Your browser doesn't support javascript.
Show: 20 | 50 | 100
Results 1 - 4 de 4
Add filters

Year range
Int J Antimicrob Agents ; : 106103, 2020 Jul 23.
Article in English | MEDLINE | ID: covidwho-664350


This systemic review and meta-analysis aimed to assess the efficacy of tocilizumab for the treatment of severe coronavirus disease-2019 (COVID-19). Candidate studies up to May 24, 2020 were identified from PubMed, Cochrane Library, Embase, MedRxiv, and BioRxiv. Treatment outcomes included mortality, risk of intensive care unit (ICU) admission, and the requirement of mechanical ventilation (MV). A total of 7 retrospective studies involving 593 adult patients with severe COVID-19, including 241 in the tocilizumab group and 352 in the control group were enrolled. All-cause mortality of severe COVID-19 patients among the tocilizumab group was 16.2% (39/241), which was lower than that in the control group (24.1%, 85/352). However, the difference did not reach statistical significance (risk ratio [RR], 0.61; 95% confidence interval [CI], 0.31-1.22, I2 = 68%). In addition, the risk of ICU admission was similar between the tocilizumab and control groups (35.0% vs. 15.8%, RR, 1.51; 95% CI, 0.33-6.78, I2 = 86%). The requirement of MV was similar between the tocilizumab and control groups (32.4% vs. 28.6%, RR, 0.72; 95% CI, 0.05-10.96, I2 = 91%). However, these nonsignificant differences between the tocilizumab and control groups may have been the result of the baseline characteristics of the tocilizumab group, which were more severe than those of the control group. Based on low-quality evidence, there is no conclusive evidence that tocilizumab would provide any additional benefit to patients with severe COVID-19. Therefore, further recommendation of tocilizumab for COVID-19 cases should be halted until high-quality evidence from randomized controlled trials is made available.

Pharmacol Res ; 159: 104959, 2020 Jun 04.
Article in English | MEDLINE | ID: covidwho-526486
Acta Pharm Sin B ; 2020 Apr 20.
Article in English | MEDLINE | ID: covidwho-88716


Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection can cause acute respiratory distress syndrome, hypercoagulability, hypertension, and multiorgan dysfunction. Effective antivirals with safe clinical profile are urgently needed to improve the overall prognosis. In an analysis of a randomly collected cohort of 124 patients with Corona Virus Disease 2019 (COVID-19), we found that hypercoagulability as indicated by elevated concentrations of D-dimers was associated with disease severity. By virtual screening of a U.S. Food and Drug Administration (FDA) approved drug library, we identified an anticoagulation agent dipyridamole (DIP) in silico, which suppressed SARS-CoV-2 replication in vitro. In a proof-of-concept trial involving 31 patients with COVID-19, DIP supplementation was associated with significantly decreased concentrations of D-dimers (P<0.05), increased lymphocyte and platelet recovery in the circulation, and markedly improved clinical outcomes in comparison to the control patients. In particular, all 8 of the DIP-treated severely ill patients showed remarkable improvement: 7 patients (87.5%) achieved clinical cure and were discharged from the hospitals while the remaining 1 patient (12.5%) was in clinical remission.

J. Clin. Med. ; 4(9)20200401.
Article in English | ELSEVIER | ID: covidwho-60425


An outbreak of novel coronavirus-related pneumonia COVID-19, that was identified in December 2019, has expanded rapidly, with cases now confirmed in more than 211 countries or areas. This constant transmission of a novel coronavirus and its ability to spread from human to human have prompted scientists to develop new approaches for treatment of COVID-19. A recent study has shown that remdesivir and chloroquine effectively inhibit the replication and infection of severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2, 2019-nCov) in vitro. In the United States, one case of COVID-19 was successfully treated with compassionate use of remdesivir in January of 2020. In addition, a clinically proven protease inhibitor, camostat mesylate, has been demonstrated to inhibit Calu-3 infection with SARS-CoV-2 and prevent SARS-2-spike protein (S protein)-mediated entry into primary human lung cells. Here, we systemically discuss the pharmacological therapeutics targeting RNA-dependent RNA polymerase (RdRp), proteinase and S protein for treatment of SARS-CoV-2 infection. This review should shed light on the fundamental rationale behind inhibition of SARS-CoV-2 enzymes RdRp as new therapeutic approaches for management of patients with COVID-19. In addition, we will discuss the viability and challenges in targeting RdRp and proteinase, and application of natural product quinoline and its analog chloroquine for treatment of coronavirus infection. Finally, determining the structural-functional relationships of the S protein of SARS-CoV-2 will provide new insights into inhibition of interactions between S protein and angiotensin-converting enzyme 2 (ACE2) and enable us to develop novel therapeutic approaches for novel coronavirus SARS-CoV-2.