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Antonia Anna Lukito

Bio: Antonia Anna Lukito is an academic researcher from University of Pelita Harapan. The author has contributed to research in topics: Medicine & Conventional PCI. The author has an hindex of 8, co-authored 21 publications receiving 513 citations.

Papers
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Journal ArticleDOI
TL;DR: Hypertension was associated with increased composite poor outcome, including mortality, severe COVID-19, acute respiratory distress syndrome (ARDS), need for intensive care unit (ICU) care and disease progression in patients with CO VID-19.
Abstract: Objective:To investigate the association between hypertension and outcome in patients with Coronavirus Disease 2019 (COVID-19) pneumonia.Methods:We performed a systematic literature search from sev...

261 citations

Journal ArticleDOI
TL;DR: In this paper, the authors performed a systematic literature search from several electronic databases up until 8 September 2020 and reported that increase in CFS was associated with increase in mortality in a linear fashion, and the potential for a nonlinear relationship based on ORs of each quantitative clinical frailty scale was examined using restricted cubic splines with a three-knots model.

123 citations

Journal ArticleDOI
TL;DR: A meta-analysis of the dose-response relationship between body mass index (BMI) and poor outcome in patients with COVID-19 demonstrated that obesity was associated with composite poor outcome.

117 citations

Journal ArticleDOI
TL;DR: Elevated NT-proBNP level was associated with increased mortality in COVID-19 pneumonia and summary receiver operating characteristic curve analysis demonstrates an area under curve of 0.90.
Abstract: Objectives This systematic review and meta-analysis aimed to assess the association between N-terminal pro-brain natriuretic peptide (NT-proBNP) and mortality in patients with COVID-19. Methods Systematic literature search from several electronic databases were performed. The outcome was mortality (non-survivor) in patients with COVID-19 pneumonia. NT-proBNP data were in continuous variable (pg/mL), dichotomous data (elevated/non-elevated) and effect estimate adjusted to cardiac injury/elevated biomarkers of cardiac injury. Results A total of 967 patients from six studies were included in this analysis. NT-proBNP was higher in non-survivor group (standardised mean difference 0.75 (0.44, 1.07), p Conclusion Elevated NT-proBNP level was associated with increased mortality in COVID-19 pneumonia.

85 citations

Journal ArticleDOI
TL;DR: It was revealed that COPD and smoking were associated with poor outcomes in patients with COVID-19, and current smokers were at higher risk of composite poor outcomes.
Abstract: OBJECTIVE: To investigate the association between chronic obstructive pulmonary disease (COPD) and smoking with outcome in patients with COVID-19.METHODS: A systematic literature search was performed using PubMed, EuropePMC, SCOPUS and the Cochrane Central Database. A composite of poor outcome, mortality, severe COVID-19, the need for treatment in an intensive care unit (ICU) and disease progression were the outcomes of interest.RESULTS: Data on 4603 patients were pooled from 21 studies. COPD was associated with an increased risk for composite poor outcome (OR 5.01, 95%CI 3.06-8.22; P < 0.001; I² 0%), mortality (OR 4.36, 95%CI 1.45-13.10; P = 0.009; I² 0%), severe COVID-19 (OR 4.62, 95%CI 2.49-8.56; P < 0.001; I² 0%), ICU care (OR 8.33, 95%CI 1.27-54.56; P = 0.03; I² 0%), and disease progression (OR 8.42, 95%CI 1.60-44.27; P = 0.01; I² 0%). Smoking was found to increase the risk of composite poor outcome (OR 1.52, 95%CI 1.16-2.00; P = 0.005; I² 12%), and subgroup analysis showed that smoking was significant for increased risk of severe COVID-19 (OR 1.65, 95%CI 1.17-2.34; P = 0.004; I² 11%). Current smokers were at higher risk of composite poor outcomes (OR 1.58, 95%CI 1.10-2.27; P = 0.01; I² 0%) than former/non-smokers.CONCLUSION: Our systematic review and meta-analysis revealed that COPD and smoking were associated with poor outcomes in patients with COVID-19.

80 citations


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01 Jan 2020
TL;DR: Prolonged viral shedding provides the rationale for a strategy of isolation of infected patients and optimal antiviral interventions in the future.
Abstract: Summary Background Since December, 2019, Wuhan, China, has experienced an outbreak of coronavirus disease 2019 (COVID-19), caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Epidemiological and clinical characteristics of patients with COVID-19 have been reported but risk factors for mortality and a detailed clinical course of illness, including viral shedding, have not been well described. Methods In this retrospective, multicentre cohort study, we included all adult inpatients (≥18 years old) with laboratory-confirmed COVID-19 from Jinyintan Hospital and Wuhan Pulmonary Hospital (Wuhan, China) who had been discharged or had died by Jan 31, 2020. Demographic, clinical, treatment, and laboratory data, including serial samples for viral RNA detection, were extracted from electronic medical records and compared between survivors and non-survivors. We used univariable and multivariable logistic regression methods to explore the risk factors associated with in-hospital death. Findings 191 patients (135 from Jinyintan Hospital and 56 from Wuhan Pulmonary Hospital) were included in this study, of whom 137 were discharged and 54 died in hospital. 91 (48%) patients had a comorbidity, with hypertension being the most common (58 [30%] patients), followed by diabetes (36 [19%] patients) and coronary heart disease (15 [8%] patients). Multivariable regression showed increasing odds of in-hospital death associated with older age (odds ratio 1·10, 95% CI 1·03–1·17, per year increase; p=0·0043), higher Sequential Organ Failure Assessment (SOFA) score (5·65, 2·61–12·23; p Interpretation The potential risk factors of older age, high SOFA score, and d-dimer greater than 1 μg/mL could help clinicians to identify patients with poor prognosis at an early stage. Prolonged viral shedding provides the rationale for a strategy of isolation of infected patients and optimal antiviral interventions in the future. Funding Chinese Academy of Medical Sciences Innovation Fund for Medical Sciences; National Science Grant for Distinguished Young Scholars; National Key Research and Development Program of China; The Beijing Science and Technology Project; and Major Projects of National Science and Technology on New Drug Creation and Development.

4,408 citations

Journal ArticleDOI
TL;DR: A systematic review and meta-analysis showed that lymphopenia on admission was associated with poor outcome in patients with COVID-19 and the association between lymphocyte count and composite poor outcome was affected by age.
Abstract: Clinical and laboratory biomarkers to predict the severity of coronavirus disease 2019 (COVID-19) are essential in this pandemic situation of which resource allocation must be urgently prepared especially in the context of respiratory support readiness. Lymphocyte count has been a marker of interest since the first COVID-19 publication. We conducted a systematic review and meta-analysis in order to investigate the association of lymphocyte count on admission and the severity of COVID-19. We would also like to analyze whether patient characteristics such as age and comorbidities affect the relationship between lymphocyte count and COVID-19. Comprehensive and systematic literature search was performed from PubMed, SCOPUS, EuropePMC, ProQuest, Cochrane Central Databases, and Google Scholar. Research articles in adult patients diagnosed with COVID-19 with information on lymphocyte count and several outcomes of interest, including mortality, acute respiratory distress syndrome (ARDS), intensive care unit (ICU) care, and severe COVID-19, were included in the analysis. Inverse variance method was used to obtain mean differences and its standard deviations. Maentel-Haenszel formula was used to calculate dichotomous variables to obtain odds ratios (ORs) along with its 95% confidence intervals. Random-effect models were used for meta-analysis regardless of heterogeneity. Restricted-maximum likelihood random-effects meta-regression was performed for age, gender, cardiac comorbidity, hypertension, diabetes mellitus, COPD, and smoking. There were a total of 3099 patients from 24 studies. Meta-analysis showed that patients with poor outcome have a lower lymphocyte count (mean difference − 361.06 μL [− 439.18, − 282.95], p < 0.001; I2 84%) compared to those with good outcome. Subgroup analysis showed lower lymphocyte count in patients who died (mean difference − 395.35 μL [− 165.64, − 625.07], p < 0.001; I2 87%), experienced ARDS (mean difference − 377.56 μL [− 271.89, − 483.22], p < 0.001; I2 0%), received ICU care (mean difference − 376.53 μL [− 682.84, − 70.22], p = 0.02; I2 89%), and have severe COVID-19 (mean difference − 353.34 μL [− 250.94, − 455.73], p < 0.001; I2 85%). Lymphopenia was associated with severe COVID-19 (OR 3.70 [2.44, 5.63], p < 0.001; I2 40%). Meta-regression showed that the association between lymphocyte count and composite poor outcome was affected by age (p = 0.034). This meta-analysis showed that lymphopenia on admission was associated with poor outcome in patients with COVID-19.

464 citations

Journal ArticleDOI
TL;DR: Individuals with underlying cardiometabolic disease and that present with evidence for acute inflammation and end‐organ damage are at higher risk of mortality due to COVID‐19 infection and should be managed with greater intensity.
Abstract: Mortality rates of coronavirus disease-2019 (COVID-19) continue to rise across the world. Information regarding the predictors of mortality in patients with COVID-19 remains scarce. Herein, we performed a systematic review of published articles, from 1 January to 24 April 2020, to evaluate the risk factors associated with mortality in COVID-19. Two investigators independently searched the articles and collected the data, in accordance with PRISMA guidelines. We looked for associations between mortality and patient characteristics, comorbidities, and laboratory abnormalities. A total of 14 studies documenting the outcomes of 4659 patients were included. The presence of comorbidities such as hypertension (odds ratio [OR], 2.5; 95% confidence interval [CI], 2.1-3.1; P < .00001), coronary heart disease (OR, 3.8; 95% CI, 2.1-6.9; P < .00001), and diabetes (OR, 2.0; 95% CI, 1.7-2.3; P < .00001) were associated with significantly higher risk of death amongst patients with COVID-19. Those who died, compared with those who survived, differed on multiple biomarkers on admission including elevated levels of cardiac troponin (+44.2 ng/L, 95% CI, 19.0-69.4; P = .0006); C-reactive protein (+66.3 µg/mL, 95% CI, 46.7-85.9; P < .00001); interleukin-6 (+4.6 ng/mL, 95% CI, 3.6-5.6; P < .00001); D-dimer (+4.6 µg/mL, 95% CI, 2.8-6.4; P < .00001); creatinine (+15.3 µmol/L, 95% CI, 6.2-24.3; P = .001); and alanine transaminase (+5.7 U/L, 95% CI, 2.6-8.8; P = .0003); as well as decreased levels of albumin (-3.7 g/L, 95% CI, -5.3 to -2.1; P < .00001). Individuals with underlying cardiometabolic disease and that present with evidence for acute inflammation and end-organ damage are at higher risk of mortality due to COVID-19 infection and should be managed with greater intensity.

444 citations

Journal ArticleDOI
TL;DR: This meta-analysis showed that an elevated serum CRP, PCT, D-dimer, and ferritin were associated with a poor outcome in COVID-19, a critically ill patients critically ill with coronavirus disease-2019.
Abstract: Background:Patients critically ill with coronavirus disease-2019 (COVID-19) feature hyperinflammation, and the associated biomarkers may be beneficial for risk stratification. We aimed to investiga...

371 citations

Journal ArticleDOI
TL;DR: In this paper, the authors reviewed the existing literature and knowledge of ACE2 in COVID-19 setting and focused on its pathophysiologic involvement in disease progression, clinical outcomes, and therapeutic potential.
Abstract: COVID-19 pandemic is caused by the novel coronavirus SARS-CoV-2. Angiotensin-converting enzyme 2 (ACE2) is not only an enzyme but also a functional receptor on cell surfaces through which SARS-CoV-2 enters the host cells and is highly expressed in the heart, kidneys, and lungs and shed into the plasma. ACE2 is a key regulator of the renin-angiotensin-aldosterone system (RAAS). SARS-CoV-2 causes ACE/ACE2 balance disruption and RAAS activation, which leads ultimately to COVID-19 progression, especially in patients with comorbidities, such as hypertension, diabetes mellitus, and cardiovascular disease. Therefore, ACE2 expression may have paradoxical effects, aiding SARS-CoV-2 pathogenicity, yet conversely limiting viral infection. This article reviews the existing literature and knowledge of ACE2 in COVID-19 setting and focuses on its pathophysiologic involvement in disease progression, clinical outcomes, and therapeutic potential.

325 citations