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1.
Estima (Online) ; 19(1): e0521, jan.-dez. 2021.
Artigo em Português | BDENF - Enfermagem | ID: biblio-1178332

RESUMO

Objetivo:relatar o caso de um paciente crítico com COVID-19 e mostrar os principais achados relacionados à lesão considerada Acute skin failure (ASF), bem como realizar seu diagnóstico diferencial com lesão por pressão (LP) evitável. Método: estudo observacional do tipo relato de caso, desenvolvido em um hospital de São Paulo, na unidade de terapia intensiva (UTI) exclusiva a pessoas diagnosticadas com COVID-19. Os dados foram coletados de um único paciente, entre os meses de março e setembro de 2020. Resultados: paciente com complicações da COVID-19 evoluiu com lesão de pele, inicialmente definida como LP e posteriormente reclassificada como ASF. Os seguintes achados corroboraram o diagnóstico: ventilação mecânica invasiva prolongada, insuficiências respiratória, renal e cardíaca e sepse de foco respiratório. Além disso, outros fatores agravantes, como o uso de droga vasoativa, instabilidade hemodinâmica com intolerância ao mínimo reposicionamento, jejum prolongado e coagulopatia intravascular disseminada associada à infecção pelo coronavírus. Conclusão: o relato mostra que existem dificuldades para o diagnóstico diferencial entre ASF e LP na prática clínica. Trata-se de conceito novo, sendo fundamental que o profissional de saúde reconheça os principais fatores associados ao aparecimento da ASF, muitos dos quais também estão relacionados ao desenvolvimento das LP, ressaltando a necessidade de análise individualizada dessas lesões, e garantia da implementação de intervenções adequadas para prevenção e tratamento.


Assuntos
Infecções por Coronavirus , Lesão por Pressão , Unidades de Terapia Intensiva , Cuidados de Enfermagem
3.
Preprint | bioRxiv | ID: ppbiorxiv-447287

RESUMO

Numerous studies have provided single-cell transcriptome profiles of host responses to SARS-CoV-2 infection. Critically lacking however is a datamine that allows users to compare and explore cell profiles to gain insights and develop new hypotheses. To accomplish this, we harmonized datasets from COVID-19 and other control condition blood, bronchoalveolar lavage, and tissue samples, and derived a compendium of gene signature modules per cell type, subtype, clinical condition, and compartment. We demonstrate approaches to probe these via a new interactive web portal (http://toppcell.cchmc.org/ COVID-19). As examples, we develop three hypotheses: (1) a multicellular signaling cascade among alternatively differentiated monocyte-derived macrophages whose tasks include T cell recruitment and activation; (2) novel platelet subtypes with drastically modulated expression of genes responsible for adhesion, coagulation and thrombosis; and (3) a multilineage cell activator network able to drive extrafollicular B maturation via an ensemble of genes strongly associated with risk for developing post-viral autoimmunity.

4.
Preprint | bioRxiv | ID: ppbiorxiv-448642

RESUMO

Overshooting immune reactions can occur during inflammatory responses that accompany severe infections, such as COVID-19. Cytokines, damage-associated molecular patterns (DAMPs), and reactive oxygen and nitrogen species can generate positive feedback loops of inflammation, leading to long-term complications such as vascular endothelialitis, thrombosis, endothelial dysfunction, neurological impairments, and chronic fatigue. Dexamethasone can limit inflammation by inhibiting the activation of pro-inflammatory transcription factors. High dose dexamethasone, however, has undesirable side effects. Here, we show that Ceylon cinnamon and its major compound cinnamaldehyde can mitigate inflammatory signaling in vitro. Cinnamaldehyde interferes with the dimerization of toll-like receptor 4 (TLR4), which can be activated by DAMPs like HSP60 and HMGB1. Our results suggest that supplementary treatment with Ceylon cinnamon may allow administration of lower doses of dexamethasone to avoid high dose steroid side effects. Moreover, preliminary results indicate that Ceylon cinnamon modulates angiogenesis, which is a reactive phenomenon in COVID-19.

5.
Preprint | bioRxiv | ID: ppbiorxiv-448358

RESUMO

Formalin-fixed paraffin-embedded (FFPE) human tissues represent the world's largest collection of accessible clinical specimens with matched, well-annotated clinical course for disease progression. Currently, FFPE sections are limited to low throughput histo- and immunological assessments. Extracting largescale molecular information remains a major technological barrier to uncover the vast potential within FFPE specimens for translation and clinical research. Two critical but understudied facets of glucose metabolism are anabolic pathways for glycogen and N-linked glycan biosynthesis. Together, these complex carbohydrates represent bioenergetics, protein-structure function, and tissue architecture in human biology. Herein, we report the high-dimensional Metabolomics-Assisted Digital pathology Imaging (Madi) workflow that combines matrix-assisted laser desorption ionization mass spectrometry imaging (MALDI-MSI) with machine learning for the comprehensive assessment of tissue heterogeneity, histopathology, and metabolism in human FFPE sections. In normal human tissue sections, Madi accurately identifies anatomical regions within liver and the brain. In human lung diseases, Madi accurately predicts major lung pathologies such as honeycomb change, late-stage fibrosis, diffuse alveolar damage (DAD), and acute fibrinous and organizing pneumonia (AFOP) from idiopathic pulmonary fibrosis (IPF) and COVID-19 pneumonia specimens with precision. In depth pathway enrichment analyses reveal unique metabolic pathways are associated with distinct pathological regions, which highlight aberrant complex carbohydrate metabolism as a previously unknown molecular event associated with disease progression that could hold key to future therapeutic interventions.

6.
Preprint | bioRxiv | ID: ppbiorxiv-446676

RESUMO

SARS-CoV-2 infection during pregnancy leads to an increased risk of adverse pregnancy outcomes. Although the placenta itself can be a target of virus infection, most neonates are virus free and are born healthy or recover quickly. Here, we investigated the impact of SARS-CoV-2 infection on the placenta from a cohort of women who were infected late during pregnancy and had tested nasal swab positive for SARS-CoV-2 by qRT-PCR at delivery. SARS-CoV-2 genomic and subgenomic RNA was detected in 23 out of 54 placentas. Two placentas with high virus content were obtained from mothers who presented with severe COVID-19 and whose pregnancies resulted in adverse outcomes for the fetuses, including intrauterine fetal demise and a preterm delivered baby still in newborn intensive care. Examination of the placental samples with high virus content showed efficient SARS-CoV-2 infection, using RNA in situ hybridization to detect genomic and replicating viral RNA, and immunohistochemistry to detect SARS-CoV-2 nucleocapsid protein. Infection was restricted to syncytiotrophoblast cells that envelope the fetal chorionic villi and are in direct contact with maternal blood. The infected placentas displayed massive infiltration of maternal immune cells including macrophages into intervillous spaces, potentially contributing to inflammation of the tissue. Ex vivo infection of placental cultures with SARS-CoV-2 or with SARS-CoV-2 spike (S) protein pseudotyped lentivirus targeted mostly syncytiotrophoblast and in rare events endothelial cells. Infection was reduced by using blocking antibodies against ACE2 and against Neuropilin 1, suggesting that SARS-CoV-2 may utilize alternative receptors for entry into placental cells.

7.
Preprint | medRxiv | ID: ppmedrxiv-21258558

RESUMO

On April 13, 2021 the Centers for Disease Control and Prevention (CDC) and Food and Drug Administration (FDA) recommended in a pause in use of the Johnson & Johnson (J&J)-Janssen COVID-19 vaccine due to reports of cerebral venous sinus thrombosis (CVST) in recently vaccinated individuals. The announcement of the pause required development of a coordinated communication strategy under extreme time pressure and careful messaging by stakeholders to mitigate reduced public confidence in COVID-19 vaccines, as was observed following the temporary suspension of the Oxford-AstraZeneca vaccine in many countries. In this survey study, we evaluated understanding and impressions of the CDCs public online information about the J&J-Janssen pause among unvaccinated US adults.

8.
Preprint | medRxiv | ID: ppmedrxiv-21258423

RESUMO

BackgroundCOVID-19 myocarditis is becoming increasingly appreciated as a complication of COVID-19. There are significant hurdles to formal diagnosis with endomyocardial biopsy or cardiac MRI whether by resource limitations, patient instability, or isolation precautions. Therefore, further exploratory analysis is needed to clinically define the characteristics and spectrum of severity of COVID-19 myocarditis. ObjectivesThe aim of this study was to describe the clinical course, echocardiographic, and laboratory testing across suspected fulminant and non-fulminant clinically defined COVID-19 myocarditis. MethodsIn a cross-sectional observational study of 19 patients with clinically defined COVID-19 myocarditis, we report presenting symptoms, clinical course, laboratory findings, and echocardiographic results stratified by non-fulminant and fulminant myocarditis. Student t-test and univariate logistic regression are used to compare laboratory findings across fulminant and non-fulminant cases. FindingsAmong 19 patients, there was no prior history of coronary artery disease, atrial fibrillation, or heart failure; 21.1% of patients died; and 78.9% of cases required supplemental oxygen. A significantly higher geometric mean D-dimer and ferritin were observed in patients with fulminant compared to non-fulminant suspected myocarditis. 26.3% of cases had pericardial effusions. 10 out of the 16 with available echocardiographic data had normal left ventricular systolic function. ConclusionsIn this cross-sectional analysis, we provide a practical clinical depiction of patients with clinical COVID-19 myocarditis across fulminant and non-fulminant cases. Statistically significant elevations in inflammatory markers in fulminant versus non-fulminant cases generate hypothesis regarding the role of systemic inflammation in driving severity of COVID-19 myocarditis.

9.
Preprint | medRxiv | ID: ppmedrxiv-21258355

RESUMO

BackgroundThe COVID-19 pandemic adversely affected the socially vulnerable and minority communities in the U.S. initially, but the temporal trends during the year-long pandemic remain unknown. ObjectiveWe examined the temporal association between the county-level Social Vulnerability Index (SVI), a percentile-based measure of social vulnerability to disasters, its subcomponents and race/ethnic composition with COVID-19 incidence and mortality in the U.S. in the year starting in March 2020. MethodsCounties (n=3091) with [≥] 50 COVID-19 cases by March 6th, 2021 were included in the study. Associations between SVI (and its subcomponents) and county level racial composition with the incidence and death per capita were assessed by fitting a negative-binomial mixed-effects model. This model was also used to examine potential time varying associations between weekly number of cases/deaths and SVI or racial composition. Data was adjusted for percentage of population aged [≥]65 years, state level testing rate, comorbidities using the average Hierarchical Condition Category (HCC) score, and environmental factors including average fine particulate matter (PM2.5), temperature and precipitation. ResultsHigher SVI, indicative of greater social vulnerability, was independently associated with higher COVID-19 incidence (adjusted incidence rate ratio [IRR] per-10 percentile increase:1.02, (95% CI 1.02, 1.03, p<0.001), and death per capita (1.04, (95% CI 1.04, 1.05, p<0.001). SVI became an independent predictor of incidence starting from March 2020, but this association became weak or insignificant by the winter, a period that coincided with a sharp increase in infection rates and mortality, and when counties with higher proportion of White residents were disproportionately represented ("third wave"). By Spring of 2021, SVI was again a predictor of COVID-19 outcomes. Counties with greater proportion of Black residents also observed similar temporal trends COVID-19-related adverse outcomes. Counties with greater proportion of Hispanic residents had worse outcomes throughout the duration of the analysis. ConclusionExcept for the winter "third wave" when majority White communities had the highest incidence of cases, counties with greater social vulnerability and proportionately higher minority populations, experienced worse COVID-19 outcomes. Article Summary/Strengths & LimitationsO_LIExamined full 12 months of county-level data in the US delineating the temporal trends in the association between social vulnerability index and COVID-19 outcomes C_LIO_LIInvestigated COVID-19 outcomes in predominantly Black and Hispanic communities in comparison to White communities in the US C_LIO_LIAnalysis is ecological, descriptive, and on the county-level rather than on an individual level C_LIO_LIAnalysis adjusted for confounders including county level age [≥] 65, comorbidities, and environmental factors C_LIO_LIAnalysis limited to the US C_LI

10.
Preprint | medRxiv | ID: ppmedrxiv-21258312

RESUMO

Background and AimsIn patients with chronic liver diseases (CLD) with or without cirrhosis, existing data on the risk of adverse outcomes with SARS-CoV-2 infection have been mixed or have limited generalizability. We used the National COVID Cohort Collaborative (N3C) Data Enclave, a harmonized electronic health record (EHR) dataset of 5.9 million nationally-representative, diverse, and gender-balanced patients, to describe outcomes in patients with CLD and cirrhosis with SARS-CoV-2. MethodsWe identified all chronic liver diseases patients with and without cirrhosis who had SARS-CoV-2 testing documented in the N3C Data Enclave as of data release date 5/15/2021. The primary outcome was 30-day all-cause mortality. Survival analysis methods were used to estimate cumulative incidences of death, hospitalization, and mechanical ventilation, and to calculate the associations of SARS-CoV-2 infection, presence of cirrhosis, and demographic and clinical factors to 30-day mortality. ResultsWe isolated 217,143 patients with CLD: 129,097 (59%) without cirrhosis and SARS-CoV-2 negative, 25,844 (12%) without cirrhosis and SARS-CoV-2 positive, 54,065 (25%) with cirrhosis and SARS-CoV-2 negative, and 8,137 (4%) with cirrhosis and SARS-CoV-2 positive. Among CLD patients without cirrhosis, 30-day all-cause mortality rates were 0.4% in SARS-CoV-2 negative patients and 1.8% in positive patients. Among CLD patients with cirrhosis, 30-day all-cause mortality rates were 4.0% in SARS-CoV-2 negative patients and 9.7% in positive patients. Compared to those who tested SARS-CoV-2 negative, SARS-CoV-2 positivity was associated with more than two-fold (aHR 2.43, 95% CI 2.23-2.64) hazard of death at 30 days among patients with cirrhosis. Compared to patients without cirrhosis, the presence of cirrhosis was associated with a three-fold (aHR 3.39, 95% CI 2.96-3.89) hazard of death at 30 days among patients who tested SARS-CoV-2 positive. Age (aHR 1.03 per year, 95% CI 1.03-1.04) was associated with death at 30 days among patients with cirrhosis who were SARS-CoV-2 positive. ConclusionsIn this study of nearly 220,000 CLD patients, we found SARS-CoV-2 infection in patients with cirrhosis was associated with 2.43-times mortality hazard, and the presence of cirrhosis among CLD patients infected with SARS-CoV-2 were associated with 3.39-times mortality hazard. Compared to previous studies, our use of a nationally-representative, diverse, and gender-balanced dataset enables wide generalizability of these findings.

11.
Preprint | medRxiv | ID: ppmedrxiv-21258862

RESUMO

IntroductionTwo waves of COVID-19 cases have overwhelmed most European countries during 2020. It is unclear if the incidence of acute kidney injury (AKI) has changed during the COVID-19 outbreaks. This study aims to evaluate the differences in incidence, risk factors and outcome of AKI in patients with SARS-CoV-2 infection during the first and second wave of COVID-19. MethodWe reviewed the health medical records of 792 consecutive patients with COVID-19 hospitalized at the University Hospital of Modena, Italy, from February 25 to December 14, 2020. ResultsAKI was diagnosed in 122 (15.4%) patients. Incidence of AKI remained steady rate during wave-1 (15.9%) and wave-2 (14.7%) (P=0.89). AKI patients were older (P=<0.001) and had a more severe respiratory impairment (PO2/FO2) (P=[≤]0.001) than their non-AKI counterparts. AKI led to a longer hospital stay (P=0.001), complicated with a higher rate of ICU admission. COVID-19-related AKI was associate with 59.7% of deaths during wave-1 and 70.6% during wave-2. At the end of the period of observation, 24% (wave-1) and 46.7% (wave-2) of survivors were discharged with a not fully recovered kidney function. Risk factors for AKI in patients with COVID-19 were diuretics (HR=5.3; 95%CI, 1.2-23.3; P=0.025) and cardiovascular disease (HR, 2.23; 95%CI, 1.05-5.1; P=0.036). ConclusionThe incidence of AKI (about 15%) remained unchanged during 2020, regardless of the trend of COVID-19. AKI occurred in patients with severe COVID-19 symptoms and was associated with a higher incidence of deaths than non-AKI patients. The risk factors of COVID-19-related AKI were diuretic therapy and cardiovascular disease.

12.
Preprint | medRxiv | ID: ppmedrxiv-21258172

RESUMO

Cerebral venous thrombosis was reported as a rare but serious adverse event in young and middle-aged vaccinees following immunization with AstraZenecas ChAdOx1-nCov-19 vaccine. As a consequence, several European governments recommended using this vaccine only in individuals older than 60 years leaving millions of ChAd primed individuals with the decision to either receive a second shot of ChAd or a heterologous boost with mRNA-based vaccines. However, such combinations have not been tested so far. We used Hannover Medical Schools COVID-19 Contact (CoCo) Study cohort of health care professionals (HCP) to monitor ChAd primed immune responses before and three weeks after booster with ChAd or BioNTech/Pfizers BNT162b2. Whilst both vaccines boosted prime-induced immunity, BNT induced significantly higher frequencies of Spike-specific CD4 and CD8 T cells and, in particular, high titers of neutralizing antibodies against the B.1.1.7, B.1.351 and the P.1 variants of concern of severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2).

13.
Preprint | medRxiv | ID: ppmedrxiv-21257656

RESUMO

The incidence of acute kidney injury (AKI) in hospitalized patients with coronavirus disease 2019 (COVID-19) is variable, being associated with worse outcomes. The objectives of the study were to evaluate the incidence, risk factors and impact of AKI in subjects hospitalized for COVID-19 in two third- level hospitals in Cordoba, Argentina. A retrospective cohort study was conducted. 448 adults who were consecutively hospitalized for COVID-19 between March and the end of October 2020 at Hospital Privado Universitario de Cordoba and Hospital Raul Angel Ferreyra were included. The incidence of AKI was 19% (n = 85). 50.6% presented AKI stage 1 (n=43), 20% stage 2 (n=17) and 29.4% stage 3 (n=25, of which 18 required renal replacement therapy). In the multivariate analysis, the variables that were independently associated with AKI were: age (adjusted Odd ratio -aOR- =1.30, 95%CI=1.04-1.63, p=0.022), history of chronic kidney disease (aOR=9.92, 95%CI=4.52-21.77, p<0.001), blood neutrophil count at admission (aOR=1.09, 95%CI=1.01-1.18, p=0.037) and requirement for mechanical ventilation (MV) (aOR=6.69, 95%CI=2.24-19.9, p=0.001). AKI was associated with longer hospitalization, greater admission and length of stay in the intensive care unit, a positive association with bacterial superinfection, sepsis, respiratory distress syndrome, MV requirement and mortality (mortality with AKI=47.1% vs without AKI=12.4%, p<0.001). AKI was independently associated with higher mortality (aOR=3.32, 95%CI=1.6-6.9, p=0.001). In conclusion, the incidence of AKI in adults hospitalized for COVID-19 was 19% and had a clear impact on morbidity and mortality. Local predisposing factors for AKI were identified.

14.
Artigo em Inglês | MEDLINE | ID: mdl-34097193

RESUMO

Patients with COVID-19 present a wide spectrum of disease severity, from asymptomatic cases in the majority to serious disease leading to critical care and even death. Clinically, four different scenarios occur within the typical disease timeline: first, an incubation and asymptomatic period; second, a stage with mild symptoms due mainly to the virus itself; third, in up to 20% of the patients, a stage with severe symptoms where a hyperinflammatory response with a cytokine storm driven by host immunity induces acute respiratory distress syndrome; and finally, a post-acute sequelae (PASC) phase, which present symptoms that can range from mild or annoying to actually quite incapacitating. Although the most common manifestation is acute respiratory failure of the lungs, other organs are also frequently involved. The clinical manifestations of the COVID-19 infection support a key role for endothelial dysfunction in the pathobiology of this condition. The virus enters into the organism via its interaction with angiotensin-converting enzyme 2-receptor that is present prominently in the alveoli, but also in endothelial cells, which can be directly infected by the virus. Cytokine release syndrome can also drive endothelial damage independently. Consequently, a distinctive feature of SARS-CoV-2 infection is vascular harm, with severe endothelial injury, widespread thrombosis, microangiopathy, and neo-angiogenesis in response to endothelial damage. Therefore, endothelial dysfunction seems to be the pathophysiological substrate for severe COVID-19 complications. Biomarkers of endothelial injury could constitute strong indicators of disease progression and severity. In addition, the endothelium could represent a very attractive target to both prevent and treat these complications. To establish an adequate therapy, the underlying pathophysiology and corresponding clinical stage should be clearly identified. In this review, the clinical features of COVID-19, the central role of the endothelium in COVID-19 and in other pathologies, and the potential of specific therapies aimed at protecting the endothelium in COVID-19 patients are addressed.

15.
Chest ; 159(6): e361-e364, 2021 06.
Artigo em Inglês | MEDLINE | ID: mdl-34099150

RESUMO

Research on COVID-19, the cause of a rapidly worsening pandemic, has led to the observation of laboratory derangements such as a propensity towards a hypercoagulable state. However, there are currently no reports on the incidence of pulmonary venous thrombosis in the setting of COVID-19. We report a case in which follow-up chest CT scans revealed an expansile filling defect in a branch of the right inferior pulmonary vein, which is consistent with pulmonary venous thrombosis. Our objective was to provide insight into an uncommon sequela of COVID-19 and consequently garner increased clinical suspicion for pulmonary VTE during hospitalization.

16.
Rheumatol Int ; 2021 Jun 07.
Artigo em Inglês | MEDLINE | ID: mdl-34100115

RESUMO

Antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) are systemic autoimmune diseases that may lead to renal failure due to the infiltration of mononuclear cells and the destruction of small- and medium-sized blood vessels. It has been shown that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) may trigger the presentation or exacerbation of autoimmune diseases. Crescentic glomerulonephritis (GN) has rarely been reported in patients with Coronavirus disease-2019 (COVID-19). We present rare two cases with AAV after a recent diagnosis of COVID-19. The first case was 26-year-old male patient, who was presented with acute kidney injury after COVID-19. Serum creatinine increased and active urine sediment was seen. Serological evaluation showed anti-myeloperoxidase antibody was at a level of 80.6 U/mL. Kidney biopsy showed necrotizing GN with cellular crescents. Methylprednisolone, cyclophosphamide and plasma exchange were administered. He was discharged with hemodialysis. Second case was a 36-year-old female who was hospitalized because of fever, cough and dyspnea. After she was diagnosed with COVID-19, she had total hearing loss, with cavitary lesions on bilateral lung parenchyma and an acute kidney injury. Serological evaluation showed an elevated anti-proteinase-3 with a level of 1:32. Kidney biopsy showed necrotizing GN with cellular crescents. Renal function improved after methylprednisolone and cyclophosphamide treatment. With a systematic review of the literature, we found four cases of new-onset AAV due to COVID-19. Herein, we discuss two cases and provide a literature review on cases of new-onset pauci-immune GN after COVID-19 infection.

17.
J Gen Intern Med ; 2021 Jun 07.
Artigo em Inglês | MEDLINE | ID: mdl-34100227

RESUMO

BACKGROUND: Black individuals have been disproportionately affected by the coronavirus disease 2019 (COVID-19). However, it remains unclear whether there are any biological factors that predispose Black patients to COVID-19-related morbidity and mortality. OBJECTIVE: To compare in-hospital morbidity, mortality, and inflammatory marker levels between Black and White hospitalized COVID-19 patients. DESIGN AND PARTICIPANTS: This single-center retrospective cohort study analyzed data for Black and White patients aged ≥18 years hospitalized with a positive SARS-CoV-2 PCR test between March 1, 2020, and August 4, 2020. MAIN MEASURES: The exposure was self-identified race documented in the medical record. The primary outcome of was in-hospital death. Secondary outcomes included intensive care unit admission, hospital morbidities, and inflammatory marker levels. KEY RESULTS: A total of 1,424 Black and White patients were identified. The mean ± SD age was 56.1 ± 17.4 years, and 663 (44.5%) were female. There were 683 (48.0%) Black and 741 (52.0%) White patients. In the univariate analysis, Black patients had longer hospital stays (8.1 ± 10.2 vs. 6.7 ± 8.3 days, p = 0.011) and tended to have higher rates of in-hospital death (11.0% vs. 7.3%), myocardial infarction (6.9% vs. 4.5%), pulmonary embolism (PE; 5.0% vs. 2.3%), and acute kidney injury (AKI; 39.4% vs. 23.1%) than White patients (p <0.05). However, after adjusting for potential confounders, only PE (adjusted odds ratio [aOR] 2.07, 95% CI, 1.13-3.79) and AKI (aOR 2.16, 95% CI, 1.57-2.97) were statistically significantly associated with Black race. In comparison with White patients, Black patients had statistically significantly higher peak plasma D-dimer (standardized ß = 0.10), erythrocyte sedimentation rate (standardized ß = 0.13), ferritin (standardized ß = 0.09), and lactate dehydrogenase (standardized ß = 0.11), after adjusting for potential confounders (p<0.05). CONCLUSIONS: Black hospitalized COVID-19 patients had increased risks of developing PE and AKI and higher inflammatory marker levels compared with White patients. This observation may be explained by differences in the prevalence and severity of underlying comorbidities and other unmeasured biologic risk factors between Black and White patients. Future research is needed to investigate the mechanism of these observed differences in outcomes of severe COVID-19 infection in Black versus White patients.

18.
Artigo em Inglês | MEDLINE | ID: mdl-34101024

RESUMO

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), also known as coronavirus disease 2019 (COVID-19) is a highly transmissible virus and has become pandemic. Part of the prevention of disease spread by the Malaysian government is by getting COVID-19 vaccine. Using the mRNA technology, the Pfizer/BioNTech vaccine is one of the vaccines been approved by the Drug Control Authority in Malaysia. Herein, we report an immediate complication of cerebral VST after the first dose of the Pfizer/BioNTech vaccine.

19.
J Neurovirol ; 2021 Jun 08.
Artigo em Inglês | MEDLINE | ID: mdl-34101087

RESUMO

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) commonly results in a respiratory illness in symptomatic patients; however, those critically ill can develop a leukoencephalopathy. We describe two patients who had novel subacute MRI findings in the context of coronavirus disease 2019 (COVID-19) leukoencephalopathy, which we hypothesize could implicate a potent small-vessel vasculitis, ischemic demyelination and the presence of prolonged ischemia. Recent evidence of the direct neuroinvasiness of SARS-CoV-2 leading to ischemia and vascular damage supports this hypothesis.

20.
Int J Clin Pract ; : e14467, 2021 Jun 09.
Artigo em Inglês | MEDLINE | ID: mdl-34107130

RESUMO

BACKGROUND: Recent findings indicate that thrombosis is one of the underlying pathophysiology and complication of COVID-19 infection. Therefore, the prognosis of the disease may be more favorable in people who were under oral anticoagulant treatment before the COVID-19 diagnosis. This study aims to evaluate the effects of chronic DOAC use on ICU admission and mortality in hospitalized patients due to COVID-19 infection. METHOD: Between 1 September and 30 November 2020, 2760 patients hospitalized in our hospital due to COVID-19 were screened. A total of 1710 patients who met the inclusion criteria were included in the study. The patients were divided into two groups as those who use DOAC due to any cardiovascular disease before the COVID-19 infection and those who do not. RESULTS: Seventy-nine patients were enrolled in the DOAC group and 1631 patients in the non-DOAC group. Median age of all study patient was 62 (52-71 IQR) and 860 (50.5%) of them were female. The need for intensive care, in-hospital stay, and mechanical ventilation were observed at higher rates in the DOAC group. Mortality was observed in 23 patients (29%) in the DOAC group and it was statistically higher in the DOAC group (p = 0.002). In the multivariable analysis, age (OR: 1.047, CI: 1.02-1.06, p <0.001), male gender (OR: 1.8, CI: 1.3-2.7, p=0.02), lymphocyte count (OR: 0.45, CI: 0.30-0.69, p <0.001), procalcitonin (OR: 1.12, CI: 1.02-1.23, p = 0.015), SaO2 (OR: 0.8, CI: 0.77-0.82, p <0.001) and creatinine (OR: 2.59, CI: 1.3-5.1, p =0.006) were found to be associated with in-hospital mortality. DOAC treatment was not found to be associated with lower in-hospital mortality in multivariable analysis (OR:1.17, CI: 0.20-6.60, p=0.850). CONCLUSION: Our study showed that the use of DOAC prior to hospitalization had no protective effect on in-hospital mortality and intensive care need in hospitalized COVID-19 patients.

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