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2.
J Med Case Rep ; 16(1): 106, 2022 Mar 14.
Article in English | MEDLINE | ID: covidwho-1745429

ABSTRACT

BACKGROUND: Glucose-6-phosphate dehydrogenase deficiency is a rarely recognized predisposing factor for rhabdomyolysis. Rhabdomyolysis with coronavirus disease 2019 has been increasingly seen during the pandemic. We report the uncommon occurrence of coronavirus disease 2019 pneumonia, severe rhabdomyolysis, and acute renal failure in the setting of glucose-6-phosphate dehydrogenase deficiency. CASE PRESENTATION: A 19-year-old African American male presented with myalgias, diaphoresis, and dark urine. Testing for severe acute respiratory syndrome coronavirus 2 was positive. He had severe rhabdomyolysis with creatine kinase levels up to 346,695 U/L. He was oliguric and eventually required hemodialysis. Progressive hypoxemia, methemoglobinemia, and hemolytic anemia occurred following one dose of rasburicase for hyperuricemia. Glucose-6-phosphate dehydrogenase deficiency was diagnosed. Full recovery followed a single volume exchange transfusion and simple packed red blood cell transfusions. CONCLUSIONS: Glucose-6-phosphate dehydrogenase deficiency may predispose individuals to rhabdomyolysis due to severe acute respiratory syndrome coronavirus 2, presumably due to altered host responses to viral oxidative stress. Early screening for glucose-6-phosphate dehydrogenase deficiency can be useful for management of patients with rhabdomyolysis.


Subject(s)
COVID-19 , Glucosephosphate Dehydrogenase Deficiency , Methemoglobinemia , Pneumonia , Rhabdomyolysis , Adult , COVID-19/complications , Glucosephosphate Dehydrogenase Deficiency/complications , Glucosephosphate Dehydrogenase Deficiency/diagnosis , Humans , Male , Methemoglobinemia/complications , Methemoglobinemia/diagnosis , Pneumonia/complications , Rhabdomyolysis/etiology , Young Adult
4.
Sci Rep ; 11(1): 19213, 2021 09 28.
Article in English | MEDLINE | ID: covidwho-1442805

ABSTRACT

Glucose-6-phosphate dehydrogenase deficiency (G6PDd) is known to suppress the antioxidant system and is likely to aggravate severity of COVID-19, which results in a pro-oxidant response. This possible association has not been explored adequately in human studies. In this research, we report that the occurrence of non-invasive ventilation, intubation or death-all of which are indicative of severe COVID-19, are not significantly different in hospitalized COVID-19 patients with and without G6PDd (4.6 vs. 6.4%, p = 0.33). The likelihood of developing any of these severe outcomes were slightly lower in patients with G6PDd after accounting for age, nationality, presence of comorbidities and drug interventions (Odds ratio 0.40, 95% confidence intervals 0.142, 1.148). Further investigation that extends to both, hospitalized and non-hospitalized COVID-19 patients, is warranted to study this potential association.


Subject(s)
COVID-19 , Glucosephosphate Dehydrogenase Deficiency/complications , Acute Disease , Adult , Age Factors , COVID-19/epidemiology , COVID-19/metabolism , COVID-19/pathology , Comorbidity , Critical Illness , Female , Glucose-6-Phosphatase/metabolism , Humans , Male , Middle Aged , SARS-CoV-2/pathogenicity
5.
PLoS One ; 16(9): e0257560, 2021.
Article in English | MEDLINE | ID: covidwho-1430541

ABSTRACT

Certain clinical indications and treatments such as the use of rasburicase in cancer therapy and 8-aminoquinolines for Plasmodium vivax malaria treatment would benefit from a point-of-care test for glucose-6-phosphate dehydrogenase (G6PD) deficiency. Three studies were conducted to evaluate the performance of one such test: the STANDARD™ G6PD Test (SD BIOSENSOR, South Korea). First, biological interference on the test performance was evaluated in specimens with common blood disorders, including high white blood cell (WBC) counts. Second, the test precision on fingerstick specimens was evaluated against five individuals of each, deficient, intermediate, and normal G6PD activity status. Third, clinical performance of the test was evaluated at three point-of-care settings in the United States. The test performed equivalently to the reference assay in specimens with common blood disorders. High WBC count blood samples resulted in overestimation of G6PD activity in both the reference assay and the STANDARD G6PD Test. The STANDARD G6PD Test showed good precision on multiple fingerstick specimens from the same individual. The same G6PD threshold values (U/g Hb) were applied for a semiquantitative interpretation for fingerstick- and venous-derived results. The sensitivity/specificity values (95% confidence intervals) for the test for G6PD deficiency were 100 (92.3-100.0)/97 (95.2-98.2) and 100 (95.7-100.0)/97.4 (95.7-98.5) for venous and capillary specimens, respectively. The same values for females with intermediate (> 30% to ≤ 70%) G6PD activity were 94.1 (71.3-99.9)/88.2 (83.9-91.7) and 82.4 (56.6-96.2)/87.6(83.3-91.2) for venous and capillary specimens, respectively. The STANDARD G6PD Test enables point-of-care testing for G6PD deficiency.


Subject(s)
Glucosephosphate Dehydrogenase Deficiency/diagnosis , Glucosephosphate Dehydrogenase/blood , Point-of-Care Systems/standards , Adolescent , Adult , Aged , Blood Specimen Collection , Child , Child, Preschool , Female , Glucosephosphate Dehydrogenase/genetics , Glucosephosphate Dehydrogenase/standards , Glucosephosphate Dehydrogenase Deficiency/complications , Hematologic Diseases/complications , Hemoglobins/analysis , Humans , Leukocyte Count , Male , Middle Aged , Reagent Kits, Diagnostic , Reference Standards , Sensitivity and Specificity , Young Adult
7.
BMJ Case Rep ; 14(3)2021 Mar 16.
Article in English | MEDLINE | ID: covidwho-1138315

ABSTRACT

We report a case of a 91-year-old Caucasian woman with a history of chronic lymphocytic leukaemia who developed acute hypoxic respiratory failure (AHRF) requiring intubation for less than 24 hours after receiving rasburicase. Laboratory workup was significant for methemoglobinemia and acute anaemia, and blood film demonstrated evidence of oxidative haemolysis with bite cells. The patient was given a presumptive diagnosis of glucose-6-phosphate dehydrogenase (G6PD) deficiency and was managed conservatively with successful resolution of AHRF and stabilisation of haemoglobin level. Seven days after admission, she passed away due to subsequent complications; hence, follow-up G6PD level could not be obtained. Haemolytic anaemia and methemoglobinemia in the setting of recent rasburicase administration should raise clinical suspicion for G6PD deficiency. In non-emergent cases, patients should be screened prior to receiving rasburicase regardless of risk factors. Because rasburicase is often needed emergently, patients at high risk of tumour lysis syndrome should be screened early for G6PD deficiency.


Subject(s)
Glucosephosphate Dehydrogenase Deficiency , Methemoglobinemia , Aged, 80 and over , Female , Glucosephosphate Dehydrogenase Deficiency/complications , Hemolysis , Humans , Methemoglobinemia/chemically induced , Methemoglobinemia/diagnosis , Methemoglobinemia/drug therapy , Urate Oxidase/adverse effects
8.
Nucleosides Nucleotides Nucleic Acids ; 40(5): 505-517, 2021.
Article in English | MEDLINE | ID: covidwho-1132307

ABSTRACT

COVID-19 has become a major public health problem since December, 2019 and no highly effective drug has been found until now. Numbers of infected people and deaths by COVID-19 are increasing every day worldwide, therefore self-isolation and protection are highly recommended to prevent the spread of the virus and especially to protect major risk groups such as the elderly population and people with comorbidities including diabetes, hypertension, cancer, cardiovascular diseases and metabolic syndrome. On the other hand, young people without any secondary disease have died by COVID-19 as well. In this study we compared two male patients infected by COVID-19 at the same age and one of them was diagnosed with G6PD deficiency. Both COVID-19 and G6PD deficiency enhance the risk of hemolysis and thrombosis. Serum biochemistry, hemogram and immunological parameters showed that risk of hemolysis and thrombosis may increase in the G6PD deficient patient infected by COVID-19.


Subject(s)
COVID-19/genetics , Glucosephosphate Dehydrogenase Deficiency/genetics , Glucosephosphate Dehydrogenase/genetics , Thrombosis/genetics , Adult , COVID-19/blood , COVID-19/complications , COVID-19/virology , Glucosephosphate Dehydrogenase Deficiency/blood , Glucosephosphate Dehydrogenase Deficiency/complications , Glucosephosphate Dehydrogenase Deficiency/pathology , Hemolysis/physiology , Humans , Male , Risk Factors , SARS-CoV-2/genetics , SARS-CoV-2/pathogenicity , Thrombosis/blood , Thrombosis/etiology , Thrombosis/virology
9.
Mol Biol Rep ; 48(3): 2973-2978, 2021 Mar.
Article in English | MEDLINE | ID: covidwho-1095719

ABSTRACT

The coronavirus disease 2019 (COVID-19) is until today a global health emergency. In an immense effort, effective drugs against COVID-19 are searched and intensive researches on possible repurposing of antiviral agents are performed. Since chloroquine (CQ) and hydroxychloroquine (HCQ) have shown in vitro anti- COVID-19 activities, the potential effect of CQ/HCQ to treat and/or prevent COVID-19 infection has caused global attention. However, concern regarding possible hemolysis in G6PD-deficient COVID-19 patients exists and for this reason, the association between HCQ and G6PD deficiency (G6PDD) is back in the limelight. This study aims to answer the question raised by Mastroianni et al. "Hydroxychloroquine: Culprit or Innocent Bystander in G6PD-Deficient Patients with COVID-19?", reporting all cases of HCQ in G6PD deficient COVID-19 patients published on PubMed (pubmed.ncbi.nlm.nih.gov), in addition to the Mastroianni's patient. In our opinion, after an accurate revision of these cases and responding the question raised by Mastroianni et al., we believe that it is difficult to reach a final verdict about the definitive role of HCQ in these patients. The COVID-19 pandemic has reopened attention on HCQ use and G6PDD. G6PD status is extremely important in modulating the level of reactive oxygen species and many cellular immune responses such as enhanced production of the pro-inflammatory cytokine and inflammasome activation. Since these processes are involved in COVID-19 infection, acute hemolytic anemia, a severe complication of the G6PDD, can occur in these patients. In this context, the role of HCQ, usually effective, safe, and well tolerated in G6PD deficient patients, must be redefined in these patients with COVID-19.As consequence, answering the question: "Hydroxychloroquine: Culprit or Innocent Bystander in G6PD-Deficient Patients with COVID-19?", we state that it is risky to believe that HCQ may be an "innocent bystander" in G6PD-deficient COVID-19 patients.


Subject(s)
Antiviral Agents , COVID-19 , Glucosephosphate Dehydrogenase Deficiency , Hydroxychloroquine , Adult , Aged , Antiviral Agents/adverse effects , Antiviral Agents/therapeutic use , COVID-19/complications , COVID-19/drug therapy , COVID-19/physiopathology , Glucosephosphate Dehydrogenase Deficiency/complications , Glucosephosphate Dehydrogenase Deficiency/physiopathology , Hemolysis , Humans , Hydroxychloroquine/adverse effects , Hydroxychloroquine/therapeutic use , Male , Middle Aged
10.
Ann Hematol ; 100(3): 667-673, 2021 Mar.
Article in English | MEDLINE | ID: covidwho-1030503

ABSTRACT

The severe pneumonia caused by the human coronavirus (hCoV)-SARS-CoV-2 has inflicted heavy casualties, especially among the elderly and those with co-morbid illnesses irrespective of their age. The high mortality in African-Americans and males, in general, raises the concern for a possible X-linked mediated process that could affect the viral pathogenesis and the immune system. We hypothesized that G6PD, the most common X-linked enzyme deficiency, associated with redox status, may have a role in severity of pneumonia. Retrospective chart review was performed in hospitalized patients with COVID19 pneumonia needing supplemental oxygen. A total of 17 patients were evaluated: six with G6PD deficiency (G6PDd) and 11 with normal levels. The two groups (normal and G6PDd) were comparable in terms of age, sex, co-morbidities, and laboratory parameters-LDH, IL-6, CRP, and ferritin, respectively. Thirteen patients needed ventilatory support ; 8 in the normal group and 5 in the G6PDd group (72% vs.83%). The main differences indicating increasing severity in normal vs. G6PDd groups included G6PD levels (12.2 vs. 5.6, P = 0.0002), PaO2/FiO2 ratio (159 vs. 108, P = 0.05), days on mechanical ventilation (10.25 vs. 21 days P = 0.04), hemoglobin level (10 vs. 8.1 P = 0.03), and hematocrit (32 vs. 26 P = 0.015). Only one patient with G6PDd died; 16 were discharged home. Our clinical series ascribes a possible biological role for G6PDd in SARS-CoV2 viral proliferation. It is imperative that further studies are performed to understand the interplay between the viral and host factors in G6PDd that may lead to disparity in outcomes. KEY POINTS: • COVID19 studies show higher mortality in men, due to severe pneumonia and ARDS, indicating possible X-linked mediated differences • G6PD, the most common X-linked enzymopathy, highly prevalent in African Americans and Italians, maintains redox homeostasis. • Preclinical studies using G6PD deficient (G6PDd) cells infected with human coronavirus (hCoV), show impaired cellular responses, viral proliferation and worsening oxidative damage. • Retrospective chart review in hospitalized patients with COVID19 pneumonia needing supplemental oxygen shows differences between the two groups (Normal and G6PDd) in hematological indices; the G6PDdgroup demonstrated prolonged PaO2/FiO2 ratio, and longer days on mechanical ventilation indicating the severity of the pneumonia.


Subject(s)
COVID-19/complications , Glucosephosphate Dehydrogenase Deficiency/complications , Respiratory Distress Syndrome/etiology , SARS-CoV-2 , African Americans , COVID-19/blood , COVID-19/diagnosis , COVID-19 Nucleic Acid Testing , Contraindications, Drug , Critical Care , Female , Genetic Predisposition to Disease , Glucosephosphate Dehydrogenase Deficiency/blood , Glucosephosphate Dehydrogenase Deficiency/ethnology , Glucosephosphate Dehydrogenase Deficiency/physiopathology , Humans , Hydroxychloroquine/adverse effects , Hydroxychloroquine/therapeutic use , Male , Middle Aged , Oxidative Stress , Respiration, Artificial , Respiratory Distress Syndrome/blood , Respiratory Distress Syndrome/therapy , Retrospective Studies , SARS-CoV-2/isolation & purification , Severity of Illness Index , Sex Distribution
11.
Free Radic Res ; 55(4): 364-374, 2021 Apr.
Article in English | MEDLINE | ID: covidwho-1010202

ABSTRACT

The COVID-19 pandemic has so far affected more than 45 million people and has caused over 1 million deaths worldwide. Infection with SARS-CoV-2, the pathogenic agent, which is associated with an imbalanced redox status, causes hyperinflammation and a cytokine storm, leading to cell death. Glucose-6-phosphate dehydrogenase (G6PD) deficient individuals may experience a hemolytic crisis after being exposed to oxidants or infection. Individuals with G6PD deficiency are more susceptible to coronavirus infection than individuals with normally functioning G6PD. An altered immune response to viral infections is found in individuals with G6PD deficiency. Evidence indicates that G6PD deficiency is a predisposing factor of COVID-19.


Subject(s)
COVID-19 , Glucosephosphate Dehydrogenase Deficiency , SARS-CoV-2/physiology , Virus Diseases , COVID-19/complications , COVID-19/epidemiology , COVID-19/genetics , COVID-19/metabolism , Disease Susceptibility , Glucosephosphate Dehydrogenase/genetics , Glucosephosphate Dehydrogenase/metabolism , Glucosephosphate Dehydrogenase Deficiency/complications , Glucosephosphate Dehydrogenase Deficiency/epidemiology , Glucosephosphate Dehydrogenase Deficiency/genetics , Glucosephosphate Dehydrogenase Deficiency/metabolism , Homeostasis/physiology , Humans , Oxidation-Reduction , Pandemics , Virus Diseases/epidemiology , Virus Diseases/genetics , Virus Diseases/metabolism
13.
Perm J ; 242020.
Article in English | MEDLINE | ID: covidwho-922950

ABSTRACT

INTRODUCTION: The growing coronavirus disease 2019 (COVID-19) pandemic initially led to widespread use of hydroxychloroquine sulfate as an off-label experimental treatment of this disease. CASE PRESENTATION: Acute hemolytic anemia developed in an African American man with COVID-19-related pneumonia and glucose-6-phosphate dehydrogenase (G6PD) deficiency who completed the standard 5-day experimental course of hydroxychloroquine. Although the trigger leading to our patient's hemolytic sequelae will never be known with certainty, his clinical course suggests that hydroxychloroquine use and/or COVID-19 infection may trigger hemolysis in susceptible patients with G6PD deficiency. DISCUSSION: This case confirms recent findings that the potential risks of hydroxychloroquine therapy for COVID-19 may outweigh the benefits.


Subject(s)
Anemia, Hemolytic/complications , COVID-19/complications , Enzyme Inhibitors/therapeutic use , Glucosephosphate Dehydrogenase Deficiency/complications , Hydroxychloroquine/therapeutic use , Anemia, Hemolytic/therapy , COVID-19/drug therapy , Enzyme Inhibitors/adverse effects , Erythrocyte Transfusion , Humans , Hydroxychloroquine/adverse effects , Male , Middle Aged
15.
Am J Case Rep ; 21: e925788, 2020 Jul 22.
Article in English | MEDLINE | ID: covidwho-665389

ABSTRACT

BACKGROUND Beta-hemoglobinopathies and glucose-6-phosphate dehydrogenase (G6PD) deficiency are genetic disorders that cause hemolytic anemia when exposed to oxidative stress. Their co-existence is, however, not proven to enhance the severity of anemia. CASE REPORT We report the case of a young man with no known co-morbidities, who came with fever and cough and was diagnosed with COVID-19 pneumonia. He was found to have hemoglobin D thalassemia and G6PD deficiency during further evaluation. Hydroxychloroquine therapy started initially, was discontinued after 3 doses once the G6PD deficiency was diagnosed. His hospital course showed a mild drop in hemoglobin with evidence of hemolysis on peripheral smear. However, the hemoglobin improved without any need for transfusion. CONCLUSIONS Hydroxychloroquine therapy can induce hemolytic crises in patients with underlying G6PD deficiency or hemoglobinopathies and should be avoided or closely monitored. Immediate intervention to stop hydroxychloroquine after 3 doses saved our patient from a major hemolytic crisis. The significance of this case report is that it is the first report that outlines the clinic course of COVID-19 pneumonia in a patient with underlying hemoglobin D disease and G6PD deficiency.


Subject(s)
Betacoronavirus , Coronavirus Infections/complications , Glucosephosphate Dehydrogenase Deficiency/complications , Hemoglobins/metabolism , Pneumonia, Viral/complications , Thalassemia/complications , Asymptomatic Diseases , COVID-19 , Coronavirus Infections/virology , Glucosephosphate Dehydrogenase Deficiency/blood , Humans , Male , Pandemics , Pneumonia, Viral/virology , SARS-CoV-2 , Thalassemia/blood , Young Adult
16.
Clin Immunol ; 219: 108544, 2020 10.
Article in English | MEDLINE | ID: covidwho-664013

ABSTRACT

Glucose 6-phosphate dehydrogenase (G6PD) deficiency facilitates human coronavirus infection due to glutathione depletion. G6PD deficiency may especially predispose to hemolysis upon coronavirus disease-2019 (COVID-19) infection when employing pro-oxidant therapy. However, glutathione depletion is reversible by N-acetylcysteine (NAC) administration. We describe a severe case of COVID-19 infection in a G6PD-deficient patient treated with hydroxychloroquine who benefited from intravenous (IV) NAC beyond reversal of hemolysis. NAC blocked hemolysis and elevation of liver enzymes, C-reactive protein (CRP), and ferritin and allowed removal from respirator and veno-venous extracorporeal membrane oxygenator and full recovery of the G6PD-deficient patient. NAC was also administered to 9 additional respirator-dependent COVID-19-infected patients without G6PD deficiency. NAC elicited clinical improvement and markedly reduced CRP in all patients and ferritin in 9/10 patients. NAC mechanism of action may involve the blockade of viral infection and the ensuing cytokine storm that warrant follow-up confirmatory studies in the setting of controlled clinical trials.


Subject(s)
Acetylcysteine/therapeutic use , Antioxidants/therapeutic use , Betacoronavirus/pathogenicity , Coronavirus Infections/drug therapy , Cytokine Release Syndrome/drug therapy , Glucosephosphate Dehydrogenase Deficiency/drug therapy , Pneumonia, Viral/drug therapy , Adult , Antirheumatic Agents/therapeutic use , Biomarkers/blood , C-Reactive Protein/metabolism , COVID-19 , Coronavirus Infections/blood , Coronavirus Infections/complications , Coronavirus Infections/virology , Cytokine Release Syndrome/blood , Cytokine Release Syndrome/complications , Cytokine Release Syndrome/virology , Drug Administration Schedule , Ferritins/blood , Fibrin Fibrinogen Degradation Products/metabolism , Glucosephosphate Dehydrogenase Deficiency/blood , Glucosephosphate Dehydrogenase Deficiency/complications , Glucosephosphate Dehydrogenase Deficiency/virology , Humans , Hydroxychloroquine/therapeutic use , Inflammation/prevention & control , Male , Pandemics , Pneumonia, Viral/blood , Pneumonia, Viral/complications , Pneumonia, Viral/virology , SARS-CoV-2 , Treatment Outcome
18.
Infect Dis (Lond) ; 52(9): 659-661, 2020 09.
Article in English | MEDLINE | ID: covidwho-526880

ABSTRACT

While the COVID-19 epidemic occurred since December 2019, as of end April 2020, no treatment has been validated or invalidated by accurate clinical trials. Use of hydroxychloroquine has been popularised on mass media and put forward as a valid treatment option without strong evidence of efficacy. Hydroxychloroquine (HCQ) has its own side effects, some of which are very serious like acute haemolysis in glucose-6-phosphate dehydrogenase (G6PD) deficient patients. Side effects may be worse than the disease itself. Belgian national treatment guidelines recommend the use of HCQ in mild to severe COVID-19 disease. As opinions, politics, media and beliefs are governing COVID-19 therapy, performance of randomised controlled blinded clinical trials became difficult. Results of sound clinical trials are eagerly awaited. We report a case of acute haemolysis leading to admission in intensive care unit and renal failure in a patient with uncovered G6PD deficiency.


Subject(s)
Coronavirus Infections/complications , Coronavirus Infections/drug therapy , Enzyme Inhibitors/adverse effects , Glucosephosphate Dehydrogenase Deficiency/complications , Hemolysis , Hydroxychloroquine/adverse effects , Pneumonia, Viral/complications , Pneumonia, Viral/drug therapy , Aged , Azithromycin/therapeutic use , Betacoronavirus/genetics , Betacoronavirus/isolation & purification , Blood Transfusion , COVID-19 , Continuous Renal Replacement Therapy , Drug Therapy, Combination , Enzyme Inhibitors/therapeutic use , Haptoglobins/analysis , Humans , Hydroxychloroquine/therapeutic use , Hypoxia/chemically induced , Hypoxia/complications , Male , Nasopharynx/virology , Pandemics , Respiratory Distress Syndrome/complications , SARS Virus/genetics , SARS Virus/isolation & purification , SARS-CoV-2
20.
Eur J Haematol ; 105(3): 357-359, 2020 Sep.
Article in English | MEDLINE | ID: covidwho-108769

ABSTRACT

Glucose-6-phosphate dehydrogenase (G6PD) deficiency is an inherited genetic disorder caused by red cell enzymatic defects and is associated with haemolytic crisis when patients are exposed to oxidative agents (fava beans, drugs, infections). Hydroxychloroquine is suspected to trigger haemolytic crisis in G6PD-deficient patients, and off-label administration of this drug to patients infected with the novel coronavirus (SARS-CoV-2) could cause concern. We report here the first case of severe haemolytic crisis in a patient with G6PD deficiency, initiated by severe COVID-19 infection and hydroxychloroquine use. With worldwide spread of COVID-19, especially in regions with a high prevalence of G6PD deficiency, our case should alert physicians to this possible correlation.


Subject(s)
Betacoronavirus , Coronavirus Infections/drug therapy , Glucosephosphate Dehydrogenase Deficiency/complications , Hemolysis/drug effects , Hydroxychloroquine/adverse effects , Pneumonia, Viral/drug therapy , Aged , COVID-19 , Comorbidity , Coronavirus Infections/complications , Coronavirus Infections/epidemiology , Glucosephosphate Dehydrogenase Deficiency/epidemiology , Humans , Hydroxychloroquine/therapeutic use , Male , Pandemics , Pneumonia, Viral/epidemiology , SARS-CoV-2
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