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1.
authorea preprints; 2024.
Preprint in English | PREPRINT-AUTHOREA PREPRINTS | ID: ppzbmed-10.22541.au.170668042.22617428.v1

ABSTRACT

Objective: To investigate the impacts of demographic, hematological, and biochemical factors on the clinical course and the prognostic outcome in adult COVID-19 patients. Methods: This retrospective study was performed in the internal medicine departments of 2 hospitals and data were extracted from the medical files of 1700 adult COVID-19 patients (836 females, 49.2%; 864 males, 50.8%) with an average age of 48.23 ± 16.68 (range: 18-93). Clinical data included baseline descriptives, prior medical history, admission date, treatment, and hematological and biochemical blood test results. The relationship between the survival, length of hospitalization, hematological, and biochemical parameters was investigated. Results: Advanced age (p<0.001), presence of at least 1 comorbid disease (p=0.045), increased length of hospitalization (p=0.006), elevated white blood cell (p=0.001) and neutrophil (p=0.002) counts, increased serum levels of glucose (p=0.027), blood urea nitrogen (p<0.001), AST (p=0.006), LDH (p<0.001), CRP (p>0.001), and D-dimer (p=0.001). In contrast, diminution of serum levels of albumin (p<0.001), ALT (p=0.028), calcium (p=0.022), and platelet count (p=0.010) were associated with increased mortality. There was a positive and weak relationship between serum D-dimer levels and length of hospitalization. Conclusion: Our data imply that identification and validation of indicators that predict COVID-19 disease progression to improve health outcomes are crucial. Age, comorbidities, immunological response, radiographic abnormalities, laboratory markers, and signs of organ dysfunction may all predict poor outcomes individually or collectively. It is critical to identify characteristics that predict COVID-19 problems to guide clinical management, improve patient outcomes, and allocation of limited resources. Keywords: SARS-Cov-2, COVID-19; severity; prognosis; outcome


Subject(s)
Hematologic Diseases , Multiple Organ Failure , COVID-19
2.
researchsquare; 2023.
Preprint in English | PREPRINT-RESEARCHSQUARE | ID: ppzbmed-10.21203.rs.3.rs-3744615.v1

ABSTRACT

Background Cadmium exposure can cause oxidative stress, induce inflammation, inhibit immune function, and therefore has significant impacts on the pathogenesis and severity of many diseases. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection can also provoke oxidative stress and the dysregulation of inflammatory and immune responses. This study aimed to assess the potential associations of cadmium exposure with the severity and clinical outcomes of patients with coronavirus disease 2019 (COVID-19).Methods We performed a retrospective, observational, bicenter cohort analysis of patients with SARS-CoV-2 infection in Taiwan between June 2022 and July 2023. Cadmium concentrations in blood and urine were measured within 3 days of the diagnosis of acute SARS-CoV-2 infection, and the severity and clinical outcomes of patients with COVID-19 were analyzed.Results A total of 574 patients were analyzed and divided into a severe COVID-19 group (hospitalized patients) (n = 252; 43.9%), and non-severe COVID-19 group (n = 322; 56.1%). The overall in-hospital mortality rate was 11.8% (n = 68), and 149 patients (26%) required invasive mechanical ventilation. The severe COVID-19 patients were older, had significantly more comorbidities, and significantly higher neutrophil/lymphocyte ratio, C-reactive protein, and interleukin-6 than the non-severe COVID-19 patients (all p < 0.05). Both blood and urine cadmium concentrations were significantly higher in the severe COVID-19 patients than in the non-severe COVID-19 patients. Among the severe COVID-19 patients, those in higher urine cadmium/creatinine quartiles had a significantly higher risk of organ failure (i.e., higher APACHE II and SOFA scores), higher neutrophil/lymphocyte ratio, lower PaO2/FiO2 requiring higher invasive mechanical ventilation support, higher risk of acute respiratory distress syndrome, and higher 60-, 90-day, and all-cause hospital mortality (all p < 0.05). Multivariate logistic regression models revealed that urine cadmium/creatinine was independently associated with severe COVID-19 (adjusted OR 1.648 [95% CI 1.064–2.552], p = 0.025), and that a urine cadmium/creatinine value > 2.05 µg/g had the highest predictive value (adjusted OR 5.391, [95% CI 1.127–25.794], p = 0.035).Conclusions Urine cadmium concentration in the early course of COVID-19 could predict the severity and clinical outcomes of patients and was independently associated with the risk of severe COVID-19.


Subject(s)
Respiratory Distress Syndrome , Inflammation , Coronavirus Infections , Multiple Organ Failure , COVID-19
3.
researchsquare; 2023.
Preprint in English | PREPRINT-RESEARCHSQUARE | ID: ppzbmed-10.21203.rs.3.rs-3492501.v1

ABSTRACT

Background: Limited data from the Chinese experience are available regarding the infection status, clinical characteristics, treatments and early outcomes of lung transplant recipients (LTRs) afflicted with coronavirus disease 2019 (COVID-19) caused by the SARS-CoV-2 Omicron Variant. Methods: We conducted a study on LTRs with COVID-19 caused by the Omicron Variant from November 17, 2022, to May 1, 2023. Clinical information was gathered through electronic medical records, questionnaires, or follow-up telephone calls. To identify potential risk factors for severe disease progression, a multivariate logistic analysis was performed. Results: 178 LTRs with COVID-19 were included, with 50% (89/178) requiring hospitalization for an average stay of 16 days (IQR: 9.5-25.5 days). The most common symptoms were fever (79.8%), dry cough (75.3%) and fatigue (61.8%). Ultimately, 17 recipients succumbed to COVID-19-related respiratory failure or secondary multiple organ dysfunction, resulting in an overall mortality rate of 9.6%. Of the 89 hospitalized patients, 41.6% (37/89) eventually progressed to severe or critical disease, forming the Severe/Critical Group (S/C group), while the remaining 58.4% (52/89) had mild to moderate disease (M/M group). In comparison to the M/M group, the S/C group had higher CRP (59.6 vs. 16.8 mg/L, P<0.01), ESR (45.5 vs. 22.5mm/h, P<0.01) and D-dimer (1.09 vs. 0.65 mg/L, P<0.05), but lower CD3+ T lymphocytes (577 vs. 962 cells/ul, P<0.01) and CD4+ T lymphocytes (217 vs. 427 cells/ul, P<0.01). The S/C group had significantly higher rates of combined pulmonary bacterial infection (67.6% vs. 38.5%, P<0.01) and pulmonary fungal infection (73.0% vs. 38.5%, P<0.01) during the course of COVID-19, nearly double that of the M/M group. In a multivariate logistic analysis, elevated CRP (>41.8mg/L), combined pulmonary fungal infection, and interstitial lung disease(ILD) as primary disease emerged as high-risk factors for developing the severe disease phenotype following Omicron variant infection in LTRs, with respective OR values of 4.23 (95% CI: 1.68-11.23), 4.76 (95% CI: 1.59-15.64), and 5.13 (95% CI: 1.19-29.17). Conclusions: LTRs displayed an increased vulnerability to combined lung bacterial or fungal infections following Omicron infection. CRP> 41.8mg/L, ILD as primary disease, and combined pulmonary fungal infection are high-risk factors for developing severe disease.


Subject(s)
Fever , Mycoses , Lung Diseases, Interstitial , Critical Illness , Bacterial Infections , Respiratory Insufficiency , Cough , Multiple Organ Failure , COVID-19 , Fatigue
4.
researchsquare; 2023.
Preprint in English | PREPRINT-RESEARCHSQUARE | ID: ppzbmed-10.21203.rs.3.rs-3142062.v1

ABSTRACT

Background Coronavirus disease 2019 (COVID-19) emerged in late December 2019 and was declared pandemic in March 2020 by the World Health Organization, causing clinically acute respiratory manifestations and corresponding symptoms, pathological inflammation and multi-organ dysfunctions. The total commitment of the scientific community to develop therapeutics to deal with this global emergency in the shortest possible period was unprecedented. In a very short time, several vaccines were approved by the EMA (European Medicines Agency) and the FDA (Food and Drug Administration). Despite this, it is conceivable that COVID-19 will continue to spread globally through evolving variants in more or less cyclic waves. With these perspectives, it is essential to quickly develop additional therapeutic tools to deal with the next wave of infection.  Methods In the present study we describe the development and characterization of neutralizing mouse monoclonal antibodies (mAbs) against the receptor binding domain (RBD) of the SARS-CoV-2 Spike (S) protein.  Results The mAbs identified are able to specifically detect the RBD of SARS-CoV-2 Spike protein in all tested applications, including enzyme-linked immunosorbent assay (ELISA), flow cytometry (FACS) and bio-layer interferometry. In addition, we show that these mAbs efficiently block entry of both SARS-CoV-2 pseudoparticles carrying the spike protein of the original SARS-CoV-2 strain and a broad set of variants of concern (VOC). Conclusions Here we report a panel of monoclonal antibodies that target RBD and inhibit SARS-CoV-2 variants  infection and enable the isolation of novel therapeutic tools to neutralize SARS-CoV-2 virus


Subject(s)
Severe Acute Respiratory Syndrome , Inflammation , Multiple Organ Failure , COVID-19
5.
medrxiv; 2023.
Preprint in English | medRxiv | ID: ppzbmed-10.1101.2023.07.01.23291847

ABSTRACT

IntroductionAt the end of 2019, in the city of Wuhan, China, a virus of the family of coronaviruses first appeared, mainly affecting the respiratory system, which was called SARS-COV-2 and causes COVID-19. Although in most patients, it occurs with mild symptomatology, however, a significant percentage (15-30%) will develop acute respiratory distress syndrome (ARDS) with increased chances of intubation and mechanical ventilation. In special cases of severe disease, where the oxygenation of the patient is not improved by the use of the ventilator, extracorporeal membrane oxygenation (ECMO) can be applied, a technique that has been used in previous pandemics that affected the respiratory system. AimTo investigate the evidence of the appliance of the ECMO, based on international literature, of the extracorporeal membrane oxygenator in patients with severe respiratory failure due to Covid-19 disease. MethodArticles were searched on the international bases of scientific studies PubMed, Cochrane Library, and Google Scholar. This review was carried out using meta-analysis and international guidelines. ResultsFour articles were included where there was an agreement on the basic characteristics of patients, which can be considered as selection criteria. The primary criteria indicate the age, where the patient must be under 65 years old, and the body mass index (BMI) should be below 40. In addition, it is very important that there is no serious underlying pathology such as multi-organ failure syndrome. Also, the mechanical ventilation should not exceed seven (7) days until the placement of the ECMO, while all the other therapeutic methods, such as the prone position, neuromuscular blockers, and the appropriate positive end-expiratory pressure of the airways (Positive end-expiratory pressure - PEEP) should be already applied. ConclusionsThe application of ECMO is widely used as a treatment for patients with severe COVID-19 disease. However, in order to have the best therapeutic results while reducing hospitalization costs, it is necessary to follow the guidelines regarding the selection of patients who will benefit substantially.


Subject(s)
Multiple Organ Failure , COVID-19 , Respiratory Distress Syndrome , Respiratory Insufficiency
6.
researchsquare; 2023.
Preprint in English | PREPRINT-RESEARCHSQUARE | ID: ppzbmed-10.21203.rs.3.rs-3130965.v1

ABSTRACT

Background Systemic inflammation is closely related to the progress of COVID-19.This study aimed to explore the role of combined detection of heparin-binding protein (HBP), interleukin-6 (IL6), and C-reactive protein (CRP) on the severity and clinical outcomes of COVID-19. Methods Our hospital conducted a retrospective analysis of 214 patients with COVID-19 from 1 December 2022 to 28 February 2023. Patients were separated into non-severe and severe categories. Based on whether there was organ failure during hospitalization, patients were further split into the non-organ failure group and the organ failure group. Records on demographics, baseline, and clinical features, as well as the levels of HBP, IL6, and CRP on admission, were collected. Results HBP, IL6, and CRP levels were positively correlated with total bilirubin, lactate dehydrogenase, serum creatinine, and D-dimer but negatively correlated with albumin. HBP, IL6, and CRP levels were remarkably higher in severe, organ failure, and non-survivor groups compared to non-severe, non-organ failure, and survivor groups (all P < 0.001). The optimal cutoff values of HBP, IL6, and CRP for predicting severe COVID-19 were 49.71 ng/mL, 11.24 pg/mL, and 39.67 mg/L, respectively. With a sensitivity and specificity of 85.10% and 95.70% for severe COVID-19, the combined detection of HBP, IL6, and CRP showed the best diagnostic effectiveness. Logistic regression revealed that HBP, IL6, and CRP were independent risk factors for severe COVID-19 and organ failure. Moreover, the risk of death predicted by any two or more of HBP, IL6, and CRP higher than the optimal cutoff value was 3.631 times that of only one of the three indicators higher than the optimal cutoff value (hazard ratio = 3.631, log-rank P = 0.003). Conclusions A combination of HBP, IL6, and CRP has higher diagnostic efficiency of severe COVID-19; combined detection can more accurately and efficiently predict COVID-19 severity, organ failure, and prognosis, which is complementary to previous studies.


Subject(s)
Death , Inflammation , Multiple Organ Failure , COVID-19
7.
biorxiv; 2023.
Preprint in English | bioRxiv | ID: ppzbmed-10.1101.2023.06.24.546363

ABSTRACT

The coronavirus disease 2019 (COVID-19) pandemic, caused by severe acute respiratory syndrome coronavirus (SARS-CoV-2) may be over, but its variants continue to emerge, and patients with mild symptoms having long COVID is still under investigation. SARS-CoV-2 infection leading to elevated cytokine levels and suppressed immune responses set off cytokine storm, fatal systemic inflammation, tissue damage, and multi-organ failure. Thus, drug molecules against virus-specific proteins that play a role in viral inflammation and simultaneous act on the host pathways participating in viral inflammation, will provide an effective antiviral therapy against emerging variants of concern. Evolutionarily conserved papain-like protease (PLpro) and main protease (Mpro) play an indispensable role in the virus life cycle and immune evasion. Direct-acting antivirals targeting both these viral proteases represent an attractive antiviral strategy that is also expected to reduce viral inflammation. The present study has evaluated the antiviral and anti-inflammatory potential of natural triterpenoids: azadirachtin, withanolide_A, and isoginkgetin. These molecules inhibit the Mpro and PLpro proteolytic activities with half-maximal inhibitory concentrations (IC50) values ranging from 1.42 to 32.7 M. Isothermal titration calorimetry (ITC) analysis validated the binding of these compounds to Mpro and PLpro. As expected, the two compounds, withanolide_A and azadirachtin exhibit potent antiviral activity with half-maximum effective concentration (EC50) values of 21.73 M and 31.19 M, respectively. The anti-inflammatory role of azadirachtin and withanolide_A when assessed using HEK293T cells were found to significantly reduce the levels of CXCL10, TNF, IL6, and IL8 cytokines, which are elevated in severe cases of COVID-19. Interestingly, azadirachtin and withanolide_A were also found to rescue the decreased type-I interferon response (IFN-1). The results of this study clearly highlight the role of triterpenoids as effective antiviral molecules that target SARS-CoV-2 specific enzymes and also host immune pathways involved in virus mediated inflammation.


Subject(s)
Severe Acute Respiratory Syndrome , Inflammation , Multiple Organ Failure , COVID-19
8.
biorxiv; 2023.
Preprint in English | bioRxiv | ID: ppzbmed-10.1101.2023.06.19.545534

ABSTRACT

The Coronavirus Disease 2019 (COVID-19) pandemic caused by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) has taken its toll on worldwide public health infrastructure. SARS-CoV-2 is reported to exhibit wide tissue tropism, contributing to its severe pathogenicity that often culminates in multiple-organ failure. The onslaught of this disease has intensified due to the emergence of variants of concern (VOC), such as Delta and Omicron. These variants have been linked to gastrointestinal (GI) symptoms, suggesting a potential fecal-oral route of viral transmission. Here we compared the broad tissue tropism of ancestral Hong-Kong SARS-CoV-2 (SARS-CoV-2 HK) against Delta and Omicron VOCs in aa hamster model by analyzing tissue samples collected from the upper and lower respiratory system and the GI tract. We observed an overall increase in vRNA load and pro-inflammatory cytokines, especially in GI tracts of animals infected with Delta virus, indicating selective virus tropism and pathology in these tissues. However, no apparent spike in Delta viral load was observed in the large intestine and fecal matter. Overall, our research investigates the wide range of tissues that various SARS-CoV-2 strains can infect in hamsters and presents evidence supporting the increased preference of Delta VOCs for infecting the GI tract.


Subject(s)
Multiple Organ Failure , Gastrointestinal Diseases , Severe Acute Respiratory Syndrome , Gastroesophageal Reflux , COVID-19
9.
Sci Rep ; 13(1): 7832, 2023 05 15.
Article in English | MEDLINE | ID: covidwho-2320255

ABSTRACT

This study evaluates the association between antivirals (Molnupiravir and Nirmatrelvir-Ritonavir) and all-cause and respiratory mortality and organ dysfunction among high-risk COVID-19 patients during an Omicron outbreak. Two cohorts, Nirmatrelvir-Ritonavir versus control and Molnupiravir versus control, were constructed with inverse probability treatment weighting to balance baseline characteristics. Cox proportional hazards models evaluated the association of their use with all-cause mortality, respiratory mortality, and all-cause sepsis (a composite of circulatory shock, respiratory failure, acute liver injury, coagulopathy, and acute liver impairment). Patients recruited were hospitalized and diagnosed with the COVID-19 Omicron variant between February 22, 2022 and April 15, 2022, and followed up until May 15, 2022. The study included 17,704 patients. There were 4.67 and 22.7 total mortalities per 1000 person-days in the Nirmatrelvir-Ritonavir and control groups respectively before adjustment (weighted incidence rate ratio, - 18.1 [95% CI - 23.0 to - 13.2]; hazard ratio, 0.18 [95% CI, 0.11-0.29]). There were 6.64 and 25.9 total mortalities per 1000 person-days in the Molnupiravir and control groups respectively before adjustment (weighted incidence rate ratio per 1000 person-days, - 19.3 [95% CI - 22.6 to - 15.9]; hazard ratio, 0.23 [95% CI 0.18-0.30]). In all-cause sepsis, there were 13.7 and 35.4 organ dysfunction events per 1000 person-days in the Nirmatrelvir-Ritonavir and control groups respectively before adjustment (weighted incidence rate ratio per 1000 person-days, - 21.7 [95% CI - 26.3 to - 17.1]; hazard ratio, 0.44 [95% CI 0.38-0.52]). There were 23.7 and 40.8 organ dysfunction events in the Molnupiravir and control groups respectively before adjustment (weighted incidence ratio per 1000 person-days, - 17.1 [95% CI, - 20.6 to - 13.6]; hazard ratio, 0.63 [95% CI 0.58-0.69]). Among COVID-19 hospitalized patients, use of either Nirmatrelvir-Ritonavir or Molnupiravir compared with no antiviral use was associated with a significantly lower incidence of 28-days all-cause and respiratory mortality and sepsis.


Subject(s)
COVID-19 , Sepsis , Humans , COVID-19 Drug Treatment , Multiple Organ Failure , Ritonavir/therapeutic use , SARS-CoV-2 , Sepsis/drug therapy , Sepsis/epidemiology , Antiviral Agents/therapeutic use
10.
Cells ; 12(9)2023 05 06.
Article in English | MEDLINE | ID: covidwho-2312262

ABSTRACT

BACKGROUND AND AIM: Here, we assess the effect of adjuvant antioxidant therapies in septic shock patients with organ dysfunction and their effect on the enzymatic and non-enzymatic antioxidant systems. METHODS: Randomized clinical trial run between 2018 and 2022. One hundred and thirty-one patients with septic shock were included in five groups with 25, 27, 24, 26 and 29 patients each. Group 1 received vitamin C (Vit C), Group 2 vitamin E (Vit E), Group 3 n-acetylcysteine (NAC), Group 4 melatonin (MT) and group 5 no treatment. All antioxidants were administered orally or through a nasogastric tube for 5 days as an adjuvant to standard therapy. RESULTS: All patients had multiple organ failure (MOF) and low Vit C levels. Vit C therapy decreased CRP, PCT and NO3-/NO2- but increased Vit C levels. The SOFA score decreased with MT in 75%, Vit C 63% and NAC 50% vs. controls 33% (p = 0.0001, p = 0.03 and p = 0.001 respectively). MT diminished lipid peroxidation (LPO) (p = 0.01) and improved total antioxidant capacity (TAC) (p = 0.04). Vit E increased thiol levels (p = 0.02) and tended to decrease LPO (p = 0.06). Selenium levels were decreased in the control group (p = 0.04). CONCLUSIONS: Antioxidants used as an adjuvant therapy in the standard treatment of septic shock decrease MOF and oxidative stress markers. They increase the TAC and thiols, and maintain selenium levels.


Subject(s)
Melatonin , Selenium , Shock, Septic , Humans , Antioxidants/therapeutic use , Shock, Septic/drug therapy , Multiple Organ Failure/drug therapy , Organ Dysfunction Scores , Vitamin E/therapeutic use , Ascorbic Acid/therapeutic use , Vitamins , Intensive Care Units
11.
Zhonghua Wei Zhong Bing Ji Jiu Yi Xue ; 35(1): 106-109, 2023 Jan.
Article in Chinese | MEDLINE | ID: covidwho-2296324

ABSTRACT

The outbreak of novel coronavirus (SARS-CoV-2) infection has brought great harm to people's life and social development. Although SARS-CoV-2 infection is more common in mild patients at present, considering the characteristics of crtical disease, rapid progress and high mortality, the treatment of critical patients are the focus of clinical attention. Immune imbalance which is characterized by cytokine storm plays a vital role in SARS-CoV-2 induced acute respiratory distress syndrome (ARDS), extrapulmonary multiple organ failure and even death. Therefore, the application of immunosuppressive agent in crtical coronavirus disease patients has a promising prospect. In this paper, different immunosuppressive agents and their application in crtical SARS-CoV-2 infection are reviewed, so as to provide reference for crtical coronavirus disease therapy.


Subject(s)
COVID-19 , Respiratory Distress Syndrome , Humans , SARS-CoV-2 , Immunosuppressive Agents/therapeutic use , Multiple Organ Failure , Respiratory Distress Syndrome/drug therapy
12.
Postgrad Med J ; 98(1164): 742-749, 2022 Oct 01.
Article in English | MEDLINE | ID: covidwho-2303151

ABSTRACT

PURPOSE: During COVID-19 infection, organ dysfunction such as respiratory failure tends to occur towards the second week of illness; however, in a subset, there may be rapid onset of organ dysfunction as early as symptom onset. We define fulminant onset COVID-19 as rapid onset of organ dysfunction such as acute respiratory failure, acute kidney injury, acute encephalopathy or shock within 4 days of symptom onset. Fulminant onset COVID-19 has not yet been systematically studied. We aimed to identify predictors and prognosis of fulminant onset COVID-19. METHODS: This retrospective study was carried out on patients admitted to a single referral hospital in South India between June 2020 and January 2022. Patients were categorised into fulminant and non-fulminant onset COVID-19. Candidate predictors for fulminant onset were chosen by an intuitive approach and analysed using logistic regression. Then, the outcome of fulminant onset COVID-19 at 30 days was studied. RESULTS: Out of 2016 patients with confirmed COVID-19, 653 (32.4%) had fulminant onset COVID-19. Age>60 years (a-OR 1.57, 95% CI 1.30 to 1.90, p<0.001), hypertension (a-OR 1.29, 95% CI 1.03 to 1.61, p=0.03) and immune-suppressed state (a-OR 5.62, 95% CI 1.7 to 18.7, p=0.005) were significant predictors of fulminant onset COVID-19. Complete vaccination lowered the odds of fulminant onset COVID-19 significantly (a-OR 0.61, 95% CI 0.43 to 0.85, p=0.004). At 30 days, the fulminant onset COVID-19 group had higher odds of mortality and need for organ support. CONCLUSION: Fulminant onset COVID-19 is not uncommon and it carries poor prognosis and deserves recognition as a distinct phenotype of COVID-19.


Subject(s)
COVID-19 , Respiratory Distress Syndrome , Humans , COVID-19/diagnosis , Retrospective Studies , Multiple Organ Failure , Prognosis
13.
researchsquare; 2023.
Preprint in English | PREPRINT-RESEARCHSQUARE | ID: ppzbmed-10.21203.rs.3.rs-2899769.v1

ABSTRACT

Background ARDS due to COVID-19 infection has a unique phenotype generating a growing need to determine the existing differences that can alter existing evidence-based management strategies for ARDS, particularly those related to ventilator management.Research Question: What differences does the clinical profile of patients with ARDS due to COVID 19 and Non-COVID 19 have?Study Design and Methods: We conducted a comparative, observational, retrospective study in the ICU of a third-level hospital in Mexico City, from March 2020 through March 2022. Clinical, echocardiographic, and laboratory variables were compared between patients with ARDS due to SARS-COV2 infection and those due to other etiologies. For qualitative variables, the chi-square test was used.Results We enrolled 140 patients with a diagnosis of ARDS. The study group of COVID-19 etiology were younger males, higher body mass index, progressed to organ dysfunction, required more frequently renal replacement therapy, and higher SOFA score. There was no difference in rates of right ventricular dysfunction.Interpretation: COVID-19 ARDS exhibit much greater severity that led to higher admission and mortality rates, whilst being younger and less comorbid.


Subject(s)
Respiratory Distress Syndrome , Severe Acute Respiratory Syndrome , Ventricular Dysfunction , Multiple Organ Failure , COVID-19
14.
medrxiv; 2023.
Preprint in English | medRxiv | ID: ppzbmed-10.1101.2023.04.27.23289234

ABSTRACT

Importance: SARS-CoV-2 infection can result in ongoing, relapsing, or new symptoms or organ dysfunction after the acute phase of infection, termed Post-Acute Sequelae of SARS-CoV-2 (PASC), or long COVID. The characteristics, prevalence, trajectory and mechanisms of PASC are poorly understood. The objectives of the Researching COVID to Enhance Recovery (RECOVER) Tissue Pathology Study (RECOVER-Pathology) are to: (1) characterize prevalence and types of organ injury/disease and pathology occurring with PASC; (2) characterize the association of pathologic findings with clinical and other characteristics; (3) define the pathophysiology and mechanisms of PASC, and possible mediation via viral persistence; and (4) establish a post-mortem tissue biobank and post-mortem brain imaging biorepository. Methods: RECOVER-Pathology is a cross-sectional study of decedents dying at least 15 days following initial SARS-CoV-2 infection. Eligible decedents must meet WHO criteria for suspected, probable, or confirmed infection and must be aged 18 years or more at the time of death. Enrollment occurs at 7 sites in four U.S. states and Washington, DC. Comprehensive autopsies are conducted according to a standardized protocol within 24 hours of death; tissue samples are sent to the PASC Biorepository for later analyses. Data on clinical history are collected from the medical records and/or next of kin. The primary study outcomes include an array of pathologic features organized by organ system. Casual inference methods will be employed to investigate associations between risk factors and pathologic outcomes. Discussion: RECOVER-Pathology is the largest autopsy study addressing PASC among US adults. Results of this study are intended to elucidate mechanisms of organ injury and disease and enhance our understanding of the pathophysiology of PASC.


Subject(s)
Multiple Organ Failure , Neurocognitive Disorders , COVID-19 , Death
15.
Zhonghua Wei Zhong Bing Ji Jiu Yi Xue ; 34(9): 900-904, 2022 Sep.
Article in Chinese | MEDLINE | ID: covidwho-2288831

ABSTRACT

OBJECTIVE: To investigate the clinical characteristics and prognosis of coronavirus disease 2019 (COVID-19) patients with Omicron variant combined with atrial fibrillation (AF). METHODS: From March 23, 2022 to May 15, 2022, 2 675 aged ≥ 50 years old COVID-19 patients with AF were admitted to Zhoupu Hospital, the designated hospital for COVID-19 in Shanghai. Patients were divided into mild symptoms group, normal group, and serious/critical group according to the symptoms. The clinical data, imaging examination and laboratory results and prognosis of the three group patients were compared. RESULTS: The median age of 2 675 COVID-19 patients was 69.0 (60.0, 81.0) years old, the incidence of AF was 5.05% (135/2 675), the age range of AF patients were from 55 to 101 years old, with a median age of 84.0 (74.0, 89.0), and the number of mild symptoms, normal, serious/critical patients were 68, 30, 37, respectively, including 9 of serious and 28 of critical patients. In the serious/critical patients, aged 55-75 years old accounted for 43.2%, the rate of 2019 novel coronavirus vaccination was 32.4%. The identified new-onset AF was the highest among the three groups, but the rate of persistent AF was the highest in the mild symptoms group (58.8%). The severe/critical group complicated with fever (29.7%), hepatic insufficiency (13.5%), renal insufficiency (46.0%), type 2 diabetes (46.0%), and heart failure were higher in NYHA classification [compared with the mild symptoms and normal group (score): 1.8±1.1 vs. 1.1±0.8, 1.2±0.7, respectively, all P < 0.05]. In term of laboratory examinations, C-reactive protein (CRP), alanine aminotransferase (ALT), and aspartate aminotransferase (AST) levels were significantly higher in serious/critical patients compared to the mild symptoms and normal groups [CRP (mg/L): 27.2 (6.0, 60.8) vs. 7.6 (3.1, 19.3), 12.8 (4.9, 26.3), ALT (U/L): 31.3±15.4 vs. 15.4±9.3, 19.3±11.7, AST (U/L): 78.0±21.7 vs. 34.7±15.6, 38.1±24.4, all P < 0.05]. The hemoglobin (Hb) and albumin (ALB) levels were significantly lower than those in the mild symptoms and normal groups [Hb (g/L): 105.3±22.5 vs. 125.8±25.4, 123.0±20.4, ALB (g/L): 33.7±6.0 vs. 39.0±5.5 and 39.6±13.1, all P < 0.05]. In addition, MB isoenzyme of creatine kinase (CK-MB) was significantly higher in the serious/critical group than that in the mild symptoms group [µg/L: 2.5 (1.5, 3.4) vs. 2.2 (1.2, 2.8), P < 0.05]. In terms of the treatment, the percentage of antiplatelet agents and low-molecular heparin ratio compared among the three groups were statistically significant, with the serious/critical group using the lowest percentage of antiplatelet agents (27.0%) and a higher percentage of low-molecular heparin usage than that in mild symptoms group [81.1% (30/37) vs. 51.5% (35/68), P < 0.05]. In terms of prognosis, the mortality of patients with AF was 18.5% (25/135), all of whom were critical ill, including 32.0% (8/25) with cerebral embolism, pulmonary embolism and cerebral hemorrhage. Among them, 40.0% (10/25) died of multiple organ failure (40.0% combined with gastrointestinal hemorrhage), 20.0% (5/25) died of heart failure, and 12.0% (3/25) died of respiratory failure; while there were no death cases recorded in the mild symptoms, normal group and 9 serious patients. CONCLUSIONS: The serious/critical patients infected with COVID-19 Omicron variant with AF, have a worse prognosis and high mortality. Multiple organ failure, heart failure, sudden cardiac death, respiratory failure and embolic disease are the major causes of death.


Subject(s)
Atrial Fibrillation , COVID-19 , Diabetes Mellitus, Type 2 , Heart Failure , Respiratory Insufficiency , Humans , Middle Aged , Aged , Aged, 80 and over , SARS-CoV-2 , Multiple Organ Failure , Platelet Aggregation Inhibitors , Retrospective Studies , China/epidemiology , C-Reactive Protein , Heparin
16.
BMC Cancer ; 23(1): 265, 2023 Mar 23.
Article in English | MEDLINE | ID: covidwho-2264861

ABSTRACT

INTRODUCTION: COVID-19 particularly impacted patients with co-morbid conditions, including cancer. Patients with melanoma have not been specifically studied in large numbers. Here, we sought to identify factors that associated with COVID-19 severity among patients with melanoma, particularly assessing outcomes of patients on active targeted or immune therapy. METHODS: Using the COVID-19 and Cancer Consortium (CCC19) registry, we identified 307 patients with melanoma diagnosed with COVID-19. We used multivariable models to assess demographic, cancer-related, and treatment-related factors associated with COVID-19 severity on a 6-level ordinal severity scale. We assessed whether treatment was associated with increased cardiac or pulmonary dysfunction among hospitalized patients and assessed mortality among patients with a history of melanoma compared with other cancer survivors. RESULTS: Of 307 patients, 52 received immunotherapy (17%), and 32 targeted therapy (10%) in the previous 3 months. Using multivariable analyses, these treatments were not associated with COVID-19 severity (immunotherapy OR 0.51, 95% CI 0.19 - 1.39; targeted therapy OR 1.89, 95% CI 0.64 - 5.55). Among hospitalized patients, no signals of increased cardiac or pulmonary organ dysfunction, as measured by troponin, brain natriuretic peptide, and oxygenation were noted. Patients with a history of melanoma had similar 90-day mortality compared with other cancer survivors (OR 1.21, 95% CI 0.62 - 2.35). CONCLUSIONS: Melanoma therapies did not appear to be associated with increased severity of COVID-19 or worsening organ dysfunction. Patients with history of melanoma had similar 90-day survival following COVID-19 compared with other cancer survivors.


Subject(s)
COVID-19 , Melanoma , Humans , COVID-19/therapy , Multiple Organ Failure , Melanoma/complications , Melanoma/therapy , Immunotherapy
17.
researchsquare; 2023.
Preprint in English | PREPRINT-RESEARCHSQUARE | ID: ppzbmed-10.21203.rs.3.rs-2844078.v1

ABSTRACT

The coronavirus disease 2019 (COVID-19), which affects multiple organs, is causing an unprecedented global public health crisis. Most COVID-19 patients recover gradually upon appropriate interventions. Viruses were reported to utilize the small extracellular vesicles (sEVs) to escape the attack from the host’s immune system. This study aimed to examine the lipid profile of plasma small extracellular vesicles of recovered COVID-19 patients (RCs). Plasma sEVs were separated from 83 RCs 3 months after discharge without underlying diseases, including 18 recovered asymptomatic patients (RAs), 32 recovered moderate patients (RMs), and 33 recovered severe and critical patients (RSs), and 19 healthy controls (HCs) by Total Exosome Isolation. Lipids were extracted from sEVs and then subjected to targeted liquid chromatography-mass spectrometry. Size, concentration, and distribution of plasma-derived sEVs from RAs, RMs, RSs, and HCs did not differ in RCs and HCs as validated by transmission electron microscopy, nanoparticle tracking analysis, and immunoblot analysis. Fifteen subclasses of 508 lipids were detected in plasma sEVs from HCs, RAs, RMs, and RSs, such as phosphatidylcholines (PCs) and diacylglycerols (DAGs), etc. Total lipid intensity displayed downregulation in RCs compared with HCs. The relative abundance of DAGs gradually dropped, whereas PCs, lysophosphatidylcholines, and sphingomyelins were higher in RCs relative to HCs, especially RSs. 88 lipids out of 241 were significantly different and a conspicuous increase in lipid profiles of RCs was revealed with disease status. The lipids alternations were found to be significantly correlated with the clinical indices in RCs and HCs, suggesting that the impact of COVID-19 on lipid metabolism lingered for a long time. The lipid abnormalities bore an intimate link with glycerophospholipid metabolism and glycosylphosphatidylinositol anchor biosynthesis. Furthermore, the lipidomic analysis showed that RCs were at higher risk of developing diabetes and sustaining hepatic impairment. The abnormality of immunomodulation in RCs might still exist. The study may offer new insights into the mechanism of organ dysfunction and help identify novel therapeutic targets in the RCs.


Subject(s)
Multiple Organ Failure , COVID-19 , Liver Diseases , Diabetes Mellitus
18.
researchsquare; 2023.
Preprint in English | PREPRINT-RESEARCHSQUARE | ID: ppzbmed-10.21203.rs.3.rs-2732946.v1

ABSTRACT

Background: Multi-system inflammatory syndrome in children (MIS-C) is a newly defined clinical syndrome characterized by systemic inflammation, fever, and multi-organ dysfunction related to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. While MIS-C is familiar to most physicians, recurrent and rebound cases of MIS-C are extremely rare, with only two such cases reported to date. Case presentation: Here, we report the case of a five-month-old boy diagnosed with rebound MIS-C (19 days apart), with the second episode being more severe and featuring a right coronary artery aneurysm. The immunodeficiency workup returned normal. Standard MIS-C treatment protocols were followed in both episodes, eventually yielding an excellent outcome. The patient remained well within 12 months of follow-up. Conclusions: We conclude that longer and closer follow-ups of MIS-C patients may be needed, perhaps with a more aggressive treatment protocol to prevent a rebound or recurrence of the disease, though further studies are required to guide clinical decision-making.


Subject(s)
Dementia, Multi-Infarct , Fever , Coronary Aneurysm , Inflammation , Coronavirus Infections , Multiple Organ Failure , Immunologic Deficiency Syndromes
19.
researchsquare; 2023.
Preprint in English | PREPRINT-RESEARCHSQUARE | ID: ppzbmed-10.21203.rs.3.rs-2718744.v1

ABSTRACT

Background Few studies have reported on mortality beyond one year after sepsis. We aim to describe trends in short- and long-term mortality among patients admitted with sepsis, and to identify clinical characteristics associated with mortality for improved monitoring, treatment and prognosis.Methods Patients ≥ 18 years admitted to all Norwegian hospitals (2008–2021) with a first sepsis episode were identified using Norwegian Patient Registry and International Classification of Diseases 10th Revision codes. Sepsis was classified as implicit (known infection site plus organ dysfunction), explicit (unknown infection site), or COVID-19 related sepsis. The outcome was all-cause mortality. We calculated age-standardized 30-day, 90-day, 1-, 5- and 10-year mortality for each admission year and estimated the annual percentage change with 95% confidence interval (CI). The association between clinical characteristics and all-cause mortality is reported as hazard ratios (HRs) from Cox regression.Results The study included 222,832 patients, of whom 127,059 (57.1%) had implicit, 92,928 (41.7%) had explicit, and 2,845 (1.3%) had COVID-19-related sepsis. Trends in overall age-standardized 30-day, 90-day, 1- and 5-year mortality decreased by 0.29 (95% CI -0.39 to -0.19), 0.43 (95% CI -0.56 to -0.29), 0.61 (95% CI -0.73 to -0.49) and 0.66 (95% CI -0.84 to -0.48) percent per year, respectively. The decrease was observed for all infections sites but was largest among patients with respiratory tract infections. Implicit, explicit and COVID-19-related sepsis had largely similar overall mortality, with explicit sepsis having a HR of 0.980 (95% CI 0.969 to 0.991) and COVID-19-related sepsis a HR of 0.916 (95% CI 0.836 to 1.003) compared to implicit sepsis. Patients with respiratory tract infections have somewhat higher mortality than those with other infection sites. Number of comorbidities was positively associated with mortality, but mortality varied considerably between different comorbidities. Similarly, number of acute organ dysfunctions was strongly associated with mortality, whereas the risk varied for each type of organ dysfunction.Conclusion Overall mortality has declined over the past 14 years among patients with a first sepsis admission. Existing comorbidity, site of infection, and acute organ dysfunction are characteristics associated with mortality and needs further attention to reduce the excess risk of long-term mortality.


Subject(s)
Respiratory Tract Infections , Acute Disease , Sepsis , Multiple Organ Failure , COVID-19
20.
medrxiv; 2023.
Preprint in English | medRxiv | ID: ppzbmed-10.1101.2023.03.09.23287043

ABSTRACT

Introduction: Infection with SARS-CoV-2 leads to coronavirus disease 2019 (COVID-19), which can result in acute respiratory distress syndrome and multiple organ failure. However, its comprehensive influence on pathological immune responses in the respiratory epithelium and peripheral immune cells is not yet fully understood. Methods: In this study, we integrated multiple public scRNA-seq datasets of nasopharyngeal swab and peripheral blood results to investigate the gene regulatory networks (GRNs) of healthy individuals and COVID-19 patients with mild/moderate and severe disease, respectively. Similar and dissimilar regulons were identified within or between epithelial and immune cells during COVID-19 severity progression. The relative transcription factors (TFs) and their targets were used to construct GRNs among different infection sites and conditions. Results: Between respiratory epithelial and peripheral immune cells, different TFs tended to be used to regulate the activity of a cell between healthy individuals and COVID-19 patients, although they had some TFs in common. For example, XBP1, FOS, STAT1, and STAT2 were activated in both the epithelial and immune cells of virus-infected individuals. In contrast, severe COVID-19 cases exhibited activation of CEBPD in peripheral immune cells, while CEBPB was exclusively activated in respiratory epithelial cells. Moreover, in patients with severe COVID-19, CEBPD upregulated S100A8 and S100A9 in CD14 and CD16 monocytes, while S100A9 genes were co-upregulated by different regulators (SPEDEF and ELF3) in goblet and squamous cells. The cell-cell communication analysis suggested that epidermal growth factor receptor signaling among epithelial cells contributes to mild/moderate disease, and chemokine signaling among immune cells contributes to severe disease. Conclusions: This study identified cell type- and condition-specific regulons in a wide range of cell types from the initial infection site to the peripheral blood, and clarified the diverse mechanisms of maladaptive responses to SARS-CoV-2 infection.


Subject(s)
Respiratory Distress Syndrome , Carcinoma, Squamous Cell , Tumor Virus Infections , Multiple Organ Failure , COVID-19
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