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1.
Egypt Heart J ; 72(1): 68, 2020 Oct 06.
Article in English | MEDLINE | ID: covidwho-2098497

ABSTRACT

BACKGROUND: Patients with established cardiovascular diseases have a poor prognosis when affected by the coronavirus disease 2019 (COVID-19). Also, the cardiovascular system, especially the heart, is affected by COVID-19. So we aimed to evaluate the angiographic and clinical characteristics of COVID-19 patients presented by ST-elevation myocardial infarction (STEMI). RESULTS: Our retrospective study showed that STEMI patients with COVID-19 had elevated inflammatory markers with mean of their CRP (89.69 ± 30.42 mg/dl) and increased laboratory parameters of thrombosis with mean D-dimer (660.15 ± 360.11 ng/ml). In 69.2% of patients, STEMI was the first clinical presentation and symptoms suggestive of COVID-19 developed during the hospital stay; about one third of patients had a non-obstructive CAD, while patients with total occlusion had a high thrombus burden. CONCLUSION: STEMI may be the initial presentation of COVID-19. A non-obstructive CAD was found in about one third of patients; on the other hand, in patients who had a total occlusion of their culprit artery, the thrombus burden was high. Identification of the underlying mechanism responsible for the high thrombus burden in these patients is important as it may result in changes in their primary management strategy, either primary PCI, fibrinolytic therapy, or a pharmaco-invasive strategy. Furthermore, adjunctive anticoagulation and antiplatelet therapy may need to be revised.

2.
Am J Med Case Rep ; 8(8): 225-228, 2020.
Article in English | MEDLINE | ID: covidwho-1989681

ABSTRACT

Coronavirus disease 2019 (COVID-19) is a pandemic that started in China in December 2019 and carries a high risk of morbidity and mortality. To-date (4-22-2020) it affected over 2.6 million people and resulted in nearly 200,000 death worldwide mainly due to severe acute respiratory syndrome coronavirus 2 (SARS-Cov-2). Among the major underlying pathophysiologic mechanisms in COVID 19 is hypercoagulability, leading to increased risk for deep vein thrombosis and pulmonary embolism that contribute to increased morbidity and mortality. In this report, we present the case of a 55-year-old man who presented with COVID-19 pneumonia, and was found to have a thrombus in transit by routine point of care ultrasound (POCUS). While computer tomography (CT) angiography is the test of choice, the utilization of point of care ultrasound (POCUS) has gained traction as an adjunctive means of surveillance for the development of VTE in patients with COVID-19. In this report, we discuss the clinical utility of POCUS in diagnosing thrombus in transit in COVID 19 populations.

3.
Hepatology ; 74(2): 1088-1100, 2021 Aug.
Article in English | MEDLINE | ID: covidwho-1274693

ABSTRACT

Infection with the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a novel coronavirus that emerged in late 2019, is posing an unprecedented challenge to global health. Coronavirus disease 2019 (COVID-19), the clinical disease caused by SARS-CoV-2, has a variable presentation ranging from asymptomatic infection to life-threatening acute respiratory distress syndrome and multiorgan failure. Liver involvement is common during COVID-19 and exhibits a spectrum of clinical manifestations from asymptomatic elevations of liver function tests to hepatic decompensation. The presence of abnormal liver tests has been associated with a more severe presentation of COVID-19 disease and overall mortality. Although SARS-CoV-2 RNA has been detected in the liver of patients with COVID-19, it remains unclear whether SARS-CoV-2 productively infects and replicates in liver cells and has a direct liver-pathogenic effect. The cause of liver injury in COVID-19 can be attributed to multiple factors, including virus-induced systemic inflammation, hypoxia, hepatic congestion, and drug-induced liver disease. Among patients with cirrhosis, COVID-19 has been associated with hepatic decompensation and liver-related mortality. Additionally, COVID-19's impact on health care resources can adversely affect delivery of care and outcomes of patients with chronic liver disease. Understanding the underlying mechanisms of liver injury during COVID-19 will be important in the management of patients with COVID-19, especially those with advanced liver disease. This review summarizes our current knowledge of SARS-CoV-2 virus-host interactions in the liver as well the clinical impact of liver disease in COVID-19.


Subject(s)
Acute-On-Chronic Liver Failure/diagnosis , COVID-19/therapy , Liver Cirrhosis/diagnosis , Liver/pathology , Acute-On-Chronic Liver Failure/epidemiology , COVID-19/mortality , Disease Progression , Global Health , Humans , Liver Cirrhosis/epidemiology , Liver Function Tests , SARS-CoV-2/isolation & purification
4.
Front Cardiovasc Med ; 8: 671669, 2021.
Article in English | MEDLINE | ID: covidwho-1247852

ABSTRACT

Covid-19 infection may be associated with a higher incidence developing cardiovascular complications, however, the underlying mechanisms contributing to cardiovascular complications are largely unknown, while endothelial cell damage may be present. We want to report a 24-year-old woman with Covid-19 infection who had undergone measurements of vascular reactivity and arterial stiffness, including flow-mediated dilation (FMD), nitroglycerin-mediated dilation (NMD), aortic pulse wave velocity (PWV), augmentation index and carotid intima-media-thickness (cIMT) at the time when Covid-19 was diagnosed. Reduced FMD of 0.0% and NMD of 15.5% were observed, while PWV (5.9 m/s), Aix (27%) and cIMT with 0.4 mm of both common carotid arteries were unremarkable. Repeated measurements of FMD, NMD, PWV, Aix, and cIMT 6 weeks after Covid-19 infection revealed persistently reduced FMD (0.0%), while NMD (17.24%), PWV (5.6 m/s) and augmentation index (13%) ameliorated. This case suggests potential impact of Covid-19 infection on endothelial function, also in young Covid-19 patients without any co-morbidity.

5.
Eur J Trauma Emerg Surg ; 47(5): 1335-1342, 2021 Oct.
Article in English | MEDLINE | ID: covidwho-1241588

ABSTRACT

PURPOSE: There is mounting evidence that surgical patients with COVID-19 have higher morbidity and mortality than patients without COVID-19. Infection is prevalent amongst the trauma population, but any effect of COVID-19 on trauma patients is unknown. We aimed to evaluate the effect of COVID-19 on a trauma population, hypothesizing increased mortality and pulmonary complications for COVID-19-positive (COVID) trauma patients compared to propensity-matched COVID-19-negative (non-COVID) patients. METHODS: A retrospective analysis of trauma patients presenting to 11 Level-I and II trauma centers in California between 1/1/2019-6/30/2019 and 1/1/2020-6/30/2020 was performed. A 1:2 propensity score model was used to match COVID to non-COVID trauma patients using age, blunt/penetrating mechanism, injury severity score, Glasgow Coma Scale score, systolic blood pressure, respiratory rate, and heart rate. Outcomes were compared between the two groups. RESULTS: A total of 20,448 trauma patients were identified during the study period. 53 COVID trauma patients were matched with 106 non-COVID trauma patients. COVID patients had higher rates of mortality (9.4% vs 1.9%, p = 0.029) and pneumonia (7.5% vs. 0.0%, p = 0.011), as well as a longer mean length of stay (LOS) (7.47 vs 3.28 days, p < 0.001) and intensive care unit LOS (1.40 vs 0.80 days, p = 0.008), compared to non-COVID patients. CONCLUSION: This multicenter retrospective study found increased rates of mortality and pneumonia, as well as a longer LOS, for COVID trauma patients compared to a propensity-matched cohort of non-COVID patients. Further studies are warranted to validate these findings and to elucidate the underlying pathways responsible for higher mortality in COVID trauma patients.


Subject(s)
COVID-19 , Humans , Injury Severity Score , Intensive Care Units , Length of Stay , Retrospective Studies , SARS-CoV-2 , Trauma Centers
6.
Sci China Life Sci ; 64(12): 2129-2143, 2021 12.
Article in English | MEDLINE | ID: covidwho-1212915

ABSTRACT

Prolonged viral RNA shedding and recurrence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in coronavirus disease 2019 (COVID-19) patients have been reported. However, the clinical outcome and pathogenesis remain unclear. In this study, we recruited 43 laboratory-confirmed COVID-19 patients. We found that prolonged viral RNA shedding or recurrence mainly occurred in severe/critical patients (P<0.05). The average viral shedding time in severe/critical patients was more than 50 days, and up to 100 days in some patients, after symptom onset. However, chest computed tomography gradually improved and complete absorption occurred when SARS-CoV-2 RT-PCR was still positive, but specific antibodies appeared. Furthermore, the viral shedding time significantly decreased when the A1,430G or C12,473T mutation occurred (P<0.01 and FDR<0.01) and increased when G227A occurred (P<0.05 and FDR<0.05). High IL1R1, IL1R2, and TNFRSF21 expression in the host positively correlated with viral shedding time (P<0.05 and false discovery rate <0.05). Prolonged viral RNA shedding often occurs but may not increase disease damage. Prolonged viral RNA shedding is associated with viral mutations and host factors.


Subject(s)
COVID-19/virology , SARS-CoV-2/pathogenicity , Adult , Antibodies, Neutralizing/blood , Antibodies, Viral/blood , COVID-19/epidemiology , COVID-19/pathology , China/epidemiology , Female , Gene Expression Profiling , Genome, Viral/genetics , Hospitalization , Humans , Longitudinal Studies , Lung/pathology , Male , Middle Aged , Mutation , RNA, Viral/genetics , RNA, Viral/metabolism , SARS-CoV-2/genetics , SARS-CoV-2/isolation & purification , SARS-CoV-2/physiology , Time Factors , Virus Replication , Virus Shedding
7.
Thromb Res ; 202: 191-198, 2021 06.
Article in English | MEDLINE | ID: covidwho-1193488

ABSTRACT

Severe COVID-19 can manifest as multiorgan dysfunction with pulmonary involvement being the most common and prominent. As more reports emerge in the literature, it appears that an exaggerated immune response in the form of unfettered complement activation and a cytokine storm may be a key driver of the widespread organ injury seen in this disease. In addition, these patients are also known to be hypercoagulable with a high rate of thrombosis and a higher-than-expected failure rate of anticoagulation. While macrovascular thrombosis is common in these individuals, the frequent finding of extensive microvascular thromboses in several series and case reports, raises the possibility of thrombotic microangiopathy (TMA) as being a contributing factor in the thrombotic and multi-organ complications of the disease. If this is correct, rapidly identifying a TMA and treating the underlying pathophysiology may allow for better outcomes in these critically ill patients. To further explore this, we reviewed the published literature on COVID-19, looking for reports describing TMA-like presentations. We summarize our findings here along with a discussion about presentation, pathophysiology, and a suggested treatment algorithm.


Subject(s)
COVID-19 , Thrombosis , Thrombotic Microangiopathies , Complement Activation , Humans , SARS-CoV-2 , Thrombotic Microangiopathies/diagnosis
8.
Allergy ; 76(2): 483-496, 2021 02.
Article in English | MEDLINE | ID: covidwho-1140084

ABSTRACT

BACKGROUND: The impacts of chronic airway diseases on coronavirus disease 2019 (COVID-19) are far from understood. OBJECTIVE: To explore the influence of asthma and chronic obstructive pulmonary disease (COPD) comorbidity on disease expression and outcomes, and the potential underlying mechanisms in COVID-19 patients. METHODS: A total of 961 hospitalized COVID-19 patients with a definite clinical outcome (death or discharge) were retrospectively enrolled. Demographic and clinical information were extracted from the medical records. Lung tissue sections from patients suffering from lung cancer were used for immunohistochemistry study of angiotensin-converting enzyme II (ACE2) expression. BEAS-2B cell line was stimulated with various cytokines. RESULTS: In this cohort, 21 subjects (2.2%) had COPD and 22 (2.3%) had asthma. After adjusting for confounding factors, COPD patients had higher risk of developing severe illness (OR: 23.433; 95% CI 1.525-360.135; P < .01) and acute respiratory distress syndrome (OR: 19.762; 95% CI 1.461-267.369; P = .025) than asthmatics. COPD patients, particularly those with severe COVID-19, had lower counts of CD4+ T and CD8+ T cells and B cells and higher levels of TNF-α, IL-2 receptor, IL-10, IL-8, and IL-6 than asthmatics. COPD patients had increased, whereas asthmatics had decreased ACE2 protein expression in lower airways, compared with that in control subjects without asthma and COPD. IL-4 and IL-13 downregulated, but TNF-α, IL-12, and IL-17A upregulated ACE2 expression in BEAS-2B cells. CONCLUSION: Patients with asthma and COPD likely have different risk of severe COVID-19, which may be associated with different ACE2 expression.


Subject(s)
Asthma/epidemiology , COVID-19/complications , Pulmonary Disease, Chronic Obstructive/epidemiology , Aged , Angiotensin-Converting Enzyme 2/biosynthesis , Asthma/immunology , Asthma/metabolism , COVID-19/immunology , Comorbidity , Female , Humans , Male , Middle Aged , Prevalence , Pulmonary Disease, Chronic Obstructive/immunology , Pulmonary Disease, Chronic Obstructive/metabolism , SARS-CoV-2
9.
Int J Obes (Lond) ; 45(6): 1163-1169, 2021 06.
Article in English | MEDLINE | ID: covidwho-1137758

ABSTRACT

The COVID-19 pandemic has emerged as a public health crisis and has placed a significant burden on healthcare systems. Patients with underlying metabolic dysfunction, such as type 2 diabetes mellitus and obesity, are at a higher risk for COVID-19 complications, including multi-organ dysfunction, secondary to a deranged immune response, and cellular energy deprivation. These patients are at a baseline state of chronic inflammation associated with increased susceptibility to the severe immune manifestations of COVID-19, which are triggered by the cellular hypoxic environment and cytokine storm. The altered metabolic profile and energy generation of immune cells affect their activation, exacerbating the imbalanced immune response. Key immunometabolic interactions may inform the development of an efficacious treatment for COVID-19. Novel therapeutic approaches with repurposed drugs, such as PPAR agonists, or newly developed molecules such as the antagomirs, which block microRNA function, have shown promising results. Those treatments, alone or in combination, target both immune and metabolic pathways and are ideal for septic COVID-19 patients with an underlying metabolic condition.


Subject(s)
COVID-19 , Diabetes Mellitus, Type 2 , Obesity , Antiviral Agents/therapeutic use , COVID-19/drug therapy , COVID-19/immunology , COVID-19/metabolism , COVID-19/physiopathology , Cytokine Release Syndrome , Diabetes Mellitus, Type 2/complications , Diabetes Mellitus, Type 2/drug therapy , Diabetes Mellitus, Type 2/physiopathology , Humans , Hypoglycemic Agents/therapeutic use , Obesity/complications , Obesity/physiopathology , SARS-CoV-2
10.
Sci Immunol ; 6(56)2021 02 23.
Article in English | MEDLINE | ID: covidwho-1099742

ABSTRACT

Hyperinflammation contributes to lung injury and subsequent acute respiratory distress syndrome (ARDS) with high mortality in patients with severe coronavirus disease 2019 (COVID-19). To understand the underlying mechanisms involved in lung pathology, we investigated the role of the lung-specific immune response. We profiled immune cells in bronchoalveolar lavage fluid and blood collected from COVID-19 patients with severe disease and bacterial pneumonia patients not associated with viral infection. By tracking T cell clones across tissues, we identified clonally expanded tissue-resident memory-like Th17 cells (Trm17 cells) in the lungs even after viral clearance. These Trm17 cells were characterized by a a potentially pathogenic cytokine expression profile of IL17A and CSF2 (GM-CSF). Interactome analysis suggests that Trm17 cells can interact with lung macrophages and cytotoxic CD8+ T cells, which have been associated with disease severity and lung damage. High IL-17A and GM-CSF protein levels in the serum of COVID-19 patients were associated with a more severe clinical course. Collectively, our study suggests that pulmonary Trm17 cells are one potential orchestrator of the hyperinflammation in severe COVID-19.


Subject(s)
COVID-19/immunology , Granulocyte-Macrophage Colony-Stimulating Factor/metabolism , Immunologic Memory , Lung/immunology , Th17 Cells/metabolism , Bronchoalveolar Lavage Fluid/cytology , Bronchoalveolar Lavage Fluid/immunology , COVID-19/complications , COVID-19/pathology , Clone Cells , Humans , Inflammation/etiology , Inflammation/immunology , Lung/pathology , Myeloid Cells , Pneumonia, Bacterial/immunology , Th17 Cells/immunology
11.
Clin J Oncol Nurs ; 25(1): 23-26, 2021 02 01.
Article in English | MEDLINE | ID: covidwho-1080876

ABSTRACT

Febrile neutropenia, a serious complication of cytotoxic chemotherapy, is an oncologic emergency associated with high rates of morbidity and mortality. Fever is often the only clinical sign of an underlying infection in neutropenic patients with cancer. Prompt treatment with empiric broad-spectrum antibiotics is crucial to ensuring best outcomes for patients; practice guidelines recommend antibiotic administration within one hour of fever onset. A quality improvement initiative to improve time to antibiotic administration among patients with febrile neutropenia presenting to a community hospital emergency department is described in this article.


Subject(s)
Febrile Neutropenia , Neoplasms , Anti-Bacterial Agents/therapeutic use , Emergency Service, Hospital , Febrile Neutropenia/chemically induced , Febrile Neutropenia/drug therapy , Fever/drug therapy , Hospitals, Community , Humans , Neoplasms/complications , Neoplasms/drug therapy
12.
Eur J Med Res ; 26(1): 18, 2021 Feb 08.
Article in English | MEDLINE | ID: covidwho-1069594

ABSTRACT

BACKGROUND: Patients with severe COVID-19 have disorders of the respiratory, cardiovascular, coagulation, skeletal muscle, and central nervous systems. These systemic failures may be associated with cytokine release syndrome, characterized by hyperpyrexia, thrombocytopenia, hyperferritinemia, and the elevation of other inflammatory markers. Rhabdomyolysis with high fever is a complication that is rarely found in COVID-19. The exact relations of these clinical conditions in patients with COVID-19 remain unknown. CASE PRESENTATION: We present the case of a 36-year-old man with severe COVID-19 complicated by rhabdomyolysis and high fever. After admission, his condition continued to deteriorate, with a high body temperature. On day 9, the patient had elevated creatine kinase and myoglobin levels consistent with rhabdomyolysis (26,046 U/L and 3668 ng/mL, respectively). In addition to viral therapy, he was immediately treated with hydration. However, the patient had persistent fever and elevated creatine kinase levels. The patient was diagnosed with malignant hyperthermia as a late complication of COVID-19, although he had no hereditary predisposition to malignant hyperthermia or neuroleptic malignant syndrome. The administration of dantrolene with muscle relaxation and anti-inflammatory function showed potential efficacy for rhabdomyolysis, high fever, and increased plasma inflammatory markers. CONCLUSIONS: Malignant hyperthermia is triggered by not only anesthetic agents but also viral infections. A possible mechanism of malignant hyperthermia is hypersensitivity of calcium release from the sarcoplasmic reticulum. These include mutations in or the activation of the skeletal muscle ryanodine receptor calcium release channel. Dantrolene is a ryanodine receptor antagonist and is used as an anti-inflammatory agent. The administration of dantrolene showed potential efficacy for rhabdomyolysis, high body temperature due to inflammation, and increased inflammatory markers. The underlying mechanism of the association of rhabdomyolysis and high fever in COVID-19 might be similar to the pathogenesis of malignant hyperthermia.


Subject(s)
COVID-19/complications , Dantrolene/therapeutic use , Muscle Relaxants, Central/therapeutic use , Rhabdomyolysis/drug therapy , Rhabdomyolysis/virology , Adult , Humans , Male , Malignant Hyperthermia/complications , Malignant Hyperthermia/virology , SARS-CoV-2
13.
BMJ Case Rep ; 14(1)2021 Jan 18.
Article in English | MEDLINE | ID: covidwho-1066835

ABSTRACT

SARS-CoV-2 is the cause of COVID-19. Since the outbreak and rapid spread of COVID-19, it has been apparent that the disease is having multi-organ system involvement. Still its effect in the endocrine system is not fully clear and data on cortisol dynamics in patients with COVID-19 are not yet available. SARS-CoV-2 can knock down the host's cortisol stress response. Here we present a case of a 51-year-old man vomiting for 10 days after having confirmed COVID-19 infection. He had hypotension and significant hyponatraemia. Work-up was done including adrenocorticotropic hormone stimulation test. He was diagnosed as suffering from adrenal insufficiency and started on steroids with subsequent improvement in both blood pressure and sodium level. COVID-19 can cause adrenal insufficiency. Clinicians must be vigilant about the possibility of an underlying relative cortisol deficiency in patients with COVID-19.


Subject(s)
Adrenal Insufficiency/physiopathology , COVID-19/physiopathology , Hyponatremia/physiopathology , Hypotension/physiopathology , Acidosis/blood , Acidosis/physiopathology , Acidosis/therapy , Adrenal Insufficiency/blood , Adrenal Insufficiency/diagnosis , Adrenal Insufficiency/drug therapy , COVID-19/blood , Fluid Therapy , Glucocorticoids/therapeutic use , Humans , Hydrocortisone/blood , Hyponatremia/blood , Hyponatremia/therapy , Hypophosphatemia/blood , Hypophosphatemia/physiopathology , Hypophosphatemia/therapy , Hypotension/therapy , Male , Middle Aged , Pituitary-Adrenal Function Tests , Prednisolone/therapeutic use , SARS-CoV-2 , Vomiting/physiopathology , Water-Electrolyte Imbalance/blood , Water-Electrolyte Imbalance/physiopathology , Water-Electrolyte Imbalance/therapy
14.
Acad Radiol ; 28(5): 595-607, 2021 05.
Article in English | MEDLINE | ID: covidwho-1062192

ABSTRACT

BACKGROUND: COVID-19 commonly presents with upper respiratory symptoms; however, studies have shown that SARS-CoV-2 infection affects multiple organ systems. Here, we review the pathophysiology and imaging characteristics of SARS-CoV-2 infection in organ systems throughout the body and explore commonalities. OBJECTIVE: Familiarity with the underlying pathophysiology and imaging characteristics is essential for the radiologist to recognize these findings in patients with COVID-19 infection. Though pulmonary findings are the most prevalent presentation, COVID-19 may have multiple manifestations and recognition of the extrapulmonary manifestations is especially important because of the potential serious and long-term effects of COVID-19 on multiple organ systems.


Subject(s)
COVID-19 , Humans , Peptidyl-Dipeptidase A , SARS-CoV-2
15.
Infect Genet Evol ; 89: 104717, 2021 04.
Article in English | MEDLINE | ID: covidwho-1051857

ABSTRACT

BACKGROUND/OBJECTIVES: COVID-19 followed a mortal course in some young patients without any underlying factors, however, it followed a very benign course in some very older individuals with multiple comorbidities. These observations question if some genetic factors may be related to the vulnerability and poor prognosis of the disease. In this study, we aimed to investigate whether MBL2 gene B variant at codon 54 (rs1800450) were related to the variabilities in clinical course of this infection. METHODS: 284 PCR-confirmed COVID-19 patients and 100 healthy controls were included in the study. COVID-19 patients were subdivided according to the clinical features and clinical characteristics were analyzed. DNAs of all patients and controls were examined for the codon 54 A/B (gly54asp: rs1800450) variation in exon 1 of the MBL2 gene. RESULTS: In univariate analysis, BB genotype of MBL2 gene was more common among COVID-19 cases compared with controls (10.9% vs 1.0%, respectively; OR = 12.1, 95%CI = 1.6-90.1, p = 0.001). Multivariate analyses, adjusted for age, sex and MBL genetic variants, revealed that when compared with the COVID-19 patients that had AA genotype (reference), the patients that had BB or AB genotypes suffered from a higher risk for severe disease (for BB genotype, odds ratio (OR) = 5.3, p < 0.001; for AB genotype, OR = 2.9, p = 0.001) and for ICU need (for BB genotype, OR = 19.6, p < 0.001; for AB genotype, OR = 6.9, p = 0.001). On the other hand, there was not any significant difference between the genotype variants in terms of mortality at 28 days or development of secondary bacterial infection. CONCLUSION: The B variants of MBL2 gene at codon 54, which were associated with lower MBL2 levels, were related to a higher risk for a more severe clinical course of COVID-19 infection in some respects. Our findings may have potential future implications, e.g. for use of MBL protein as potential therapeutics or prioritize the individuals with B variants during vaccination strategies.


Subject(s)
COVID-19/genetics , COVID-19/pathology , Mannose-Binding Lectin/genetics , Mutation, Missense , Adult , Aged , Aged, 80 and over , COVID-19/virology , Case-Control Studies , Comorbidity , Female , Genetic Predisposition to Disease , Humans , Male , Mannose-Binding Lectin/metabolism , Middle Aged , Protein Interaction Maps , SARS-CoV-2/isolation & purification , Severity of Illness Index , Young Adult
16.
PLoS Biol ; 18(12): e3000963, 2020 12.
Article in English | MEDLINE | ID: covidwho-1040033

ABSTRACT

Approximately 28% of the human population have been exposed to Mycobacterium tuberculosis (MTB), with the overwhelming majority of infected individuals not developing disease (latent TB infection (LTBI)). While it is known that uncontrolled HIV infection is a major risk factor for the development of TB, the effect of underlying LTBI on HIV disease progression is less well characterized, in part because longitudinal data are lacking. We sorted all participants of the Swiss HIV Cohort Study (SHCS) with at least 1 documented MTB test into one of the 3 groups: MTB uninfected, LTBI, or active TB. To detect differences in the HIV set point viral load (SPVL), linear regression was used; the frequency of the most common opportunistic infections (OIs) in the SHCS between MTB uninfected patients, patients with LTBI, and patients with active TB were compared using logistic regression and time-to-event analyses. In adjusted models, we corrected for baseline demographic characteristics, i.e., HIV transmission risk group and gender, geographic region, year of HIV diagnosis, and CD4 nadir. A total of 13,943 SHCS patients had at least 1 MTB test documented, of whom 840 (6.0%) had LTBI and 770 (5.5%) developed active TB. Compared to MTB uninfected patients, LTBI was associated with a 0.24 decreased log HIV SPVL in the adjusted model (p < 0.0001). Patients with LTBI had lower odds of having candida stomatitis (adjusted odds ratio (OR) = 0.68, p = 0.0035) and oral hairy leukoplakia (adjusted OR = 0.67, p = 0.033) when compared to MTB uninfected patients. The association of LTBI with a reduced HIV set point virus load and fewer unrelated infections in HIV/TB coinfected patients suggests a more complex interaction between LTBI and HIV than previously assumed.


Subject(s)
HIV Infections/complications , Latent Tuberculosis/complications , Latent Tuberculosis/diagnosis , AIDS-Related Opportunistic Infections/complications , AIDS-Related Opportunistic Infections/etiology , AIDS-Related Opportunistic Infections/microbiology , Adult , CD4-Positive T-Lymphocytes , Cohort Studies , Disease Progression , Female , HIV Infections/metabolism , HIV-1/pathogenicity , Humans , Interferon-gamma , Latent Tuberculosis/metabolism , Male , Middle Aged , Mycobacterium tuberculosis/pathogenicity , Opportunistic Infections/complications , Risk , Tuberculosis/complications , Tuberculosis/diagnosis , Viral Load/immunology
17.
Thromb Res ; 200: 1-8, 2021 04.
Article in English | MEDLINE | ID: covidwho-1032457

ABSTRACT

BACKGROUND: The novel coronavirus SARS-CoV-2, responsible for the 2019-2020 global (COVID-19) pandemic, is a respiratory virus associated with the development of thromboembolic complications and respiratory failure in severe cases. Increased risk of pulmonary embolism and thrombosis has been identified in COVID-19 patients, alongside accompanying elevations in potential prognostic biomarkers, including D-dimer, IL-6 and cardiac specific troponins. Our aim was to provide a scoping review of the available literature regarding thrombosis risk, other cardiovascular implications, and their biomarkers in COVID-19 to highlight potential disease mechanisms. METHODS: Authors conducted a literature search in PubMed using MeSH headings "disseminated intravascular coagulation", "pulmonary embolism", "thromb*", "stroke", "myocardial infarction" and "acute lung injury", as well as terms "COVID-19", "SARS-CoV-2", "2019 novel coronavirus" and "2019-nCoV". RESULTS AND CONCLUSIONS: COVID-19 disease is characterised by the interactions between hyperactive coagulation and complement systems - induced by hyper-inflammatory conditions, resulting in a pro-thrombotic state and diffuse tissue injury. There are several promising prognostic markers of disease severity, with D-dimer the most significant. The presence of thrombocytopenia appears to be a key indicator of patient deterioration. Further research is required to understand the underlying pathophysiology in COVID-19 and its implications in disease progression and patient management. Randomised trials are urgently needed to determine the safety of proposed therapeutic anticoagulation with heparin and the role for anti-platelet agents, such as Ticagrelor, in patient management.


Subject(s)
COVID-19/complications , Thromboembolism/virology , Thrombosis/virology , Biomarkers , Humans , Thrombocytopenia/virology
18.
Neurology ; 96(2): e294-e300, 2021 01 12.
Article in English | MEDLINE | ID: covidwho-1028474

ABSTRACT

OBJECTIVE: To explore whether hospitalized patients with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and neurologic symptoms have evidence of CNS infection, inflammation, and injury using CSF biomarker measurements. METHODS: We assessed CSF SARS-CoV-2 RNA along with CSF biomarkers of intrathecal inflammation (CSF white blood cell count, neopterin, ß2-microglobulin, and immunoglobulin G index), blood-brain barrier integrity (albumin ratio), and axonal injury (CSF neurofilament light chain protein [NfL]) in 6 patients with moderate to severe coronavirus disease 2019 (COVID-19) and neurologic symptoms who had undergone a diagnostic lumbar puncture. Neurologic symptoms and signs included features of encephalopathies (4 of 6), suspected meningitis (1 of 6), and dysgeusia (1 of 6). SARS-CoV-2 infection was confirmed by real-time PCR analysis of nasopharyngeal swabs. RESULTS: SARS-CoV-2 RNA was detected in the plasma of 2 patients (cycle threshold [Ct] value 35.0-37.0) and in CSF at low levels (Ct 37.2, 38.0, 39.0) in 3 patients in 1 but not in a second real-time PCR assay. CSF neopterin (median 43.0 nmol/L) and ß2-microglobulin (median 3.1 mg/L) were increased in all. Median immunoglobulin G index (0.39), albumin ratio (5.35), and CSF white blood cell count (<3 cells/µL) were normal in all, while CSF NfL was elevated in 2 patients. CONCLUSION: Our results in patients with COVID-19 and neurologic symptoms suggest an unusual pattern of marked CSF inflammation in which soluble markers were increased but white cell response and other immunologic features typical of CNS viral infections were absent. While our initial hypothesis centered on CNS SARS-CoV-2 invasion, we could not convincingly detect SARS-CoV-2 as the underlying driver of CNS inflammation. These features distinguish COVID-19 CSF from other viral CNS infections and raise fundamental questions about the CNS pathobiology of SARS-CoV-2 infection.


Subject(s)
COVID-19/cerebrospinal fluid , COVID-19/complications , Nervous System Diseases/cerebrospinal fluid , Nervous System Diseases/etiology , SARS-CoV-2/isolation & purification , Adult , Aged , Aged, 80 and over , Biomarkers/cerebrospinal fluid , Blood-Brain Barrier/diagnostic imaging , Blood-Brain Barrier/metabolism , COVID-19/diagnostic imaging , Female , Humans , Male , Middle Aged , Nervous System Diseases/diagnostic imaging
19.
J Integr Med ; 19(3): 226-231, 2021 05.
Article in English | MEDLINE | ID: covidwho-1026228

ABSTRACT

OBJECTIVE: To observe the early interventions of traditional Chinese Medicine (TCM) on the conversion time of nucleic acid in patients with coronavirus disease 2019 (COVID-19), and find possible underlying mechanisms of action. METHODS: A retrospective cohort study was conducted on 300 confirmed COVID-19 patients who were treated with TCM, at a designated hospital in China. The patients were categorized into three groups: TCM1, TCM2 and TCM3, who respectively received TCM interventions within 7, 8-14, and greater than 15 days of hospitalization. Different indicators such as the conversion time of pharyngeal swab nucleic acid, the conversion time of fecal nucleic acid, length of hospital stay, and inflammatory markers (leukocyte count, and lymphocyte count and percentage) were analyzed to observe the impact of early TCM interventions on these groups. RESULTS: The median conversion times of pharyngeal swab nucleic acid in the three groups were 5.5, 7 and 16 d (P < 0.001), with TCM1 and TCM2 being statistically different from TCM3 (P < 0.01). TCM1 (P < 0.05) and TCM3 (P < 0.01) were statistically different from TCM2. The median conversion times of fecal nucleic acid in the three groups were 7, 9 and 17 d (P < 0.001). Conversion times of fecal nucleic acid in TCM1 were statistically different from TCM3 and TCM2 (P < 0.01). The median lengths of hospital stay in the three groups were 13, 16 and 21 d (P < 0.001). TCM1 and TCM2 were statistically different from TCM3 (P < 0.01); TCM1 and TCM3 were statistically different from TCM2 (P < 0.01). Both leucocyte and lymphocyte counts increased gradually with an increase in the length of hospital stay in TCM1 group patients, with a statistically significant difference observed at each time point in the group (P < 0.001). Statistically significant differences in lymphocyte count and percentage in TCM2 (P < 0.001), and in leucocyte count (P = 0.043) and lymphocyte count (P = 0.038) in TCM3 were observed. The comparison among the three groups showed a statistically significant difference in lymphocyte percentage on the third day of admission (P = 0.044). CONCLUSION: In this study, it was observed that in COVID-19 patients treated with a combination of Chinese and Western medicines, TCM intervention earlier in the hospital stay correlated with faster conversion time of pharyngeal swab and fecal nucleic acid, as well as shorter length of hospital stay, thus helping promote faster recovery of the patient. The underlying mechanism of action may be related to improving inflammation in patients with COVID-19.


Subject(s)
COVID-19/drug therapy , Medicine, Chinese Traditional , SARS-CoV-2 , Adult , Aged , Female , Humans , Length of Stay , Male , Middle Aged , Retrospective Studies
20.
Front Cardiovasc Med ; 7: 568720, 2020.
Article in English | MEDLINE | ID: covidwho-993345

ABSTRACT

Overlapping commonalities between coronavirus disease of 2019 (COVID-19) and cardio-oncology regarding cardiovascular toxicities (CVT), pathophysiology, and pharmacology are special topics emerging during the pandemic. In this perspective, we consider an array of CVT common to both COVID-19 and cardio-oncology, including cardiomyopathy, ischemia, conduction abnormalities, myopericarditis, and right ventricular (RV) failure. We also emphasize the higher risk of severe COVID-19 illness in patients with cardiovascular disease (CVD) or its risk factors or cancer. We explore commonalities in the underlying pathophysiology observed in COVID-19 and cardio-oncology, including inflammation, cytokine release, the renin-angiotensin-aldosterone-system, coagulopathy, microthrombosis, and endothelial dysfunction. In addition, we examine common pharmacologic management strategies that have been elucidated for CVT from COVID-19 and various cancer therapies. The use of corticosteroids, as well as antibodies and inhibitors of various molecules mediating inflammation and cytokine release syndrome, are discussed. The impact of angiotensin converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) is also addressed, since these drugs are used in cardio-oncology and have received considerable attention during the COVID-19 pandemic, since the culprit virus enters human cells via the angiotensin converting enzyme 2 (ACE2) receptor. There are therefore several areas of overlap, similarity, and interaction in the toxicity, pathophysiology, and pharmacology profiles in COVID-19 and cardio-oncology syndromes. Learning more about either will likely provide some level of insight into both. We discuss each of these topics in this viewpoint, as well as what we foresee as evolving future directions to consider in cardio-oncology during the pandemic and beyond. Finally, we highlight commonalities in health disparities in COVID-19 and cardio-oncology and encourage continued development and implementation of innovative solutions to improve equity in health and healing.

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