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1.
Preprint em Inglês | medRxiv | ID: ppmedrxiv-22283193

RESUMO

ObjectivesWe assessed the causal association of three COVID-19 phenotypes with insulin-like growth factor 1 (IGF-1), estrogen, testosterone, dehydroepiandrosterone (DHEA), thyroid-stimulating hormone (TSH), thyrotropin-releasing hormone (TRH), luteinizing hormone (LH), and follicle-stimulating hormone (FSH). MethodsWe used a bidirectional two-sample univariate and multivariable Mendelian randomization (MR) analysis to evaluate the direction, specificity, and causality of the association between CNS-regulated hormones and COVID-19 phenotypes. Genetic instruments for CNS-regulated hormones were selected from the largest publicly available genome-wide association studies in the European population. Summary-level data on COVID-19 severity, hospitalization, and susceptibility were obtained from the COVID-19 host genetic initiative. ResultsDHEA was associated with increased risks of very severe respiratory syndrome (OR=4.21, 95% CI: 1.41-12.59), consistent with the results in multivariate MR (OR=3.72, 95% CI: 1.20-11.51), and hospitalization (OR = 2.31, 95% CI: 1.13-4.72) in univariate MR. LH was associated with very severe respiratory syndrome (OR=0.83; 95% CI: 0.71-0.96) in univariate MR. Estrogen was negatively associated with very severe respiratory syndrome (OR=0.09, 95% CI: 0.02-0.51), hospitalization (OR=0.25, 95% CI: 0.08-0.78), and susceptibility (OR=0.50, 95% CI: 0.28-0.89) in multivariate MR. ConclusionsWe found strong evidence for the causal relationship of DHEA, LH, and estrogen with COVID-19 phenotypes.

2.
Artigo em Chinês | WPRIM (Pacífico Ocidental) | ID: wpr-964189

RESUMO

@#ObjectiveTo review the efficacy and safety in secondary prevention of ischemic stroke with cilostazol or aspirin.Methodswe searched Cochrane Library(the 4th issue, 2009 ), PubMed(1980.1~2009.11), EMBASE(1980.1~2009.11), CBM(1978.1~2009.11), CNKI(1979.1~2009.11) and some other databases, then collected all of the studies describing the outcomes in curing the ischemic stroke after taking cilostazol or aspirin. According to the strict inclusion and exclusion criteria, two reviewers independently selected trials, extracted datas, made cross-checking and methodological quality assessment of the homogeneity studies by using the Cochrane systematic review methods, then made Meta analysis using RevMan 5.0 software.ResultsThis systematic review study included two randomized controlled trials and a cross-over trial, which contained a total of 838 participants. The evidence quality of one of the randomized controlled trials was high, however, the evidence quality of another randomized controlled trial and the cross-over trial was poor. Meta analysis results suggested that the effectiveness of cilostazol and aspirin in the secondary prevention of ischemic stroke performed no significantly statistical difference: primary endpoint(30 d[RR=3.00, 95%CI(0.31,28.70)]; 90 d[RR=1.67, 95%CI(0.40,6.92)]; 180 d[RR=1.25, 95%CI(0.50, 3.13)]; 360 d[RR=0.65, 95%CI(0.33, 1.29)]; 540 d[RR=0.80,95%CI(0.54, 1.18)]); combined endpoint(30 d[RR=4.00, 95%CI(0.45,35.61)]; 90 d [RR=1.75,95%CI(0.52,5.93)]; 180 d[RR=1.00, 95%CI(0.48, 2.07)]; 360 d [RR=0.77, 95%CI(0.45, 1.29)]; 540 d[RR=0.66,95%CI(0.40,1.09)]); the recurrence of ischemic stroke: cilostazol group: RR=0.64, 95%CI(0.31,1.30),aspirin group: RR=0.21, 95%CI(0.04,1.06); PDMP[RR=1.00, 95%CI(0.39, 2.58)]. But in terms of the probability of intracranial hemorrhage ([RR=7.14, 95%CI(0.7,58.33)]) and other safety standards, taking cilostazol performed lower than taking aspirin.ConclusionThe side effects of cilostazol and aspirin in the treatment for ischemic stroke were similar to each other, but in terms of the probability of dizziness, headache, tachycardia and palpitation, taking cilostazol performed higher than taking aspirin, however, taking cilostazol performed lower in the probability of intracranial hemorrhage and other organ hemorrhage than taking aspirin. Since this study included a small amount of studies, in which the evidence quality of one of the randomized controlled trials and the cross-over study was poor, therefore, it would be necessary to make a further validation with lots of high-quality clinical trials.

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