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Some studies suggest that the respiratory microbiome of COVID-19 patients differs from that of healthy individuals, infected patients may have reduced diversity and increased levels of opportunistic bacteria, however, the role of the microbiome in fatal SARS-CoV-2 infection remains poorly understood. Our study aimed to determine whether there are differences in the respiratory microbiome between patients who recovered from COVID-19 and those who died, by characterizing the bacterial communities of both groups. A total of 24 patients who recovered from COVID-19 and 24 who died were included in the study, patient data were analyzed for signs, symptoms and clinical variables. Airway samples were collected and the 16 S rRNA variable regions V3-V4 were amplified and sequenced using the Illumina MiSeq platform. Elevated levels of blood urea nitrogen, creatinine and lactate dehydrogenase, and higher frequencies of cardiovascular disease, diabetes mellitus and renal disease were observed in patients with a fatal outcome. Compared to patients who recovered from COVID-19, patients who died exhibited a microbiome enriched in periodontal and pathogenic bacteria such as Klebsiella pneumoniae. Our results highlighted a dual relationship between SARS CoV-2 infection and an exacerbated periodontopathogen-induced immune response.

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BACKGROUND: Rapid progression of symptoms and development of Acute Respiratory Distress Syndrome (ARDS) frequently occurred during COVID-19 pandemic, while CT-Scan was useful to assess severity of lung damage, with classic patterns like early Ground Glass Opacity and/or late consolidation. Likewise, lung injury has been related to activation of the coagulation-fibrinolysis systems and pro-inflammatory mediators; where D-Dimer acquires prognostic relevance. The present study aimed to evaluate whether the extent of lung involvement and pattern of lung injury, as determined by chest CT-scan, are related with D-Dimer; and further impact clinical prognosis in patients with ARDS due to COVID-19. METHODS: Longitudinal, prospective, observational, multi-center study. Patients diagnosed with ARDS due to COVID-19, without previous lung damage, clotting disorder and/or anticoagulants use, who were attended at the Intensive Care Unit and Internal Medicine Department from March to June 2020. Tomographic extent of lung involvement was analyzed by image software, as well as damage patterns, assessed by experienced radiologists. Endpoints included relation of lung injury with coagulopathy markers like D-Dimer, and prognostic outcome including mortality, mechanical ventilation and hospitalization time. RESULTS: One-hundred and four patients mean aged 55 years old, 66% males, main comorbidities obesity, hypertension and diabetes mellitus. Larger lung damage was associated with older age, male gender and higher pro-inflammatory mediators like leukocytes and ferritin; whilst consolidation pattern was related to higher Body Mass Index. Higher values of D-Dimer were related either to a larger extent of lung involvement or late consolidation pattern. In addition, the extent of lung involvement was related with longer hospital stay, higher requirement of mechanical ventilation (HR 0.12, p < 0.01) and mortality rate (HR 0.13, p < 0.01); whereas late consolidation was mainly associated with requirement of mechanical ventilation (HR 0.23, p < 0.01). CONCLUSION: Tomographic extent of lung involvement and the pattern of lung injury are related with coagulopathy severity markers like D-Dimer, and own prognostic clinical ability in ARDS.

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This study reports the first documented case of COVID-19-associated pulmonary aspergillosis (CAPA) caused by Aspergillus welwitschiae in the Americas, which occurred in a rural area of Sao Paulo State, Brazil. The case involves a 52-year-old woman with COVID-19, hypertension, and dyslipidemia, who was admitted following severe respiratory deterioration. Imaging tests revealed extensive pulmonary involvement, including nodular and cavitary lesions indicative of CAPA. Bronchoalveolar lavage (BAL) analysis identified Aspergillus spp. using morphological and molecular techniques, and sequencing of the benA gene confirmed the isolate as A. welwitschiae, closely related to the reference strain CBS 139.54. Matrix-assisted laser desorption/ionization-time of flight mass spectrometry further validated this identification. Traditionally recognized as a plant pathogen, A. welwitschiae has recently been implicated in human diseases, such as otomycosis, and is increasingly detected in respiratory samples. However, its association with CAPA remains underreported globally, particularly in the Americas. This case highlights the critical importance of accurate fungal diagnosis, as overlapping morphological features among Aspergillus species can hinder clinical management. The identification of A. welwitschiae in this context raises concerns about its potential as an emerging pathogen in agricultural regions, where environmental exposure may drive its epidemiological relevance. Given the growing recognition of A. welwitschiae as a CAPA agent, this report underscores its importance in the epidemiology of the disease and its potential role in regions with high agricultural activity. Accurate identification is essential for guiding targeted interventions and addressing the public health risks posed by this emerging fungal threat toCOVID-19 patients.

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Myiasis, a condition stemming from the parasitic infestation of Diptera fly larvae, constitutes a complication for cancer patients, particularly those with malignant skin wounds. The factors that contribute to myiasis include old age, inadequate hygiene, poor living conditions, vascular disease, and diabetes. Cases of myiasis in neoplastic wounds in the head and neck region are rare and guidelines or recommendations regarding the best treatment approach remain lacking. Herein, we describe a case of myiasis that developed into an extensive squamous cell carcinoma of the lip in an older male adult due to the delay in oncological treatment stemming from the COVID-19 pandemic. Patients with oral squamous cell carcinoma, especially those residing in rural areas, face a notable risk of developing oral myiasis. Therefore, it is imperative that patients and caregivers adopt strict preventive measures to avoid fly infestations in wounds. Maintaining optimal hygiene (including meticulous cleaning with antiseptic solutions before daily dressing changes) is essential to prevent myiasis. Adequate wound coverage is crucial, especially during warmer seasons.

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BACKGROUND: The long-term health impacts of COVID-19, including post-acute sequelae of SARS-CoV-2, remain insufficiently explored, especially concerning pre-existing cardiovascular risk factors in older adults. This study examines the association between these risk factors and post-acute sequelae of SARS-CoV-2 in this population. METHODS: A retrospective study of Brazilian adults aged = 60 years assessed the persistence of post-acute sequelae of SARS-CoV-2 three months after infection in 2020. Cardiovascular risk factors (obesity, smoking, high blood pressure, diabetes mellitus, hypercholesterolemia, and chronic kidney disease) were analyzed in relation to sequelae and adjusting for sociodemographic variables. Data were obtained from the Department of Epidemiological Surveillance in Roraima, Brazil. RESULTS: Of the 1,322 participants (55% female; mean age 70.4 years, SD = 7.87), 61.7% (95% CI: 59.1-63.9) reported at least one post-acute sequelae of SARS-CoV-2 at the three-month follow-up. The likelihood of post-acute sequelae of SARS-CoV-2 was significantly higher in participants with diabetes mellitus (OR = 4.39; 95% CI: 3.42-5.66), tobacco use (OR = 3.93; 95% CI: 2.47-6.23), hypertension (OR = 3.62; 95% CI: 2.73-4.78), or hypercholesterolemia (OR = 3.58; 95% CI: 2.80-4.59). Chronic kidney disease (OR = 2.28; 95% CI: 1.59-3.25) and obesity (OR = 1.83; 95% CI: 1.28-2.61) were less strongly associated. CONCLUSIONS: Pre-existing cardiovascular risk factors are linked to a higher likelihood of long-term COVID-19 sequelae in adults aged = 60 years old. Preventing and managing these factors are crucial for reducing the long-term effects of COVID-19, particularly during a pandemic.

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BACKGROUND: COVID-19 became a pandemic disease in 2020, with multisystem involvement and high renal morbidity during the acute phase. Some affected patients began to present new or persistent symptoms in a condition known as Long COVID. The study aimed to evaluate renal function using clinical and laboratory findings, and to establish the frequency and staging of renal function decline in Long COVID patients, as well as the associated factors. METHODS: This is a cross-sectional observational study that selected participants from a Long COVID clinical care program between 2020 and 2022. RESULTS: A total of 246 patients were selected for this study, and renal function decline was found in 83 (33.7%). Patients over 60 years (29.6%) and those who developed glycaemic alterations (41.8%) exhibited a higher prevalence of renal outcomes in long COVID. Some laboratory test as LDH levels and glycated hemoglobin seems to have a statistic relation with a decrease in renal function (p < 0.05). CONCLUSION: A decline in renal function was common in patients with Long COVID in this study, and older age and glycaemic alterations were relevant to this condition. Some laboratory markers can be used to predict this outcome.

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Although most cases of COVID-19 are mild cases, severe cases requiring hospitalization and mechanical ventilation were sufficient to overwhelm healthcare systems worldwide, leading to more than 6 million deaths and the increase in healthcare associated infections (HAIs). The incidence of HAIs in COVID-19 hospitalized patients has been addressed in systematic reviews, but in these there was no description of mortality related to these infections. Therefore, the aim of this review was to evaluate the impact of HAIs on mortality of hospitalized patients with COVID-19, specially by multidrug resistant bacteria as Acinetobacter baumannii. A systematic review was carried out in the PubMed database on July 2022 using the keywords "healthcare-associated infection" OR "nosocomial infection" AND "COVID-19" AND "Acinetobacter baumannii". The incidence of HAIs in COVID-19 patients was 18.85%, with 42.17% of mortality rate and relative risk (RR) 2.08 (95%CI 1.61-2.68). Considering that the risk of death was twice greater in co-infection COVID-19/HAI, it is essential the broad vaccination against COVID-19 and the adoption of measures to reduce HAI incidence in hospitalized patients and mortality by superinfections.

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Dysregulated renin-angiotensin system (RAS) signaling contributes to elevated blood pressure (BP), inflammation, and organ damage in systemic arterial hypertension (HTN). We have demonstrated that hypertensive humans and rats exhibit higher expression of classic RAS components and lower expression of counterregulatory RAS components in the lungs compared with normotensive counterparts. Here, we investigated whether BP control could restore the balance between classic [angiotensin I-converting enzyme 2 (ACE)/angiotensin II (Ang II)] and counterregulatory [angiotensin I-converting enzyme 2 (ACE2)/Ang (1-7)] RAS, thereby mitigating lung inflammation. Male spontaneously hypertensive rats (SHRs) were treated with either losartan or amlodipine, both of which effectively reduced BP. These interventions up-regulated lung Ace2 and down-regulated Ace gene expression. Pulmonary membrane ACE2 abundance and activity were higher in losartan- and amlodipine-treated SHRs than in vehicle-treated SHRs, whereas ACE protein and function remained unchanged. Drug-treated SHRs exhibited lower levels of lung Ang II and higher levels of Ang (1-7) than vehicle-treated SHRs. Rebalancing the pulmonary RAS remarkably reduced macrophage number and down-regulated pro-inflammatory genes in SHR lungs, with lower expression of lung pro-inflammatory genes correlating with lower circulating levels of ACE2. Serum analysis in healthy and hypertensive individuals supported these findings, showing higher ACE2 levels in uncontrolled compared with controlled hypertension and normotension. Collectively, these findings suggest that high blood pressure may induce lung inflammation via an ACE/ACE2 imbalance. BP control with either an RAS inhibitor or a calcium channel blocker rebalances RAS in SHR lungs and alleviates inflammation. Furthermore, this study provides a mechanistic link between inflammatory lung diseases (such as COVID-19) and hypertension as a major risk factor.

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BACKGROUND: The COVID-19 pandemic has resulted in a critical shortage of respiratory ventilators, highlighting the urgent need to explore alternative treatment options for patients with acute respiratory distress syndrome (ARDS) caused by respiratory viruses, as an alternative to invasive mechanical ventilation (IMV) in future pandemics. OBJECTIVES: The objective of this study was to assess the effectiveness of alternative noninvasive oxygenation and ventilation strategies in comparison to invasive mechanical ventilation (IMV) in patients with virus-induced acute respiratory failure (ARF). The primary outcome was the all-cause ICU mortality rate. METHODS: A systematic review was conducted following the Cochrane guidelines and PRISMA reporting guidelines. The search encompassed databases such as Medline, Cochrane CENTRAL, and Embase to identify relevant indexed literature. Additionally, gray literature was included by consulting regulatory agencies. The included studies compared various oxygenation and ventilatory alternatives, such as high-flow nasal cannula (HFNC), continuous positive airway pressure (CPAP), or noninvasive mechanical ventilation (NIMV) with IMV. An exploratory meta-analysis was performed by calculating the risk ratio (RR) by random effects and meta-regression to explore possible sources of heterogeneity and to compare ventilatory alternatives against IMV to reduce mortality, length of stay (LOS) days in ICU, nosocomial infection, and barotrauma. RESULTS: A total of forty-seven studies were included in this systematic review. NIMV had an RR of 0.70 (0.58-0.85), HFNC had an RR of 0.54 (0.42-0.71), and CPAP had an RR of 0.80 (0.71-0.90), with meta-regression models that reduced heterogeneity to 0%. For LOS days in ICU, NIMV had 0.38 (- 0.69: - 0.08) lower days and HFNC 0.29 (- 0.64: 0.06) lower days with meta-regression models that reduction heterogeneity to 0% for HFNC and 50% for NIMV. Not enough studies reported nosocomial infection or barotrauma to evaluate them in a meta-analysis. The overall quality of evidence, as assessed by GRADE evaluation, was determined to be from very low to medium certainty depending on the ventilatory strategy and outcome. CONCLUSIONS: The findings of this systematic review support the use of alternative noninvasive oxygenation and ventilation strategies as viable alternatives to conventional respiratory ventilation for managing viral-induced ARF. Although it is essential to interpret these findings with caution given the overall low to medium certainty of the evidence, the integration of these modalities as part of the management strategies of these patients could help reduce the utilization of ICU beds, invasive ventilators, and costs in both developed and developing countries.

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INTRODUCTION: SARS-CoV-2 can cause mild upper respiratory tract involvement to pulmonary disease of varying severity, as well as cardiovascular complications with increased mortality. The prevalence is similar in men and women, although there are sex differences in disease characteristics and outcome. In this study, we analyze the clinical characteristics, progression, and in-hospital outcome by sex of patients included in the RACCOVID-19 registry. MATERIALS AND METHODS: We included data from 2750 patients consecutively admitted to 50 centers in 11 provinces of the country, from May 18 to October 31, 2020. RESULTS: A total of 1541 men (60.2%) and 1018 women (39.8%) were included (p<0.001). The prevalence of cardiovascular risk factors (because of current smoking) was higher in men. During hospitalization, men had a higher incidence of cardiovascular complications (17.9% vs. 12.5%; p=0.0002) and mortality (20.8% vs. 16.8%; p=0.01). Poor performance status on hospital admission was more common in men (53.9% vs. 42.6%, p<0.0001). On multivariate analysis, male sex, the presence of hypertension and diabetes, and a history of other medical conditions were independent predictors of inhospital mortality. DISCUSSION: In the RACCOVID-19 registry, men had worse performance status and higher incidence of cardiovascular complications with higher in-hospital mortality. Male sex, hypertension, diabetes, and history of other diseases were independent predictors of in-hospital mortality.

Introducción: SARS-CoV-2 puede causar desde afección leve de la vía área superior hasta enfermedad pulmonar con diferentes niveles de gravedad, así como también complicaciones cardiovasculares, con mayor mortalidad. La prevalencia es similar en hombres y mujeres, aunque existen diferencias en cuanto a las características de la enfermedad y su evolución según el sexo. En este trabajo, se analizan las características clínicas, evolución y pronóstico intrahospitalario de los pacientes incluidos en el registro RACCOVID-19, de acuerdo al sexo. Materiales y métodos: Se incluyen datos de 2750 pacientes ingresados consecutivamente en 50 centros de 11 provincias del país, desde el 18 de mayo hasta el 31 de octubre de 2020. Resultados: Se incluyeron 1541 hombres (60.2%) y 1018 mujeres (39.8%) (p<0.001). Se observóen el sexo masculino una mayor prevalencia de factores de riesgo cardiovascular, en especial el tabaquismo. En la evolución intrahospitalaria, los varones presentaron mayor incidencia de complicaciones cardiovasculares (17.9% vs. 12.5%; p=0.0002) así como una mayor mortalidad (20.8% vs. 16.8%; p=0.01). El estado clínico comprometido fue mayor en varones (53.9 vs. 42.6%; p<0.0001). En el análisis multivariado, el sexo masculino, la presencia de hipertensión arterial, diabetes y otros antecedentes patológicos fueron predictores independientes de mortalidad hospitalaria. Discusión: Los hombres en el RACCOVID-19 presentaron peor estado clínico y más complicaciones cardiovasculares con una mayor mortalidad intrahospitalaria. El sexo masculino, la hipertensión arterial, la diabetes y la presencia de otros antecedentes patológicos fueron predictores independientes de mortalidad hospitalaria.

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INTRODUCTION: Severe acute respiratory syndrome coronavirus infection is responsible for multisystemic disease and has high transmissibility. It culminated in a pandemic, challenging scientific knowledge and care capacity. Neurological symptoms are highly prevalent, and cases of encephalitis have been described, in both peri- and postinfectious periods. However, pathogenesis and prognosis are unclear. Thus, we aim to describe the clinical findings in cases of encephalitis in patients infected with severe acute respiratory syndrome coronavirus, together with a 1-year follow-up of self-perception of recovery and remaining neuropsychiatric symptoms. METHODS: This is a retrospective observational study in which patients with cerebrospinal fluid collection and a recent diagnosis of severe acute respiratory syndrome coronavirus infection were screened for encephalitis through analysis of medical records. We describe their clinical and paraclinical findings using descriptive statistics, together with their long-term outcome, through a self-assessment questionnaire. RESULTS: Among the 135 patients screened, 11 patients were included. Most of them were admitted for neurological symptoms (73%), and in 63% of cases, those symptoms occurred within the first 7 days of systemic symptoms. Most patients had minor pulmonary involvement assessed on chest computed tomography. On cerebrospinal fluid analysis, the most relevant finding was hyperproteinorrachia. Three patients (27%) had positive changes on magnetic resonance studies. In the outcome analysis, most patients (77%) reported gait difficulties and 66% reported memory and concentration problems. CONCLUSION: Encephalitis associated with severe acute respiratory syndrome coronavirus 2 infection is rare but responsible for chronic sequelae in cognitive and motor aspects. The pathophysiology seems to be associated with both the immune-mediated and inflammatory processes, and the low frequency of paraclinical findings demands a high clinical suspicion.

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COVID-19 has significant long-term impacts, including a chronic syndrome known as long-COVID, characterized by persistent symptoms post-recovery. The inflammatory response during acute infection is hypothesized to influence long-term outcomes. This study aimed to identify inflammatory biomarkers predictive of functional outcomes one year after hospital discharge. A prospective cohort study was conducted with 213 COVID-19 patients admitted to ICUs in Southern Brazil between June and November 2020. After exclusions and follow-ups, 109 patients were evaluated for one-year post-discharge. Plasma levels of Th1 (TNF-α, INF-γ, IL-12), Th2 (IL-4, IL-5, IL-6, IL-10, IL-13), and Th17 (IL-17, IL-22) cytokines were measured. Functional outcomes in psychiatric, cognitive, general health, and health perception domains were assessed. Statistical analyses included multivariate regression, regularized partial correlation network analysis, and K-means clustering. We demonstrate that plasma levels of various cytokines, along with demographic and clinical characteristics, can predict four distinct domains of functional outcomes one year following hospital discharge due to COVID-19 and that an hyperinflammatory phenotype was associated with the occurrence of a worse in psychiatric, general health, and health perception domains. The network analysis highlighted complex interconnections among immune markers and clinical variables, elucidating their roles in long-term health. These findings support using biomarkers for patient stratification and indicate potential targets for therapeutic interventions.

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The pandemic due to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) resulted in over 7 million global fatalities and billions of individuals diagnosed with COVID-19. Acute and chronic muscle impairment associated with SARS-CoV-2 infection affected a substantial number of patients, leading to the development of symptoms such as fatigue, muscle pain, and exercise intolerance. Our study introduces an animal model to improve understanding of the pathogenicity caused by SARS-CoV-2 in human skeletal muscle. In this investigation, human angiotensin-converting enzyme 2 under a cytokeratin 18 promoter transgenic mice were subjected to intratracheal instillation with either inactivated SARS-CoV-2 or the virus-free culture medium, with or without pre-treatment with the P2X receptor inhibitor Brilliant Blue G (BBG). Muscle strength, morphology, and inflammatory mediators were measured. Inactivated SARS-CoV-2 induced a significant decrease in mice muscle strength, accompanied by histopathological changes in gastrocnemius and diaphragm muscles, including leukocytic infiltrates, cytoplasmic vacuoles, and centralized nuclei. Also, a notable increase in caspase 3 amount was observed, suggesting muscle apoptosis. Significant elevations were noted in inflammatory mediators in the muscle of inactivated SARS-CoV-2 mice, including high mobility group box-1, tumor necrosis factor-alpha, phospho-nuclear factor kappa B, caspase 11, and pannexin-1. On the other hand, pyroptosis markers such as caspase 1, interleukin-1ß, and gasdermin D remained unaltered in all experimental groups. Treatment with BBG mitigated the observed effects, indicating that inhibition of purinergic signaling pathways protects muscles from the inflammatory impact induced by inactivated SARS-CoV-2. This study emphasizes the potential efficacy of purinergic inhibition in ameliorating SARS-CoV-2-induced muscular impairments.

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BACKGROUND: Post-acute COVID-19 Syndrome (PACS) occurs in some COVID-19 patients long after acute infection and significantly affects patients' health. However, the mechanism by which PACS develops is unknown. Myosin light chain 9 (Myl9), produced by activated platelets, plays a role in immune dysregulation and microthrombi formation during acute COVID-19. However, in the PACS phase, the association between Myl9 and residual symptoms remains unclear, and further investigation is needed. METHODS: In this prospective cohort study, serum Myl9 concentrations were measured in 195 COVID-19 patients during hospitalization and at 3- and 6-month follow-up visits. Gaussian mixture modeling was used to identify groups on the basis of Myl9 levels. Relationships between Myl9 levels and residual symptoms were evaluated. Clinical characteristics influencing Myl9 levels were analyzed via logistic regression. RESULTS: A total of 304 serum samples from 195 patients were collected. Two distinct groups were identified in the Myl9 distribution with a cutoff of 386 ng/mL by Gaussian mixture modeling in this cohort. The high-Myl9 group presented significant residual respiratory symptoms at 6 months post-infection (p < 0.05). Elevated Myl9 levels at 6 months were correlated with increased neutrophil counts (p < 0.01) and respiratory comorbidities at diagnosis (p < 0.05) according to univariate regression analysis. Multivariate regression analysis confirmed the relationship between the neutrophil count and high Myl9 levels. CONCLUSION: Prolonged high Myl9 levels are associated with respiratory symptoms, suggesting the potential involvement of prolonged inflammation or endothelial damage in PACS.

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INTRODUCTION: Patients diagnosed with COVID-19 may present sequelae which are called Post COVID-19 Syndrome or Long COVID in which physical, psychological and/or social complications are evident. The objective of this study was to evaluate the agreement of the Post-COVID-19 Functional Status Scale (PCFS) of the evaluator-administered version vs patient self-assessed in post-COVID-19 patients. METHODS: Observational study in patients diagnosed with COVID-19 with subsequent recovery. Once the project was approved by the ethics committee and the patients signed the informed consent, a survey was carried out to collect sociodemographic and clinical data and the application of the PCFS scale, in its two forms, self-administered and by an evaluator. RESULTS: 97 patients entered the study, 57.7% being women. The agreement analysis determined a concordance index of 0.857 95% CI (0.7-0.934) (almost perfect agreement). The agreement for women was 0.817 95% CI 0.700-0.934 and for men 0.907 95% CI (0.806-1). CONCLUSION: The use of the Spanish version of the PCFS scale carried out by the health professional compared to the version self-assessed by patients, demonstrates adequate agreement.

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INTRODUCTION: Persistent elevation of biomarkers associated with endothelial dysfunction in convalescent COVID-19 patients has been linked to an increased risk of long-term cardiovascular complications, including long COVID syndrome. Sulodexide, known for its vascular endothelial affinity, has demonstrated pleiotropic protective properties. This study aims to evaluate the impact of sulodexide on serum levels of endothelial dysfunction biomarkers in patients during the convalescent phase of COVID-19. METHODS: We conducted a double-blind, single-center, randomized, placebo-controlled trial in Mexico, comparing sulodexide (250 LRU orally, twice daily) with placebo over 8 weeks in adult patients during early COVID-19 convalescence. Differences in serum biomarkers between the groups were analyzed using repeated measures and post hoc tests, with Thrombomodulin (TM) as the primary endpoint. RESULTS: Among 206 analyzed patients (103 in each group), at week 8, the sulodexide group exhibited significantly lower mean levels of Thrombomodulin (TM) (25.2 ± 7.9 ng/mL vs 29.9 ± 14.7 ng/mL, P = .03), von Willebrand Factor (vWF) (232 ± 131 U/dL vs 266 ± 122 U/dL, P = .02) and Interleukin-6 (IL-6) (12.5 ± 13.2 pg/mL vs 16.2 ± 16.5 pg/mL, P = .03) compared to the placebo group. D-dimer and C reactive protein (CRP) in the sulodexide group were also lowered. No significant differences were observed for P-selectin, fibrinogen, VCAM-1, or ICAM-1 levels. CONCLUSIONS: Patients in the convalescent phase of COVID-19 who received sulodexide for eight weeks showed a reduction in TM, vWF, D-dimer, CRP, and IL-6 serum levels compared to placebo. These findings suggest a potential protective effect of sulodexide against thromboinflammation and endothelial damage.

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BACKGROUND: Neurological manifestations associated with COVID-19 remain partially described, mainly in low- and middle-income countries where diagnostic tools are limited. To address this, we assembled medical centers in Brazil with the goal of describing neurological syndromes associated with COVID-19 during the first wave of the pandemic. METHODS: From June 1st, 2020 to June 1st, 2021, non-consecutive adult patients with new onset of six neurological syndromes up to 60 days after confirmed COVID-19 were included. Data were compiled from four tertiary centers and compared with general local COVID-19 data, as well as with a previous cohort focused on vascular syndrome. RESULTS: 197 patients were included, presenting with vascular syndromes (81), encephalopathy (68), encephalitis (19), Guillain-Barré syndrome (13), other neuropathies (12), and myelitis (4). The incidence curve of neurocovid mirrored that of COVID-19. Neurological syndromes were present regardless of COVID-19 severity. The median time from COVID-19 to onset of neurological symptoms was 14 days, suggesting a post-infectious immune-mediated mechanism. Patients were 10 times more likely to die (χ2 (1) = 356.55, p < 0.01, OR = 10.89) and 38 times more likely to be hospitalized than other COVID-19 patients (χ2 (1) = 1167.9, p < 0.01, OR = 38.22). Those developing vascular syndromes patients were 3 times more likely to require ICU (χ2 (1) = 37.12, p < 0.01, OR = 3.78) and 4 times more likely to die (χ2 (1) = 58.808, p < 0.01, OR = 4.73) than patients with vascular syndromes due to different etiologies. CONCLUSIONS: Our study corroborates the association of neurological syndromes with COVID-19. The incidence correlated with local waves of COVID-19, and patients with neurocovid exhibited a higher susceptibility to adverse outcomes compared to other COVID-19 patients. Among all neurological syndromes, vascular syndromes were the most common, and their severity surpassed that of vascular syndromes not attributed to COVID-19.

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Background and Objectives: This study aimed to evaluate and compare the functional capacity of post-COVID-19 patients with a control group and analyze cardiac hemodynamics and muscle tissue oxygenation responses during assessment protocols in both groups. Materials and Methods: A cross-sectional study was conducted involving patients with COVID-19 and a control group who were all aged ≥18 years. Participants underwent two functional capacity tests: the one-minute sit-stand test (1-STS) and the six-minute walk test (6MWT). Cardiac hemodynamic responses were evaluated using impedance during the 1-STS, and tissue perfusion responses in the oxygenation were recorded during and after both tests. The Friedman test was used for within-group and the Mann-Whitney test was used for between-group comparisons. Results: Thirty-six post-COVID-19 patients (median age 36 years, BMI 26.51 kg/m2) and eleven control subjects (median age 25 years, BMI 23.71 kg/m2) were enrolled. The post-COVID-19 group showed a 20% decrease in 6MWT distance (p = 0.0001) and a 28% decrease in 1-STS repetitions (p = 0.01) versus the control group. Cardiac hemodynamic differences were observed in the post-COVID-19 group during the 1-STS, with reductions in the stroke volume index (18%, p = 0.004), cardiac index (21%, p = 0.0009), Contractility Index (78%, p = 0.0001), and Ejection Fraction (29%, p = 0.0003) and increases in Systemic Vascular Resistance (25%, p = 0.03) and the Systemic Vascular Resistance Index (27%, p = 0.0007). Tissue oxygenation during the 6MWT and 1-STS showed no significant differences between groups. Conclusions: The post-COVID-19 subjects exhibited a reduction in functional capacity, changes in hemodynamic responses related to cardiac and systemic vascular resistance, and a similar pattern of muscle oxygen delivery and consumption in both tests.

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INTRODUCTION: Acute kidney injury (AKI) in the setting of COVID-19 is associated with worse clinical and renal outcomes, with limited long-term data. AIM: To evaluate critically ill COVID-19 patients with AKI that required nephrologist consultation (NC-AKI) in a tertiary hospital. METHODS: Prospective single-center cohort of critically ill COVID-19 adult patients with NC-AKI from May 1st, 2020, to April 30th, 2021. Kidney replacement therapy (KRT), recovery of kidney function, and death at 90-day and 1-year follow-up were evaluated. RESULTS: 360 patients were included, 60.6% were male, median age was 66.0 (57.0-72.0) years, 38.1% had diabetes, and 68.6% had hypertension. AKI stages 1, 2, and 3 were detected in 3.6%, 5.6%, and 90.8% of patients, respectively. KRT was indicated in 90% of patients. At the 90-day follow-up, 88.1% of patients died and 10.0% had recovered kidney function. Female gender (p = 0.047), older age (p = 0.047), AKI stage 3 (p = 0.005), requirement of KRT (p < 0.0001), mechanical ventilation (p < 0.0001), and superimposed bacterial infection (p < 0.0001) were significantly associated death within 90 days. At 1 year, mortality was 89.3%. Amongst surviving patients, 72% recovered kidney function, although with significantly lower eGFR compared to baseline (85.5 ± 23.6 vs. 65.9 ± 24.8 mL/min, p = 0.003). CONCLUSION: Critically ill COVID-19 patients with NC-AKI presented a high frequency of AKI stage 3 and KRT requirement, with a high 90-day mortality. Surviving patients had high rates of recovery of kidney function, with a lower eGFR at one-year follow-up compared to baseline.

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BACKGROUND: Cirrhosis has been pointed out as a clinical entity that leads to worse clinical prognosis in COVID-19 patients. However, this concept is controversial in the literature. We aimed to evaluate clinical outcomes by comparing patients with cirrhosis to those without cirrhosis in a Brazilian cohort. METHODS: Data from 20,164 COVID-19 inpatients were collected from 41 hospitals in Brazil between March to September 2020 and March 2021 to August 2022. We compared 117 patients with cirrhosis to 632 matched controls. A propensity score model was used to adjust for potential confounding variables, incorporating some predictors: age, sex at birth, number of comorbidities, hospital of admission, whether it was an in-hospital clinical manifestation of COVID-19, and admission year. Closeness was defined as being within 0.16 standard deviations of the logit of the propensity score. RESULTS: The median age was 61 (IQR 50-70) years old, and 63.4% were men. There were no significant differences in the self-reported symptoms. Patients with cirrhosis had lower median hemoglobin levels (10.8 vs. 13.1 g/dl), lower platelets (127,000 vs. 200,000 cells/mm3), and leukocyte counts, as well as lower median C-reactive protein (63.0 vs. 76.0 p = 0.044) when compared to controls. They also had higher mortality compared to matched controls (51.3% vs. 21.7%, p < 0.001). They also had higher frequencies of admission in an intensive care unit (51.3% vs. 38.0%, p = 0.007), invasive mechanical ventilation (43.9% vs. 26.6%, p < 0.001), dialysis (17.9% vs. 11.1%, p = 0.038), septic shock (23.9% vs. 14.9%; p = 0.015) and institution of palliative care (19.7% vs. 7.4%; p < 0.001). CONCLUSIONS: This study has shown that COVID-19 inpatients with cirrhosis had significantly higher incidence of severe outcomes, as well as higher frequency of institution of palliative care when compared to matched controls. Our findings underscore the need for these patients to receive particular attention from healthcare teams and allocated resources.