence is lacking. In the study we detected and evaluated the severity of myocardial dysfunction in COVID-19 patient population using two-dimensional speckle-tracking echocardiography (2-D STE). A total of 218 consecutive patients with confirmed diagnosis of COVID-19 who had no underlying cardiovascular diseases were enrolled and underwent transthoracic echocardiography. This study cohort included 52 (23.8%) critically ill and 166 noncritically ill patients. Global longitudinal strains (GLSs) and layer-specific longitudinal strains (LSLSs) were obtained using 2-D STE. Changes in GLS were correlated with the clinical parameters. We showed that GLS was reduced (<-21.0%) in about 83% of the patients. GLS reduction was more common in critically sick patients (98% vs. 78.3%, P < 0.001), and the mean GLS was significantly lower in the critically sick patients than those noncritical (-13.7% ± 3.4% vs. -17.4% ± 3.2%, P < 0.001). The alteration of GLS was more prominent in the subepicardium than in the subendocardium (P < 0.001). GLS was correlated to mean serum pulse oxygen saturation (SpO2, RR = 0.42, P < 0.0001), high-sensitive C-reactive protein (hsCRP, R = -0.20, P = 0.006) and inflammatory cytokines, particularly IL-6 (R = -0.21, P = 0.003). In conclusions, our results demonstrate that myocardial dysfunction is common in COVID-19 patients, particularly those who are critically sick. Changes in indices of myocardial strain were associated with indices of inflammatory markers and hypoxia, suggesting partly secondary nature of myocardial dysfunction.


Subject(s)
COVID-19/complications , Echocardiography , Ventricular Dysfunction, Left/diagnostic imaging , Ventricular Function, Left , Aged , COVID-19/diagnosis , Critical Illness , Cross-Sectional Studies , Female , Humans , Male , Middle Aged , Predictive Value of Tests , Prospective Studies , Severity of Illness Index , Ventricular Dysfunction, Left/etiology , Ventricular Dysfunction, Left/physiopathology
7.
Front Med (Lausanne) ; 7: 584870, 2020.
Article in English | MEDLINE | ID: covidwho-963101

ABSTRACT

Background: Statins have multiple protective effects on inflammation, immunity and coagulation, and may help alleviate pneumonia. However, there was no report focusing on the association of statin use with in-hospital outcomes of patients with coronavirus disease 2019 (COVID-19). We investigated the association between the use of statins and in-hospital outcomes of patients with COVID-19. Methods: In this retrospective case series, consecutive COVID-19 patients admitted at 2 hospitals in Wuhan, China, from March 12, 2020 to April 14, 2020 were analyzed. A 1:1 matched cohort was created by propensity score-matched analysis. Demographic data, laboratory findings, comorbidities, treatments and in-hospital outcomes were collected and compared between COVID-19 patients taking and not taking statins. Result: A total of 2,147 patients with COVID-19 were enrolled in this study. Of which, 250 patients were on statin therapy. The mortality was 2.4% (6/250) for patients taking statins while 3.7% (70/1,897) for those not taking statins. In the multivariate Cox model, after adjusting for age, gender, admitted hospital, comorbidities, in-hospital medications and blood lipids, the risk was lower for mortality (adjusted HR, 0.428; 95% CI, 0.169-0.907; P = 0.029), acute respiratory distress syndrome (ARDS) (adjusted HR, 0.371; 95% CI, 0.180-0.772; P = 0.008) or intensive care unit (ICU) care (adjusted HR, 0.319; 95% CI, 0.270-0.945; P = 0.032) in the statin group vs. the non-statin group. After propensity score-matched analysis based on 18 potential confounders, a 1:1 matched cohort (206:206) was created. In the matched cohort, the Kaplan-Meier survival curves showed that the use of statins was associated with better survival (P = 0.025). In a Cox regression model, the use of statins was associated with lower risk of mortality (unadjusted HR, 0.254; 95% CI, 0.070-0.926; P = 0.038), development of ARDS (unadjusted HR, 0.240; 95% CI, 0.087-0.657; P = 0.006), and admission of ICU (unadjusted HR, 0.349; 95% CI, 0.150-0.813; P = 0.015). The results remained consistent when being adjusted for age, gender, total cholesterol, triglyceride, low density lipoprotein cholesterol, procalcitonin, and brain natriuretic peptide. The favorable outcomes in statin users remained statistically significant in the first sensitivity analysis with comorbid diabetes being excluded in matching and in the second sensitivity analysis with chronic obstructive pulmonary disease being added in matching. Conclusion: In this retrospective analysis, the use of statins in COVID-19 patients was associated with better clinical outcomes and is recommended to be continued in patients with COVID-19.

8.
Cell Metab ; 33(1): 65-77.e2, 2021 01 05.
Article in English | MEDLINE | ID: covidwho-956992

ABSTRACT

COVID-19 caused by SARS-COV-2 infection can lead to multi-organ injuries and significant mortality in severe and critical patients, especially among those individuals with type 2 diabetes (T2D) as a comorbidity. While attenuated mortality was observed with aggressive glucose control, it was unclear whether therapeutic regimens including insulin treatment were beneficial for patients with COVID-19 and T2D. This retrospective study investigated 689 patients with COVID-19 and T2D from a cohort of 3,305 cases from Wuhan, China. Unexpectedly, we found that insulin treatment for patients with COVID-19 and T2D was associated with a significant increase in mortality (27.2% versus 3.5%; adjusted HR, 5.38 [2.75-10.54]). Further analysis showed that insulin treatment was associated with enhanced systemic inflammation and aggravated injuries of vital organs. Therefore, insulin treatment for patients with COVID-19 and T2D should be used with caution.


Subject(s)
COVID-19/drug therapy , COVID-19/mortality , Diabetes Mellitus, Type 2/drug therapy , Diabetes Mellitus, Type 2/mortality , Insulins/adverse effects , Aged , COVID-19/complications , COVID-19/metabolism , Cohort Studies , Diabetes Mellitus, Type 2/complications , Diabetes Mellitus, Type 2/metabolism , Dose-Response Relationship, Drug , Female , Humans , Insulins/metabolism , Insulins/therapeutic use , Male , Middle Aged , Retrospective Studies
9.
SSRN; 2020.
Preprint | SSRN | ID: ppcovidwho-1093

ABSTRACT

Background: Overall death cause of COVID-19 patients has been reported but attribution of myocardial injury remains undetermined. br br Methods: We extracted d

10.
J Mol Cell Cardiol ; 147: 74-87, 2020 10.
Article in English | MEDLINE | ID: covidwho-722814

ABSTRACT

BACKGROUND: Cardiac injury, as measured by troponin elevation, has been reported among hospitalized coronavirus disease 2019 (COVID-19) patients and portends a poor prognosis. However, how the dynamics of troponin elevation interplay with inflammation and coagulation biomarkers over time is unknown. We assessed longitudinal follow-up of cardiac injury, inflammation and coagulation markers in relation to disease severity and outcome. METHODS: We retrospectively assessed 2068 patients with laboratory-confirmed COVID-19 between January 29 and April 1, 2020 at Tongji Hospital in Wuhan, China. We defined cardiac injury as an increase in high sensitivity cardiac troponin-I (hs-cTnI) above the 99th of the upper reference limit. We explored the dynamics of elevation in hs-cTnI and the relationship with inflammation (interleukin [IL]-6, IL-8, IL-10, IL-2 receptor, tumor necrosis factor-α, C-reactive protein) and coagulation (d-dimer, fibrinogen, international normalized ratio) markers in non-critically ill versus critically ill patients longitudinally and further correlated these markers to survivors and non-survivors. RESULTS: Median age was 63 years (first to third quartile 51-70 years), 51.4% of whom were women. When compared to non-critically ill patients (N = 1592, 77.0%), critically ill (defined as requiring mechanical ventilation, in shock or multiorgan failure) patients (N = 476, 23.0%), had more frequent cardiac injury on admission (30.3% vs. 2.3%, p < 0.001), with increased mortality during hospitalization (38.4% vs. 0%, p < 0.001). Among critically ill patients, non-survivors (N = 183) had a continuous increase in hs-cTnI levels during hospitalization, while survivors (N = 293) showed a decrease in hs-cTnI level between day 4 and 7 after admission. Specifically, cardiac injury is an independent marker of mortality among critically ill patients at admission, day 4-7 and 8-14. Consistent positive correlations between hs-cTnI and interleukin (IL)-6 on admission (r = 0.59), day 4-7 (r = 0.66) and day 8-14 (r = 0.61; all p < 0.001) and d-dimer (at the same timepoints r = 0.54; 0.65; 0.61, all p < 0.001) were observed. A similar behavior was observed between hs-cTnI and most of other biomarkers of inflammation and coagulation. CONCLUSIONS: Cardiac injury commonly occurs in critically ill COVID-19 patients, with increased levels of hs-cTnI beyond day 3 since admission portending a poor prognosis. A consistent positive correlation of hs-cTnI with IL-6 and d-dimer at several timepoints along hospitalization could suggest nonspecific cytokine-mediated cardiotoxicity.


Subject(s)
Coronavirus Infections/pathology , Cytokines/blood , Heart Injuries/pathology , Pneumonia, Viral/pathology , Troponin I/blood , Aged , Betacoronavirus , Biomarkers/blood , Blood Coagulation/physiology , COVID-19 , Coronavirus Infections/blood , Critical Illness , Female , Heart Injuries/blood , Heart Injuries/diagnosis , Humans , Inflammation , Longitudinal Studies , Male , Middle Aged , Pandemics , Pneumonia, Viral/blood , Prognosis , Retrospective Studies , SARS-CoV-2
12.
Pharmacol Ther ; 215: 107628, 2020 11.
Article in English | MEDLINE | ID: covidwho-640973

ABSTRACT

The coronavirus disease 2019 (COVID-19) pandemic is caused by a newly emerged coronavirus (CoV) called Severe Acute Respiratory Syndrome coronavirus 2 (SARS-CoV-2). COVID-19 patients with cardiovascular disease (CVD) comorbidities have significantly increased morbidity and mortality. The use of angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor type 1 blockers (ARBs) improve CVD outcomes; however, there is concern that they may worsen the prognosis of CVD patients that become infected with SARS-CoV-2 because the virus uses the ACE2 receptor to bind to and subsequently infect host cells. Thus, some health care providers and media sources have questioned the continued use of ACE inhibitors and ARBs. In this brief review, we discuss the effect of ACE inhibitor-induced bradykinin on the cardiovascular system, on the renin-angiotensin-aldosterone system (RAAS) regulation in COVID-19 patients, and analyze recent clinical studies regarding patients treated with RAAS inhibitors. We propose that the application of RAAS inhibitors for COVID-19 patients with CVDs may be beneficial rather than harmful.


Subject(s)
Angiotensin Receptor Antagonists/pharmacology , Angiotensin-Converting Enzyme Inhibitors/pharmacology , Betacoronavirus , Cardiovascular Diseases , Coronavirus Infections , Pandemics , Pneumonia, Viral , Betacoronavirus/drug effects , Betacoronavirus/physiology , COVID-19 , Cardiovascular Diseases/drug therapy , Cardiovascular Diseases/epidemiology , Cardiovascular Diseases/metabolism , Comorbidity , Coronavirus Infections/epidemiology , Coronavirus Infections/therapy , Coronavirus Infections/virology , Humans , Pneumonia, Viral/epidemiology , Pneumonia, Viral/therapy , Pneumonia, Viral/virology , SARS-CoV-2
13.
Sci China Life Sci ; 63(10): 1617-1618, 2020 Oct.
Article in English | MEDLINE | ID: covidwho-625919

ABSTRACT

1. In the abstract, we missed a piece of information. The correct sentence should be "In this retrospective study, we included 550 critically ill COVID-19 patients who need mechanical ventilation (63.5%) and oxygen therapy (35.6%) in Tongji Hospital, Wuhan, from February 1, 2020 to April 4, 2020." 2. We mistakenly put an approval number from Tongji Hospital ethics committee in the paper (IRBID: TJ-C20200113). The correct number should be TJ-IRB20200229. 3. We mistakenly filled some data in Table 1 and the correct Table 1 (the corrected data are in boldface) should be as follows.

14.
Sci China Life Sci ; 63(11): 1678-1687, 2020 11.
Article in English | MEDLINE | ID: covidwho-610883

ABSTRACT

Coronavirus disease 2019 (COVID-19) is a global pandemic which has caused numerous deaths worldwide. The present study investigated the roles of hypoproteinemia in the clinical outcome and liver dysfunction of COVID-19 patients. In this retrospective study, we extracted data from 2,623 clinically confirmed adult COVID-19 patients (>18 years old) between January 29, 2020 and March 6, 2020 in Tongji Hospital, Wuhan, China. The patients were divided into three groups-non-critically ill, critically ill, and death groups-in accordance with the Chinese Clinical Guideline for COVID-19. Serum albumin, low-density lipoproteins cholesterol (LDL-C), and high-density lipoproteins cholesterol (HDL-C) concentrations and inflammatory cytokines levels were measured and compared among these three groups. The median age of these 2,623 patients was 64 years old (interquartile range (IQR), 52-71). Among the patients enrolled in the study, 2,008 (76.6%) were diagnosed as non-critically ill and 615 (23.4%) were critically ill patients, including 383 (14.6%) critically ill survivors and 232 (8.8%) critically ill deaths in the hospital. Marked hypoalbuminemia occurred in 38.2%, 71.2%, and 82.4% patients in non-critically ill, critically ill, and death groups, respectively, on admission and 45.9%, 77.7%, and 95.6% of these three groups, respectively, during hospitalization. We also discovered that serum low-density lipoprotein (LDL) and HDL levels were significantly lower in critically ill and death groups compared to non-critically ill group. Meanwhile, the patients displayed dramatically elevated levels of serum inflammatory factors, while a markedly prolonged activated partial thromboplastin time (APTT) in critically ill patients reflected coagulopathy. This study suggests that COVID-19-induced cytokine storm causes hepatotoxicity and subsequently critical hypoalbuminemia, which are associated with exacerbation of disease-associated inflammatory responses and progression of the disease and ultimately leads to death for some critically ill patients.


Subject(s)
COVID-19/blood , COVID-19/complications , Coronavirus Infections/blood , Coronavirus Infections/complications , Liver Diseases/etiology , Serum Albumin, Human/metabolism , Aged , COVID-19/mortality , China , Cholesterol, HDL/blood , Cholesterol, LDL/blood , Coronavirus Infections/mortality , Critical Illness , Cytokines/blood , Female , Humans , Liver Diseases/blood , Male , Middle Aged , Prognosis , Retrospective Studies , Risk Factors , SARS-CoV-2 , Thromboplastin/metabolism , Time Factors
15.
Sci China Life Sci ; 63(10): 1515-1521, 2020 10.
Article in English | MEDLINE | ID: covidwho-276142

ABSTRACT

Coronavirus disease 2019 (COVID-19) is a pandemic with no specific drugs and high fatality. The most urgent need is to find effective treatments. We sought to determine whether hydroxychloroquine (HCQ) application may reduce the death risk of critically ill COVID-19 patients. In this retrospective study, we included 550 critically ill COVID-19 patients who need mechanical ventilation in Tongji Hospital, Wuhan, from February 1, 2020 to April 4, 2020. All 550 patients received comparable basic treatments including antiviral drugs and antibiotics, and 48 of them were treated with oral HCQ treatment (200 mg twice a day for 7-10 days) in addition to the basic treatments. Primary endpoint is fatality of patients, and inflammatory cytokine levels were compared between HCQ and non-hydroxychloroquine (NHCQ) treatments. We found that fatalities are 18.8% (9/48) in HCQ group, which is significantly lower than 47.4% (238/502) in the NHCQ group (P<0.001). The time of hospital stay before patient death is 15 (10-21) days and 8 (4-14) days for the HCQ and NHCQ groups, respectively (P<0.05). The levels of inflammatory cytokine IL-6 were significantly reduced from 22.2 (8.3-118.9) pg mL-1 at the beginning of the treatment to 5.2 (3.0-23.4) pg mL-1 (P<0.05) at the end of the treatment in the HCQ group but there is no change in the NHCQ group. These data demonstrate that addition of HCQ on top of the basic treatments is highly effective in reducing the fatality of critically ill patients of COVID-19 through attenuation of inflammatory cytokine storm. Therefore, HCQ should be prescribed as a part of treatment for critically ill COVID-19 patients, with possible outcome of saving lives. hydroxychloroquine, IL-6, mortalities, COVID-19.


Subject(s)
Coronavirus Infections/drug therapy , Coronavirus Infections/mortality , Hydroxychloroquine/administration & dosage , Pneumonia, Viral/drug therapy , Pneumonia, Viral/mortality , COVID-19 , China , Critical Illness , Humans , Inflammation , Interleukin-6/blood , Length of Stay , Pandemics , Retrospective Studies , Treatment Outcome
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