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1.
Nutrients ; 13(5)2021 May 10.
Article in English | MEDLINE | ID: covidwho-1224082

ABSTRACT

BACKGROUND: Acute and chronic alcohol abuse has adverse impacts on both the innate and adaptive immune response, which may result in reduced resistance to severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection and promote the progression of coronavirus disease 2019 (COVID-19). However, there are no large population-based data evaluating potential causal associations between alcohol consumption and COVID-19. METHODS: We conducted a Mendelian randomization study using data from UK Biobank to explore the association between alcohol consumption and risk of SARS-CoV-2 infection and serious clinical outcomes in patients with COVID-19. A total of 12,937 participants aged 50-83 who tested for SARS-CoV-2 between 16 March to 27 July 2020 (12.1% tested positive) were included in the analysis. The exposure factor was alcohol consumption. Main outcomes were SARS-CoV-2 positivity and death in COVID-19 patients. We generated allele scores using three genetic variants (rs1229984 (Alcohol Dehydrogenase 1B, ADH1B), rs1260326 (Glucokinase Regulator, GCKR), and rs13107325 (Solute Carrier Family 39 Member 8, SLC39A8)) and applied the allele scores as the instrumental variables to assess the effect of alcohol consumption on outcomes. Analyses were conducted separately for white participants with and without obesity. RESULTS: Of the 12,937 participants, 4496 were never or infrequent drinkers and 8441 were frequent drinkers. Both logistic regression and Mendelian randomization analyses found no evidence that alcohol consumption was associated with risk of SARS-CoV-2 infection in participants either with or without obesity (All q > 0.10). However, frequent drinking, especially heavy drinking (HR = 2.07, 95%CI 1.24-3.47; q = 0.054), was associated with higher risk of death in patients with obesity and COVID-19, but not in patients without obesity. Notably, the risk of death in frequent drinkers with obesity increased slightly with the average amount of alcohol consumed weekly (All q < 0.10). CONCLUSIONS: Our findings suggest that alcohol consumption has adverse effects on the progression of COVID-19 in white participants with obesity, but was not associated with susceptibility to SARS-CoV-2 infection.


Subject(s)
Adaptor Proteins, Signal Transducing/genetics , Alcohol Dehydrogenase/genetics , Alcohol Drinking , Biological Specimen Banks , COVID-19 , Cation Transport Proteins/genetics , Obesity , Polymorphism, Single Nucleotide , SARS Virus , Aged , Alcohol Drinking/genetics , Alcohol Drinking/mortality , COVID-19/genetics , COVID-19/mortality , Disease-Free Survival , Female , Humans , Male , Mendelian Randomization Analysis , Middle Aged , Obesity/genetics , Obesity/mortality , Survival Rate , United Kingdom/epidemiology
2.
Virol J ; 18(1): 67, 2021 03 31.
Article in English | MEDLINE | ID: covidwho-1166917

ABSTRACT

BACKGROUND: Risk scores are needed to predict the risk of death in severe coronavirus disease 2019 (COVID-19) patients in the context of rapid disease progression. METHODS: Using data from China (training dataset, n = 96), prediction models were developed by logistic regression and then risk scores were established. Leave-one-out cross validation was used for internal validation and data from Iran (test dataset, n = 43) was used for external validation. RESULTS: A NSL model (area under the curve (AUC) 0.932) and a NL model (AUC 0.903) were developed based on neutrophil percentage and lactate dehydrogenase with and without oxygen saturation (SaO2) using the training dataset. AUCs of the NSL and NL models in the test dataset were 0.910 and 0.871, respectively. The risk scoring systems corresponding to these two models were established. The AUCs of the NSL and NL scores in the training dataset were 0.928 and 0.901, respectively. At the optimal cut-off value of NSL score, the sensitivity and specificity were 94% and 82%, respectively. The sensitivity and specificity of NL score were 94% and 75%, respectively. CONCLUSIONS: These scores may be used to predict the risk of death in severe COVID-19 patients and the NL score could be used in regions where patients' SaO2 cannot be tested.


Subject(s)
COVID-19/mortality , Hospital Mortality , L-Lactate Dehydrogenase/blood , Models, Theoretical , Neutrophils/cytology , Oxygen/blood , Aged , COVID-19/therapy , China , Disease Progression , Female , Humans , Iran , Male , Middle Aged , Prognosis , Retrospective Studies , Risk Assessment
3.
medRxiv ; 2020 Nov 30.
Article in English | MEDLINE | ID: covidwho-955706

ABSTRACT

Background: Acute and chronic alcohol abuse have adverse impacts on both the innate and adaptive immune response, which may result in reduced resistance to severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection and promote the progression of coronavirus disease 2019 (COVID-19). However, there are no large population-based data evaluating potential causal associations between alcohol consumption and COVID-19. Method: We conducted a Mendelian randomization study using data from UK Biobank to explore the association between alcohol consumption and risk of SARS-CoV-2 infection and serious clinical outcomes in patients with COVID-19. A total of 12,937 participants aged 50-83 who tested for SARS-CoV-2 between 16 March to 27 July 2020 (12.1% tested positive) were included in the analysis. The exposure factor was alcohol consumption. Main outcomes were SARS-CoV-2 positivity and death in COVID-19 patients. We generated weighted and unweighted allele scores using three genetic variants (rs1229984, rs1260326, and rs13107325) and applied the allele scores as the instrumental variables to assess the effect of alcohol consumption on outcomes. Analyses were conducted separately for white participates with and without obesity. Results: Of the 12,937 participants, 4,496 were never or infrequent drinkers and 8,441 were frequent drinkers. (including 1,156 light drinkers, 3,795 moderate drinkers, and 3,490 heavy drinkers). Both logistic regression and Mendelian randomization analyses found no evidence that alcohol consumption was associated with risk of SARS-CoV-2 infection in participants either with (OR=0.963, 95%CI 0.800-1.159; q =1.000) or without obesity (OR=0.891, 95%CI 0.755-1.053; q =.319). However, frequent drinking (HR=1.565, 95%CI 1.012-2.419; q =.079), especially heavy drinking (HR=2.071, 95%CI 1.235-3.472; q =.054), was associated with higher risk of death in patients with obesity and COVID-19, but not in patients without obesity. Notably, the risk of death in frequent drinkers with obesity increased slightly with the average amount of alcohol consumed weekly (HR=1.480, 95%CI 1.059-2.069; q =.099). Conclusions: Our findings suggested alcohol consumption may had adverse effects on the progression of COVID-19 in white participants with obesity, but was not associate with susceptibility to SARS-CoV-2 infection.

5.
Food Chem Toxicol ; 145: 111767, 2020 Nov.
Article in English | MEDLINE | ID: covidwho-778851

ABSTRACT

Currently, coronavirus disease 2019 (COVID-19), has posed an imminent threat to global public health. Although some current therapeutic agents have showed potential prevention or treatment, a growing number of associated adverse events have occurred on patients with COVID-19 in the course of medical treatment. Therefore, a comprehensive assessment of the safety profile of therapeutic agents against COVID-19 is urgently needed. In this study, we proposed a network-based framework to identify the potential side effects of current COVID-19 drugs in clinical trials. We established the associations between 116 COVID-19 drugs and 30 kinds of human tissues based on network proximity and gene-set enrichment analysis (GSEA) approaches. Additionally, we focused on four types of drug-induced toxicities targeting four tissues, including hepatotoxicity, renal toxicity, lung toxicity, and neurotoxicity, and validated our network-based predictions by preclinical and clinical evidence available. Finally, we further performed pharmacovigilance analysis to validate several drug-tissue toxicities via data mining adverse event reporting data, and we identified several new drug-induced side effects without labeling in Food and Drug Administration (FDA) drug instructions. Overall, this study provides forceful approaches to assess potential side effects on COVID-19 drugs, which will be helpful for their safe use in clinical practice and promoting the discovery of antiviral therapeutics against SARS-CoV-2.


Subject(s)
Antineoplastic Agents/adverse effects , Antiviral Agents/adverse effects , Coronavirus Infections/drug therapy , Immunologic Factors/adverse effects , Pharmacovigilance , Pneumonia, Viral/drug therapy , Antineoplastic Agents/therapeutic use , Antiviral Agents/therapeutic use , Betacoronavirus/drug effects , COVID-19 , Clinical Trials as Topic , Humans , Immunologic Factors/therapeutic use , Pandemics , SARS-CoV-2
6.
Postgrad Med ; 132(7): 604-613, 2020 Sep.
Article in English | MEDLINE | ID: covidwho-526926

ABSTRACT

Coronavirus Disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is spreading worldwide. Antiviral therapy is the most important treatment for COVID-19. Among the drugs under investigation, anti-malarials, chloroquine (CQ) and hydroxychloroquine (HCQ), are being repurposed as treatment for COVID-19. CQ/HCQ were shown to prevent receptor recognition by coronaviruses, inhibit endosome acidification, which interferes with membrane fusion, and exhibit immunomodulatory activity. These multiple mechanisms may work together to exert a therapeutic effect on COVID-19. A number of in vitro studies revealed inhibitory effects of CQ/HCQ on various coronaviruses, including SARS-CoV-2 although conflicting results exist. Several clinical studies showed that CQ/HCQ alone or in combination with a macrolide may alleviate the clinical symptoms of COVID-19, promote viral conversion, and delay disease progression, with less serious adverse effects. However, recent studies indicated that the use of CQ/HCQ, alone or in combination with a macrolide, did not show any favorable effect on patients with COVID-19. Adverse effects, including prolonged QT interval after taking CQ/HCQ, may develop in COVID-19 patients. Therefore, current data are not sufficient enough to support the use of CQ/HCQ as therapies for COVID-19 and increasing caution should be taken about the application of CQ/HCQ in COVID-19 before conclusive findings are obtained by well-designed, multi-center, randomized, controlled studies.


Subject(s)
Antiviral Agents/therapeutic use , Chloroquine/therapeutic use , Coronavirus Infections/drug therapy , Hydroxychloroquine/therapeutic use , Pneumonia, Viral/drug therapy , Angiotensin-Converting Enzyme 2 , Antiviral Agents/pharmacology , Betacoronavirus/drug effects , Betacoronavirus/metabolism , COVID-19 , Chloroquine/pharmacology , Coronavirus 229E, Human/drug effects , Cytokines/drug effects , Cytokines/metabolism , Glycosylation , Humans , Hydroxychloroquine/pharmacology , Immunity, Innate , In Vitro Techniques , Long QT Syndrome/chemically induced , Lymphocyte Activation/drug effects , MAP Kinase Signaling System , Middle East Respiratory Syndrome Coronavirus/drug effects , Pandemics , Peptidyl-Dipeptidase A/drug effects , Peptidyl-Dipeptidase A/metabolism , Reactive Oxygen Species , SARS Virus/drug effects , SARS-CoV-2 , Signal Transduction , T-Lymphocytes , Toll-Like Receptors/drug effects , Toll-Like Receptors/metabolism , Treatment Outcome , Virus Internalization/drug effects
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