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Severe pneumonia is a condition with a high risk of death and mandatory hospitalization in the intensive care unit. The incidence of severe pneumonia has increased dramatically during the pandemic of new coronavirus infection. Timely diagnosis and early initiation of adequate treatment of severe pneumonia are crucial for improving survival of critically ill patients. The aim of this review was to analyze published scientific research on molecular markers that allow to objectively assess the severity of pneumonia and to determine treatment tactics based on the predicted outcome upon admission to the hospital. A systematic search was conducted in the electronic databases PubMed, Medline, Web of Science for the period 2019 - 2022. Conclusion. The review focuses on the prognostic role of a number of markers of immune response, vascular transformation, as well as angiotensin II and angiotensin converting enzyme-2. Further prospective studies of potential predictors of severe pneumonia will enable using marker molecules in a comprehensive clinical and laboratory diagnosis for early prediction of the hospitalized patient's condition and expected outcome.Copyright © Volchkova E.V. et al., 2023.
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COVID-19, a viral respiratory illness, is caused by Severe Acute Respiratory Syndrome Corona Virus 2 (SARS-CoV-2), which was first identified in Wuhan, China, in 2019 and rapidly spread worldwide. Testing and isolation were essential to control the virus's transmission due to the severity of the disease. In this context, there is a global interest in the feasibility of employing nano-biosensors, especially those using graphene as a key material, for the real-time detection of the virus. The exceptional properties of graphene and the outstanding performance of nano-biosensors in identifying various viruses prompted a feasibility check on this technology. This paper focuses on the recent advances in using graphene-based electrochemical biosensors for sensing the SARS-CoV-2 virus. Specifically, it reviews various types of electrochemical biosensors, including amperometric, potentiometric, and impedimetric biosensors, and discusses the current challenges associated with biosensors for SARS-CoV-2 detection. The conclusion of this review discusses future directions in the field of electrochemical biosensors for SARS-CoV-2 detection, underscoring the importance of continued research and development in this domain.
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The recent ongoing COVID-19 pandemic caused by the SARS-CoV-2 virus saw many hospitalizations and deaths among elderly patients. It has been reported that the most common underlying conditions in these patients were obesity and diabetes. While both type 1 and type 2 diabetes pose a higher risk of severe or fatal COVID-19 infections, patients with type 2 diabetes required ICU treatment at a greater frequency than those with type 1 diabetes. However, whether diabetes affects susceptibility for COVID-19 has yet to be explored. This chapter focuses on both type 1 and type 2 diabetes, with the main goal of understanding this chronic condition during the pandemic, based on currently available case studies. © 2023 Elsevier Inc. All rights reserved.
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BackgroundAnti-MDA5 antibody-positive dermatomyositis (anti-MDA5+DM) is a rare autoimmune disease associated with a high mortality rate due to rapid-progressive interstitial lung disease (RP-ILD), particularly in East Asia[1]. MDA5, acts as a cytoplasmic sensor of viral RNA, thus activating antiviral responses including the type I interferon (IFN) signaling pathway[2]. The involvement of type 1 IFN in the pathogenesis of MDA5+DM has been proposed based on the significantly elevated expression of its downstream stimulated genes(ISG) in muscle, skin, lung, and peripheral blood[3;4]. Janus kinase inhibitor, which targets the IFN pathway, combined with glucocorticoid could improve the survival of early-stage MDA5+DM-ILD patients[5]. In clinical practice, there is still an urgent demand for sensitive biomarkers to facilitate clinical risk assessment and precise treatment.ObjectivesThis study aimed to investigate the clinical significance of interferon score, especially IFN-I score, in patients with anti-MDA5+DM.MethodsDifferent subtypes of idiopathic inflammatory myopathy, including anti-MDA5+DM(n=61), anti-MDA5-DM(n=20), antisynthetase syndrome(ASS,n=22),polymyositis(PM,n=6) and immune-mediated necrotizing myopathy(IMNM,n=9), and 58 healthy controls were enrolled.. A multiplex quantitative real-time PCR(RT-qPCR) assay using four TaqMan probes was utilized to evaluate two type I ISGs (IFI44, MX1, which are used for IFN-I score), one type II ISG (IRF1), and one housekeeping gene (HRPT1). Clinical features and disease activity index were compared between high and low IFN-I score groups in 61 anti-MDA5+DM patients. The association between laboratory findings and the predictive value of baseline IFN-I score level for mortality was analyzed.ResultsThe IFN scores were significantly higher in patients with anti-MDA5+DM than in HC (Figure 1A). The IFN-I score correlated positively with serum IFN α(r = 0.335, P =0.008), ferritin (r = 0.302, P = 0.018), and Myositis Disease Activity Assessment Visual Analogue Scale (MYOACT) score(r=0.426, P=0.001). Compared with patients with low IFN-I scores, patients with high IFN-I scores showed increased MYOACT score, CRP, AST, ferritin, and the percentages of plasma cells (PC%) but decreased lymphocyte count, natural killer cell count, and monocyte count. The 3-month survival rate was significantly lower in patients with IFN-I score > 4.9 than in those with IFN-I score ≤ 4.9(72.9% vs. 100%, P=0.044)(Figure 1B).ConclusionIFN score, especially IFN-I score, detected by multiplex RT-qPCR, can be a valuable biomarker for monitoring disease activity and predicting mortality in anti-MDA5+DM patients.References[1]I.E. Lundberg, M. Fujimoto, J. Vencovsky, R. Aggarwal, M. Holmqvist, L. Christopher-Stine, A.L. Mammen, and F.W. Miller, Idiopathic inflammatory myopathies. Nat Rev Dis Primers 7 (2021) 86.[2]G. Liu, J.H. Lee, Z.M. Parker, D. Acharya, J.J. Chiang, M. van Gent, W. Riedl, M.E. Davis-Gardner, E. Wies, C. Chiang, and M.U. Gack, ISG15-dependent activation of the sensor MDA5 is antagonized by the SARS-CoV-2 papain-like protease to evade host innate immunity. Nat Microbiol 6 (2021) 467-478.[3]G.M. Moneta, D. Pires Marafon, E. Marasco, S. Rosina, M. Verardo, C. Fiorillo, C. Minetti, L. Bracci-Laudiero, A. Ravelli, F. De Benedetti, and R. Nicolai, Muscle Expression of Type I and Type II Interferons Is Increased in Juvenile Dermatomyositis and Related to Clinical and Histologic Features. Arthritis Rheumatol 71 (2019) 1011-1021.[4]Y. Ye, Z. Chen, S. Jiang, F. Jia, T. Li, X. Lu, J. Xue, X. Lian, J. Ma, P. Hao, L. Lu, S. Ye, N. Shen, C. Bao, Q. Fu, and X. Zhang, Single-cell profiling reveals distinct adaptive immune hallmarks in MDA5+ dermatomyositis with therapeutic implications. Nat Commun 13 (2022) 6458.[5]Z. Chen, X. Wang, and S. Ye, Tofacitinib in Amyopathic Dermatomyositis–Associated Interstitial Lung Disease. New England Journal of Medicine 381 (2019) 291-293.AcknowledgementsThis work was supported by the National Natural Science Foundation of China [81974251], and Shanghai Hospital Develop ent Center, Joint Research of New Advanced Technology Project [SHDC12018106]Disclosure of InterestsNone Declared.
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BACKGROUND: According to the results of the ESSE-RF study, the frequency of obesity in the population reached 29.7%. Obesity is one of the main risk factors for the development of cardiovascular diseases. Features of the course of COVID-19 in patients with obesity is a very urgent problem. AIM: The aim of the study was a comparative investigation of clinical and laboratory-instrumental parameters in AH patients with or without obesity who had COVID-19 associated pneumonia, to identify the role of obesity as a potential predictor of post-COVID cardiovascular complications 3 months after discharge from the hospital. MATERIALS AND METHODS: Materials and methods. The study included 174 patients with COVID-19-associated pneumonia. Group 1 included 78 patients with AH without obesity, group 2 - 96 patients with AH and obesity. All patients were tested with a blood sample at the time of admission and 3 months after discharge from the hospital. We assessed parameters of general blood test, biochemistry, hemostasis, inflammation biomarkers - concentration of C-reactive protein (CRP), highly sensitive CRP (hs-CRP), homocysteine, IL-6, etc. All patients initially underwent computed tomography of the chest. In both groups, 24-hour blood pressure monitoring was performed using BPLaB device, according to the standard protocol;echocardiography using an expert class ultrasound diagnostic system Vivid S70. The study is registered with the Clinical Trials.gov database Identifier: NCT04501822. RESULT(S): Results. The biomarker that significantly distinguished the both groups of patients, as well as subgroups according to the degree of obesity was the concentration of maxCRP and hs-CRP, which was significantly higher in group 2. In addition, the registered maximum values of MPO, NT-proBNP, IL-1,6, TNA-alpha and NRL parameters in group 2 of patients with 2-3 degrees of obesity, may indicate the highest probability of developing delayed adverse cardiovascular complications in this group of patients. Mean systolic blood pressure, variability of systolic and diastolic blood pressure, and heart rate at night were significantly higher in AH patients with obesity. Numerous correlations of obesity with laboratory and instrumental parameters have been registered, which may indicate an increased likelihood of delayed unwanted cardiovascular complications in this particular group of patients. Multiple regression showed that obesity is an independent predictor of an increase in LDH, hs-CRP and right atrium. CONCLUSION(S): Dynamic control of the studied parameters in patients with AH and OB registered an increased concentration of CRP at the initial stage and 3 months after treatment, with a general trend towards a decrease in the increased initial structural parameters of ECHO CG. The logistic regression method showed that the presence of OB in patients with AH is an independent factor causing increased levels of immune inflammation (CRP), a marker of tissue destruction (LDH), and load on the right atrium.Copyright © Endocrinology Research Centre, 2022.
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Background: D-dimer and LDH are crucial biomarkers, particularly in view of the fact that they have been strongly linked to COVID-19 infection and have been linked to worse consequences in people who have severe viral infections. Objectives: To determine how D-dimer and LDH correlated with clinical effects in COVID-19 patients who were hospitalised and how they forecasted the severity of COVID-19 patients. Material and Methods: This was cross-sectional research conducted relatively early in the second wave of the pandemic. A total of 110 patients diagnosed with COVID-19 and admitted to the ICU from January 2021 to June 2021, were included in the study. The clinical outcome was evaluated in terms of discharge and death among patients requiring various forms of assisted ventilation. Results: The average age of patients was 53.16 years (+or- 18.47 years). 35.5% of the patients were with comorbidities of which diabetes, hypertension, and COPD were around 80%. D-dimer was deranged in 2.7% of the subjects and LDH was deranged in 60% of the study subjects at the time of admission. Coming on to the outcome, all patients were put on assisted ventilation with 71.8% on NIV, 20% on HFNO, 1% on CPAP, and 7.2% on MV. During their hospital stays, 6 (5.45%) patients died and the remaining patients were discharged. A higher D-dimer value (> 1.5 g/ml) during the hospital stay was found to be statistically significant with assisted ventilation and deaths of the admitted study subjects. Conclusion: In our investigation, the biomarker D-dimer value was more associated than LDH with mortality in patients with COVID-19 infection.
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Background and objectives: Mucormycosis is a complication in post-coronavirus disease 2019 (COVID-19) patients in India. This study was done to evaluate the prognostic value of clinical, histopathologic findings, microbiological features, and biochemical parameters such as D-dimer, lactate dehydrogenase, and serum ferritin in post- COVID-19-patients with rhino-orbital mucormycosis. Methods: This retrospective observational study was carried out on biopsies taken from 50 post-COVID-19 patients suspected of mucormycosis. The biopsy specimens were processed and stained with hematoxylin and eosin, periodic acid– schiff, and Wright-Giemsa. In addition, 10–20% potassium hydroxide wet mount and culture on sabouraud dextrose agar were performed to detect Mucor. The biochemical parameters were measured using ARCHITECT ci8200 chemistry analyzer. Results: Overall, 30 cases (60%) were positive for fungal elements, and growth of Mucor spp. was found in 28 cases (56%). In histopathology, 70% of cases (n=35) showed broad, aseptate, ribbon-like hyphae with wide-angled branching diagnostic of mucormycosis. There seemed to be a site-wise overlap between the nasal/maxillary sinus and rhinoorbital/rhino-cerebral variety. There was no difference between the patients in terms of gender. The most common risk factor was diabetes mellitus (observed in 80% of cases). In patients with invasive mucormycosis, inflammatory biomarkers such as serum ferritin, serum lactate dehydrogenase, C-reactive protein, and Ddimer were greater than the normal range, whereas procalcitonin was within the reference range. Conclusion: It can be concluded that raised metabolic markers, direct 10% KOH examination and histological features including angioinvasion as well as rhino-orbital and cerebral extension might assist doctors in diagnosis, progression, and survival rate. [ FROM AUTHOR] Copyright of Medical Laboratory Journal is the property of Golestan University of Medical Sciences, Deputy of Research & Technology and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full . (Copyright applies to all s.)
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Strong collaboration critical as trial development advances Prior to the COVID-19 pandemic, biotech and emerging biopharma companies were increasingly turning to contract research organizations (CROs) to contain costs and secure therapeutic and clinical trial expertise to help meet their individual objectives. Therapeutic and clinical trial expertiseWith exploratory drug development often focused on multiple indications, a CRO with depth of tic expertise optimize clinical delivery enhancing quality and reducing timelines. Furthermore, years of therapeutic expertise and interaction with investigational sites ensure site engagement with heightened interest and attention to the target patient population.
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Currently, there are no reliable biomarkers for identifying COVID-19 patients and no definite therapeutics to control this deadly disease. MicroRNAs (miRNA) have been explored in several human diseases for their potential role as biomarkers and their therapeutic potential. However, there is very little information available about the roles of miRNAs in COVID-19 infection. This chapter outlines the recent updates and developments of miRNAs in COVID-19 such as miRNAs as potential biomarkers for COVID-19, the molecular basis of miRNAs in COVID-19 infection, and the use of miRNAs as therapeutics targets for COVID-19. While a few potential miRNAs have been researched for the aforementioned reasons, more research is needed to determine the roles of individual miRNAs in COVID-19 infection. © 2023 Elsevier Inc. All rights reserved.
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The critical element, of course, is that there can be no compromise on trial design, execution and data collection to deliver a robust drug development package. AUM's strategy is to reverse this flow and go from Asia to the West, satisfying the need of the Asian population for innovative and affordable drug development and reducing the cost of health care in Western countries by introducing drugs at an "Asian" price point. [...]the dislocation in services from widespread lockdowns resulted in significant delays in data collection and management of research samples. Even when we could transfer them to appropriate laboratories for analysis, the staff shortages, backlog of samples, and supply chain disruption of critical reagents and parts caused troubling delays in obtaining and analyzing data.
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The new coronavirus was first reported in China and caused a widespread global outbreak of pneumonia that spread rapidly across this country and many other countries. Acute kidney injury is one of the important complications of COVID-19, which has been shown in some cases. Exploring the diagnostic features of biomarkers of kidney function in COVID-19 patients may lead to better patient management. We collected laboratory data from 206 people with confirmed COVID-19 disease and evaluated their renal biomarkers, Blood Urea Nitrogen (BUN), and creatinine. The age range of the patients was almost 62 years old. The mean age in the dead patients and recovered patients was 71 and 54 years old, respectively. The average LDH value was 755 U/L, and creatine phosphokinase (CPK) was 267 U/L in the patients. The average BUN was 59.1 U/L, and creatinine was 1.5 U/L in COVID-2019 patients. Among all 193 patients, laboratory results revealed that 163 (85.4%) patients had an elevated BUN level. Based on creatinine levels for total patients, laboratory results revealed that 49 (25.4%) patients had an elevated value. The average BUN value in dead patients was 85 mg/dL, while in recovered patients was 40.5 mg/dL (P<0.0001). Also, the average creatinine level in dead patients was 1.86 mg/dL, while in recovered patients was 1.24 mg/dL (P=0.0004). Inflammation following COVID-19 disease causes kidney damage and elevated urea and creatinine levels, which may increase the risk of death in these patients.Copyright © 2023 Tehran University of Medical Sciences.
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Different stakeholders have different definitions of success, said Bill Barry, PhD, senior statistical research scientist, Rho Inc. They will all approach the trial design differently-intent to treat? Trials todsy are more tailored than necessary, said Ken Getz, MBA, founder and board chair, CISCRP and director and professor, Tufts Center for the Study of Drug Development, Tufts University School of Medicine. [...]pragmatic studies have different roadblocks. Because these trials are based on wherever the data are gathered-patient's home, doctor's office, healthcare system- the reliance on EMRs is often frustrating. In the early 2010s, the NCI and the UK's National Institute for Health Research were funding a handful of trials.5 In the UK, the first master protocol approach-using multiple treatments against one control arm-was Stampede, which started recruiting in the mid- 2000s.
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BackgroundD-dimer and fibrinogen elevation has been observed in severe acute respiratory syndrome coronavirus 2 (SARS-CoV2) infection which is associated with higher incidence of venous thromboembolism (VTE) and higher mortality rates. [1-3]. Autoimmune Rheumatic Diseases (ARDs) are associated with higher rates of VTE compared to general population [4]. Whether patients with ARDs infected with SARS-CoV2 have similar D-dimer and fibrinogen trends compared to patients without ARDs is unknown.ObjectivesCompare D-dimer and fibrinogen levels in patients with ARDs infected with SARS-CoV2 to patients without ARDs.MethodsPatients with ARDs infected with SARS-CoV2 were identified retrospectively from the electronic medical records (EMR) of Hamad Medical Corporation and matched (age and sex) to controls (1:3). D-dimer and fibrinogen levels were extracted electronically from EMR and stratified into six-time intervals defined in table 1. Day 0 was defined as the date of positive nasopharyngeal polymerase chain reaction swab test. 2 Independent Samples test (Mann-Whitney U) was used to compare the median (25th - 75th interquartile range [IQR]) level of D-dimer and fibrinogen between both study groups at the defined intervals.ResultsThe study included 203 cases and 551 controls with a mean (SD) age of 45.3 (11.7) and 44 (12.5) years, females were (122 [60.1%] vs. 297 [53.9%], p = 0.129), respectively.Distribution of ARDs was rheumatoid arthritis 86 (42.4%), spondyloarthropathy 33 (16.1%) and systemic lupus erythematosus 31 (15.7%) cases. 67% were on conventional synthetic disease modifying anti-rheumatic drugs (Cs-DMARDs), 15.8% on biological DMARDs and 4.9% on rituximab. About 83% of the ARDs group were in remission or low disease activity and 13% were in moderate or high disease activity.The median (25th - 75th IQR) level of D-dimer and fibrinogen were comparable between study groups in all defined intervals with insignificant p values except at interval 4, fibrinogen was significantly higher in the cases, p 0.006. Table 1ConclusionThere was no significant difference in the trend of D-dimer and fibrinogen levels during SARS-CoV2 infection between patients with ARDs and those without ARDs. Additional studies are needed to quantify the actual risk of VTE in patients with ARDs during SARS-CoV2 in correlation with serum markers of VTE.References[1]Eljilany I, Elzouki AN. D-Dimer, Fibrinogen, and IL-6 in COVID-19 Patients with Suspected Venous Thromboembolism: A Narrative Review. Vasc Health Risk Manag. 2020;16:455-62.[2]Li JY, Wang HF, Yin P, Li D, Wang DL, Peng P, et al. Clinical characteristics and risk factors for symptomatic venous thromboembolism in hospitalized COVID-19 patients: A multicenter retrospective study. J Thromb Haemost. 2021;19(4):1038-48.[3]Zhan H, Chen H, Liu C, Cheng L, Yan S, Li H, et al. Diagnostic Value of D-Dimer in COVID-19: A Meta-Analysis and Meta-Regression. Clin Appl Thromb Hemost. 2021;27:10760296211010976.[4]Lee JJ, Pope JE. A meta-analysis of the risk of venous thromboembolism in inflammatory rheumatic diseases. Arthritis Res Ther. 2014;16(5):435.Table 1.Differences in D-dimer and fibrinogen during SARS-CoV2 infection between patients with ARDs and those without at the defined intervals.Case N = 203Control N = 551P valueMedian (25th - 75th IQR), D-dimer (mg/L)(0 to < 3 days)0.56 (0.34 – 1.31)0.86 (0.54 – 1.41)0.096(≤ 3 to < 6 days)0.67 (0.35 – 2.58)1.11 (0.44 – 1.11)0.340(≤ 6 to < 9 days)0.81 (0.33 – 5.12)1.12 (0.56 – 3.28)0.299(≤ 9 to 12 days)0.94 (0.72 – 5.44)5.20 (1.0 – 15.05)0.058(≤ 12 to < 15 days)2.88 (0.72 – 5.53)4.96 (0.57 – 9.98)0.681(≤ 15 to 18 days)1.81 (0.89 – 2.55)5.56 (2.60 – 15.1)0.086Median (25th – 75th IQR), fibrinogen (mg/L)(0 to < 3 days)6.53 (2.0 - 6.53)5.65 (3.75 – 7.17)1.000(≤ 3 to < 6 days)6.25 (3.72 – 8.3)4.6 (4.1 – 5.6)0.385(≤ 6 to < 9 days)3.53 (3.29 – 4.62)3.4 (3.2 – 3.92)0.328(≤ 9 to 12 days)4.3 (2.82 – 4.78)2.2 (1.65 – 3.05)0.006(≤ 12 to < 15 days)4.4 (2.37 – 5.13)3.1 (1.7 – 4.45)0.170(≤ 15 to 18 days)3.6 ( – 5.7)3.7 (2.0 – 4.88)0.524Acknowledgements:NIL.Disclosure of InterestsNone Declared.
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Acute respiratory distress syndrome (ARDS) is a life-threatening lung condition that arises from multiple causes, including sepsis, pneumonia, trauma, and severe coronavirus disease 2019 (COVID-19). Given the heterogeneity of causes and the lack of specific therapeutic options, it is crucial to understand the genetic and molecular mechanisms that underlie this condition. The identification of genetic risks and pharmacogenetic loci, which are involved in determining drug responses, could help enhance early patient diagnosis, assist in risk stratification of patients, and reveal novel targets for pharmacological interventions, including possibilities for drug repositioning. Here, we highlight the basis and importance of the most common genetic approaches to understanding the pathogenesis of ARDS and its critical triggers. We summarize the findings of screening common genetic variation via genome-wide association studies and analyses based on other approaches, such as polygenic risk scores, multi-trait analyses, or Mendelian randomization studies. We also provide an overview of results from rare genetic variation studies using Next-Generation Sequencing techniques and their links with inborn errors of immunity. Lastly, we discuss the genetic overlap between severe COVID-19 and ARDS by other causes.
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Background: Lung weight may be measured with quantitative chest computed tomography (CT) in patients with COVID-19 to characterize the severity of pulmonary edema and assess prognosis. However, this quantitative analysis is often not accessible, which led to the hypothesis that specific laboratory data may help identify overweight lungs. Methods: This cross-sectional study was a secondary analysis of data from SARITA2, a randomized clinical trial comparing nitazoxanide and placebo in patients with COVID-19 pneumonia. Adult patients (≥18 years) requiring supplemental oxygen due to COVID-19 pneumonia were enrolled between April 20 and October 15, 2020, in 19 hospitals in Brazil. The weight of the lungs as well as laboratory data [hemoglobin, leukocytes, neutrophils, lymphocytes, C-reactive protein, D-dimer, lactate dehydrogenase (LDH), and ferritin] and 47 additional specific blood biomarkers were assessed. Results: Ninety-three patients were included in the study: 46 patients presented with underweight lungs (defined by ≤0% of excess lung weight) and 47 patients presented with overweight lungs (>0% of excess lung weight). Leukocytes, neutrophils, D-dimer, and LDH were higher in patients with overweight lungs. Among the 47 blood biomarkers investigated, interferon alpha 2 protein was higher and leukocyte inhibitory factor was lower in patients with overweight lungs. According to CombiROC analysis, the combinations of D-dimer/LDH/leukocytes, D-dimer/LDH/neutrophils, and D-dimer/LDH/leukocytes/neutrophils achieved the highest area under the curve with the best accuracy to detect overweight lungs. Conclusion: The combinations of these specific laboratory data: D-dimer/LDH/leukocytes or D-dimer/LDH/neutrophils or D-dimer/LDH/leukocytes/neutrophils were the best predictors of overweight lungs in patients with COVID-19 pneumonia at hospital admission. Clinical trial registration: Brazilian Registry of Clinical Trials (REBEC) number RBR-88bs9x and ClinicalTrials.gov number NCT04561219.
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BACKGROUND: AKI is one of the COVID-19 complications with high prognostic significance. In our research, we studied the prognostic role of several biomarkers that could help us understand AKI pathogenesis in patients with COVID-19. METHODS: We evaluated the medical data of 500 patients hospitalized with COVID-19 in Tareev Clinic from 5 October 2020 to 1 March 2022. The diagnosis of COVID-19 was confirmed with positive RNA PCR in nasopharyngeal swabs and/or typical radiological findings on CT scans. Kidney function was assessed in accordance with KDIGO criteria. In the selected 89 patients, we evaluated serum levels of angiopoetin-1, KIM-1, MAC, and neutrophil elastase 2 and their prognostic significance. RESULTS: The incidence of AKI in our study was 38%. The main risk factors for kidney injury were male sex, cardiovascular diseases, and chronic kidney disease. High serum angiopoetin-1 levels and a decrease in blood lymphocyte count and fibrinogen level also increased the risk of AKI. CONCLUSIONS: AKI is an independent risk factor for death in patients with COVID-19. We propose the prognostic model of AKI development, which includes the combination of serum levels of angiopoetin-1 and KIM-1 on admission. Our model can help to prevent AKI development in patients with coronavirus disease.
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Since the outbreak of the 2019 pandemic coronavirus disease (COVID-19), great attention has been given to identifying the main clinical features of the disease. Identification of laboratory parameters able to classify patients based on their risk is mandatory to improve their clinical management. We retrospectively evaluated twenty-six laboratory tests measured in COVID-19 positive patients admitted to the hospital in March and April 2020 to find any correlation between their changes and the risk of death. We divided them into surviving and non-surviving patients. A total of 1587 patients were recruited, 854 males with median age of 71 (IQR 56-81) and 733 females with median age of 77 (IQR 61-87). On admission, death was found to be positively correlated with age (p=0.001), but not with sex (p=0.640) or with hospitalization in days (p=0.827). Brain natriuretic peptide (BNP), creatinine, C-reactive protein (CRP), INR, leukocyte count, lymphocyte count, neutrophil count, and procalcitonin (PCT) demonstrated a statistically significant difference between the two groups (p<0.001), suggesting their role as markers of disease severity; only lymphocyte count resulted as an independent risk factor for death.
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COVID-19 , Male , Female , Humans , COVID-19/epidemiology , Retrospective Studies , Prognosis , Hospitalization , Hospitals, Urban , BiomarkersABSTRACT
The liver is one of the common extrapulmonary organs involved in the coronavirus disease 2019 (COVID-19) infection. We aimed to find the prevalence of liver injury at hospital admission and its effects on outcomes. Methods: This is a single-center prospective observational study. All consecutive patients with COVID-19 admitted during the months of May to August 2021 were included in the study. Liver injury was defined as at least 2 times elevation of aspartate transaminase, alanine transaminase, alkaline phosphatase, and bilirubin above the upper limits on normal. The predictive efficacy of liver injury was measured as its effects on outcome variables, that is duration of hospital stay, requirement of ICU admission, mechanical ventilation, and mortality. Presence of liver injury compared with existing biomarkers markers of severe disease, that is lactate dehydrogenase, D-dimer, and C-reactive protein. Results: A total of 245 consecutive adult patients with COVID-19 infection were included in the study. Liver injury was present in 102 (41.63%) of patients. There was a significant association between the presence of liver injury and duration of hospital stay (10.74 vs. 8.9 days; P=0.013), the requirement of ICU admission (12.7 vs. 10.2%; P=0.018), mechanical ventilation (10.6% vs. 6.5%; P=0.003), and mortality (13.1% vs. 6.1%; P<0.001). Liver injury was significantly associated (P<0.001) with the corresponding elevation of serum biomarkers of severity. Conclusion: The presence of liver injury in patients with COVID-19 infection at the time of hospital admission is the independent predictor of poor outcomes and can also be used as the marker of disease severity.