Severe Coronavirus Disease 2019 Patients Research Articles

Relationship Between BMI and Disease Severity in COVID-19 Patients.

Obesity and increased body mass index (BMI) are associated with coronavirus disease 2019 (COVID-19)-related complications and severity. They can exacerbate the cytokine storm and lead to severe symptoms or death in obese patients. This cross-sectional descriptive study included patients with COVID-19 admitted to the Razi Hospital in Ahvaz, Iran, from January 2019 to December 2020. We evaluated the effect of BMI of patients admitted to the general ward and invasive unit care (ICU) on the length of hospitalization. We included a total of 466 patients (male: 281 or 60.3% vs. female: 185 or 39.7%) with a mean age of 59.49 ± 14.5 years in the study. Also, 47 (10.1%) patients were admitted to the ICU, and 418 (89.7%) patients to the general ward. A higher BMI was associated with longer hospitalization (P < 0.001). Patients with BMI in the range of 18.5 - 24.9 experienced a longer hospitalization (10-20 days) (P < 0.001). BMI had no significant effect on ICU hospitalization (P = 0.36). Also, there was no significant difference between the two groups regarding the length of hospitalization (P = 0.49). Furthermore, non-diabetic patients were less likely to be admitted to the ICU (73.3% vs. 26.7%) (P < 0.001). The number of discharged patients was higher in patients admitted to the general ward compared to those admitted to the ICU (93.8% vs. 63.8%) (P < 0.001). According to our results, a higher BMI was a risk factor for COVID-19, especially in the early stage of infection.

Reconstructed Genome-Scale Metabolic Model Characterizes Adaptive Metabolic Flux Changes in Peripheral Blood Mononuclear Cells in Severe COVID-19 Patients.

Coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) poses a mortal threat to human health. The elucidation of the relationship between peripheral immune cells and the development of inflammation is essential for revealing the pathogenic mechanism of COVID-19 and developing related antiviral drugs. The immune cell metabolism-targeting therapies exhibit a desirable anti-inflammatory effect in some treatment cases. In this study, based on differentially expressed gene (DEG) analysis, a genome-scale metabolic model (GSMM) was reconstructed by integrating transcriptome data to characterize the adaptive metabolic changes in peripheral blood mononuclear cells (PBMCs) in severe COVID-19 patients. Differential flux analysis revealed that metabolic changes such as enhanced aerobic glycolysis, impaired oxidative phosphorylation, fluctuating biogenesis of lipids, vitamins (folate and retinol), and nucleotides played important roles in the inflammation adaptation of PBMCs. Moreover, the main metabolic enzymes such as the solute carrier (SLC) family 2 member 3 (SLC2A3) and fatty acid synthase (FASN), responsible for the reactions with large differential fluxes, were identified as potential therapeutic targets. Our results revealed the inflammation regulation potentials of partial metabolic reactions with differential fluxes and their metabolites. This study provides a reference for developing potential PBMC metabolism-targeting therapy strategies against COVID-19.

Circulating tumor necrosis factor receptors are associated with mortality and disease severity in COVID-19 patients.

BackgroundAlthough hyperinflammatory response influences the severity of coronavirus disease 2019 (COVID-19), little has been reported about the utility of tumor necrosis factor (TNF)-related biomarkers in reflecting the prognosis. We examined whether TNF receptors (TNFRs: TNFR1, TNFR2) and progranulin (PGRN) levels, in addition to interleukin 6 (IL-6) and C-reactive protein (CRP), are associated with mortality or disease severity in COVID-19 patients.MethodsThis retrospective study was conducted at Juntendo University Hospital. Eighty hospitalized patients with various severities of COVID-19 were enrolled. Furthermore, serum levels of TNF-related biomarkers were measured using enzyme-linked immunosorbent assay.ResultsTwenty-five patients died during hospitalization, and 55 were discharged. The median (25th and 75th percentiles) age of the study patients was 70 (61–76) years, 44 (55.0%) patients were males, and 26 (32.5%) patients had chronic kidney disease (CKD). When comparing with patients who received and did not receive treatment at the intensive care unit (ICU), the former had a higher tendency of being male and have diabetes, hypertension, and CKD; had higher levels of white blood cells, D-dimer, and lactate dehydrogenase; and had lower body mass index, estimated glomerular filtration rate, and lymphocyte counts. Significant differences were observed in TNFR, PGRN, IL-6, and CRP levels between each severity (mild–severe) group. Furthermore, the serum levels of TNFR, IL-6, and CRP, but not PGRN, in ICU patients were significantly higher than in the patients who were not admitted to the ICU. Multivariate logistic regression analysis demonstrated that high levels of TNFR2 were only associated with mortality in patients with COVID-19 even after adjustment for relevant clinical parameters.ConclusionsHigh TNFR2 level might be helpful for predicting mortality or disease severity in patients with COVID-19.

INFLAMMATION OVERDRIVE: A CONFIRMED DIAGNOSIS OF HEMOPHAGOCYTIC LYMPHOHISTIOCYTOSIS RESULTING FROM COVID-19

INFLAMMATION OVERDRIVE: A CONFIRMED DIAGNOSIS OF HEMOPHAGOCYTIC LYMPHOHISTIOCYTOSIS RESULTING FROM COVID-19

Comparative Upper Respiratory Tract Transcriptomic Profiling Reveals a Potential Role of Early Activation of Interferon Pathway in Severe COVID-19.

Infection with SARS-CoV-2 results in Coronavirus disease 2019 (COVID-19) is known to cause mild to acute respiratory infection and sometimes progress towards respiratory failure and death. The mechanisms driving the progression of the disease and accumulation of high viral load in the lungs without initial symptoms remain elusive. In this study, we evaluated the upper respiratory tract host transcriptional response in COVID-19 patients with mild to severe symptoms and compared it with the control COVID-19 negative group using RNA-sequencing (RNA-Seq). Our results reveal an upregulated early type I interferon response in severe COVID-19 patients as compared to mild or negative COVID-19 patients. Moreover, severely symptomatic patients have pronounced induction of interferon stimulated genes (ISGs), particularly the oligoadenylate synthetase (OAS) family of genes. Our results are in concurrence with other studies depicting the early induction of IFN-I response in severe COVID-19 patients, providing novel insights about the ISGs involved.

Neutrophil-to-Lymphocyte Ratio and Platelet-to-Lymphocyte Ratio Can Predict the Severity in COVID-19 Patients from Ethiopia: A Retrospective Study.

BackgroundCoronaviruses are a broad family of pathogens that can cause mild to severe respiratory illnesses. Due to a strong inflammatory response and a weak immunological response, viral pneumonia inflammation, like Coronavirus Disease 2019 (COVID-19), displays an unbalanced immune response. Therefore, circulating biomarkers of inflammation and the immune system can serve as reliable predictors of a patient’s prognosis for COVID-19. Hematological ratios are reliable markers of inflammation that are frequently utilized in pneumonia, primarily in viral infections with low cost in developing countries.PurposeTo examine the neutrophil-to-lymphocyte ratio (NLR), lymphocyte-to-monocyte ratio (LMR), and platelet-to-lymphocyte ratio (PLR) in predicting the severity of COVID-19 patients.MethodsAn institutional-based retrospective study was done on 105 hospitalized COVID-19 patients at the University of Gondar comprehensive specialized referral hospital, Northwest Ethiopia. The laboratory evaluations that were gathered, evaluated, and reported on included the total leucocyte count (TLC), absolute neutrophil count (ANC), absolute lymphocyte count (ALC), absolute monocyte count (AMC), NLR, LMR, and PLR. The Kruskal–Wallis test and Wilcoxon matched-pairs signed test were used to see whether there were any differences between the continuous variables. Receiver operating curve (ROC) analysis was used to determine the appropriate cut-off values for NLR, PLR, and LMR. P-value <0.05 was considered a statistically significant association.ResultsANC, NLR, and PLR were highest in the critical group (p = 0.001), while this group had the least ALC and LMR (p = 0.001). We calculated the optimal cut-off values of the hematological ratios; NLR (8.4), LMR (1.4), and PLR (18.0). NLR had the highest specificity and sensitivity, at 83.8% and 80.4%, respectively.ConclusionOur research showed that NLR and PLR were good indicators of severity in COVID-19. However, our findings indicate that MLR is not a reliable predictor.

Highlights of clinical and laboratory parameters among severe COVID-19 patients treated with tocilizumab: a retrospective observational study.

ABSTRACTBACKGROUND:Coronavirus disease 2019 (COVID-19) can cause cytokine release syndrome (CRS), which leads to high mortality rates. Tocilizumab suppresses CRS by blocking the signal transduction of interleukin-6 (IL-6).OBJECTIVE:To evaluate the clinical and laboratory parameters associated with mortality among patients receiving tocilizumab treatment.DESIGN AND SETTING:Retrospective observational study conducted in the chest disease departments of two different training and research hospitals in the center of Ankara, Turkey.METHODS:Patients who were hospitalized and treated with tocilizumab in September 2020 were retrospectively analyzed. Their laboratory parameters and clinical characteristics were obtained from the hospital information system database. Comparative analyses were performed between the patients who died and the ones who survived.RESULTS:A total of 58 patients who received tocilizumab treatment were included in this study, among whom 35 (60.3%) died. There was no difference between the mortality and survival groups in terms of white blood cell (WBC), neutrophil, lymphocyte, ferritin or C-reactive protein (CRP) levels detected on admission. WBC, lymphocyte, neutrophil and CRP levels measured on the third and fifth days after tocilizumab administration were found to be significantly lower in the survival group (P < 0.05). In multiple logistic regression analysis, age and oxygen saturation were determined to be independent risk factors for mortality.CONCLUSION:Persistently high WBC, CRP and neutrophil levels and low lymphocyte levels could be considered to be valuable indicators of mortality among COVID-19 patients treated with tocilizumab. Age and low oxygen saturation are independent risk factors for mortality among patients receiving tocilizumab treatment.

EXTRACORPOREAL MEMBRANE OXYGENATION: A HOPE FOR THE SICKEST PATIENTS WITH COVID-19

EXTRACORPOREAL MEMBRANE OXYGENATION: A HOPE FOR THE SICKEST PATIENTS WITH COVID-19

Persistent but dysfunctional mucosal SARS-CoV-2-specific IgA and low lung IL-1β associate with COVID-19 fatal outcome: A cross-sectional analysis.

The role of the mucosal pulmonary antibody response in coronavirus disease 2019 (COVID-19) outcome remains unclear. Here, we found that in bronchoalveolar lavage (BAL) samples from 48 patients with severe COVID-19-infected with the ancestral Wuhan virus, mucosal IgG and IgA specific for S1, receptor-binding domain (RBD), S2, and nucleocapsid protein (NP) emerged in BAL containing viruses early in infection and persist after virus elimination, with more IgA than IgG for all antigens tested. Furthermore, spike-IgA and spike-IgG immune complexes were detected in BAL, especially when the lung virus has been cleared. BAL IgG and IgA recognized the four main RBD variants. BAL neutralizing titers were higher early in COVID-19 when virus replicates in the lung than later in infection after viral clearance. Patients with fatal COVID-19, in contrast to survivors, developed higher levels of mucosal spike-specific IgA than IgG but lost neutralizing activities over time and had reduced IL-1β in the lung. Altogether, mucosal spike and NP-specific IgG and S1-specific IgA persisting after lung severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) clearance and low pulmonary IL-1β correlate with COVID-19 fatal outcome. Thus, mucosal SARS-CoV-2-specific antibodies may have adverse functions in addition to protective neutralization.HighlightsMucosal pulmonary antibody response in COVID-19 outcome remains unclear. We show that in severe COVID-19 patients, mucosal pulmonary non-neutralizing SARS-CoV-2 IgA persit after viral clearance in the lung. Furthermore, low lung IL-1β correlate with fatal COVID-19. Altogether, mucosal IgA may exert harmful functions beside protective neutralization.

280 Emergency Department Predictors of Mortality for Adult Patients With Severe Coronavirus Disease-19 (COVID-19) in a Tertiary Hospital: A Retrospective Cohort Study

The data regarding the predictors of mortality in Coronavirus disease-19 (COVID-19) patients remains limited since the disease entity is very novel. Determining the factors affecting the mortality of these patients are needed in the development of guidelines and other significant health policies concerning triaging and patient management. This study aims to determine the variables affecting the mortality of severe and critical COVID-19 patients based on their initial presentation and work-up in the emergency department (ED).

Correlation of antigen-specific immune response with disease severity among COVID-19 patients in Bangladesh.

Coronavirus disease 2019 (COVID-19) is a protean disease causing different degrees of clinical severity including fatality. In addition to humoral immunity, antigen-specific T cells may play a critical role in defining the protective immune response against SARS-CoV-2, the virus that causes this disease. As a part of a longitudinal cohort study in Bangladesh to investigate B and T cell-specific immune responses, we sought to evaluate the activation-induced marker (AIM) and the status of different immune cell subsets during a COVID-19 infection. We analyzed a total of 115 participants, which included participants with asymptomatic, mild, moderate, and severe clinical symptoms. We observed decreased mucosal-associated invariant T (MAIT) cell frequency on the initial days of the COVID-19 infection in symptomatic patients compared to asymptomatic patients. However, natural killer (NK) cells were found to be elevated in symptomatic patients just after the onset of the disease compared to both asymptomatic patients and healthy individuals. Moreover, we found a significant increase of AIM+ (both OX40+CD137+ and OX40+CD40L+) CD4+ T cells in moderate and severe COVID-19 patients in response to SARS-CoV-2 peptides (especially spike peptides) compared to pre-pandemic controls who are unexposed to SARS-CoV-2. Notably, we did not observe any significant difference in the CD8+ AIMs (CD137+CD69+), which indicates the exhaustion of CD8+ T cells during a COVID-19 infection. These findings suggest that patients who recovered from moderate and severe COVID-19 were able to mount a strong CD4+ T-cell response against shared viral determinants that ultimately induced T cells to mount further immune responses to SARS-CoV-2.

Low muscle mass and high visceral fat mass predict mortality in patients hospitalized with moderate-to-severe COVID-19: a prospective study.

IntroductionThe severity of coronavirus disease 2019 (COVID-19) has been positively correlated with several comorbidities. The primary outcome of the study was to assess the relationship between the mortality and severity of COVID-19 and obesity classes according to BMI, visceral adipose tissue (VAT) area, s.c. adipose tissue area, muscle area (MA), and leptin levels.MethodsIn this prospective cohort study, 200 patients hospitalized with moderate-to-severe COVID-19 underwent an unenhanced CT of the thorax and laboratory tests, and leptin levels between June and August 2020 were obtained.ResultsOur study included 200 patients (male 52%; mean age: 62 (49–74) years; obesity (BMI > 30): 51.5%)). Fifty-eight patients (23.5%) were admitted to the intensive care unit and 29 (14.5%) died. In multivariate logistic regression (corrected for leptin, sex, age, and serum biomarkers) and receiver operating characteristic curve analyses, high VAT > 150 cm2 (odds ratio (OR): 6.15; P < 0.002), MA < 92 cm2 (OR: 7.94; P < 0.005), and VAT/MA ratio > 2 (OR: 13.9; P < 0.0001) were independent risk factors for mortality. Indeed, the Kaplan–Meier curves showed that patients with MA < 92 cm2 and without obesity (BMI < 30) had a lower survival rate (hazard ratio between 3.89 and 9.66; P < 0.0006) than the other groups. Leptin levels were not related to mortality and severity.ConclusionThis prospective study reports data on the largest number of hospitalized severe COVID-19 patients and pinpoints VAT area and MA calculated by CT as predictors of COVID-19 mortality.

Importance of Insulin Resistance in the COVID-19 Era: A Retrospective Analysis of a Single Center in Mexico.

Introduction and objectivesType 2 diabetes mellitus (T2DM) has been one of the main risk factors associated with mortality from the coronavirus disease 2019 (COVID-19). Insulin resistance (IR) is a preceding and underlying condition of T2DM, which has been thought that it could increase mortality from COVID-19 since it favors the entry of severe acute respiratory syndrome coronavirus type 2 in the host cell. This article reports a biochemical study that estimated the prevalence of IR in COVID-19 patients and non-diabetic patients without COVID-19 history. It also assesses the prognostic role of IR in the evolution of patients with COVID-19.Materials and methodsIn this single-center, retrospective and cross-sectional design, we included patients with severe and critical COVID-19 and non-diabetic patients without COVID-19 history. We calculated the Homeostatic Model Assessment Insulin Resistance (HOMA-IR) and defined IR with a HOMA-IR >2.6. We estimated the prevalence of IR in both groups and used x2 to assess the association between IR and mortality from severe and critical COVID-19.ResultsOne hundred and twenty-three COVID-19 patients were included with a mean age of 53±15 years: 77 (62.6%) were men and 46 (37.4%) were women. Eighty (65%) patients were critical while the rest were severe. Forty-three (35%) patients died. Seventy-one (57.7%) patients had IR; there was no evidence of an association between IR and mortality from severe or critical COVID-19. Fifty-five non-diabetic patients without COVID-19 history were included with a median age of 40 (26-60) years; 35 (63.6%) were men and 20 (36.4%) were women. Nineteen (34.5%) people had IR.ConclusionIR was more prevalent in patients with severe and critical COVID-19 than in non-diabetic patients without COVID-19 history. Our results showed no evidence of the association between IR and mortality from severe and critical COVID-19.

SARS-CoV-2 infection increases the gene expression profile for Alzheimer’s disease risk

The coronavirus disease 2019 (COVID-19) pandemic has caused over 600,000,000 infections globally thus far. Up to 30% of individuals with mild to severe disease develop long COVID, exhibiting diverse neurologic symptoms including dementias. However, there is a paucity of knowledge of molecular brain markers and whether these can precipitate the onset of Alzheimer’s disease (AD). Herein, we report the brain gene expression profiles of severe COVID-19 patients showing increased expression of innate immune response genes and genes implicated in AD pathogenesis. The use of a mouse-adapted strain of SARS-CoV-2 (MA10) in an aged mouse model shows evidence of viral neurotropism, prolonged viral infection, increased expression of tau aggregator FKBP51, interferon-inducible gene Ifi204, and complement genes C4 and C5AR1. Brain histopathology shows AD signatures including increased tau-phosphorylation, tau-oligomerization, and α-synuclein expression in aged MA10 infected mice. The results of gene expression profiling of SARS-CoV-2-infected and AD brains and studies in the MA10 aged mouse model taken together, for the first time provide evidence suggesting that SARS-CoV-2 infection alters expression of genes in the brain associated with the development of AD. Future studies of common molecular markers in SARS-CoV-2 infection and AD could be useful for developing novel therapies targeting AD.

Characteristics of Albumin Levels and Liver Function in Patients With COVID-19 at H. Adam Malik Hospital, Medan

Background: COVID-19 (Corona Virus Disease-2019) pandemic has a high mortality rate especially in Medan, Indonesia. Serum albumin and liver function tests are believed to be predictive biomarkers for prognosis in patients with infectious diseases, including COVID-19. This study aimed to investigate the association between the mortality events and severely ill COVID-19 patients' serum albumin and liver enzymes. Method: This is a cross-sectional study using secondary data from the medical records of H. Adam Malik Hospital patients with COVID-19 who were confirmed by RT-PCR from August to December 2020. All patients were analyzed for age, sex, hypoalbuminemia, increased liver enzymes and outcome using Chi-square tests (P&lt;0.05). Results: The average age of severe COVID-19 patients at H. Adam Malik Hospital ranged from 41 to 60 years, with more women prevalence than men. Most of the patients had hypoalbuminemia (84.2%), an increase in AST (59.4)% and ALT (45.5%). There was no significant association between hypoalbuminemia and the disease outcome (P=0.12). There was a significant association between elevated liver enzymes and mortality in severely ill COVID-19 patients (P&lt;0.001). Conclusion: We found that hypoalbuminemia is common in patients with severe COVID-19. However, we found that albumin levels had no association with the patients' mortality rate. Liver enzymes levels appear to be a predictive biomarker for outcomes in COVID-19 patients of H. Adam Malik Hospital. We found that higher ALT and AST levels were associated with significantly higher mortality.

Patients with severe coronavirus disease 2019 have high frequency of factor 5 Leiden and prothrombin gene mutations.

We investigated the frequency of factor 5 Leiden (FVL) and prothrombin gene (PTG) mutations in patients with severe coronavirus disease 2019 (COVID-19). Our primary aim is to reveal whether these mutations are associated with severity of disease and mortality. A total of 249 patients were included in this cross-sectional study. Severe COVID-19 cases (with oxygen saturation of less than 90 mmHg and who received ventilation support invasively or noninvasively) were included. FVL and PTG mutations were identified by real time- PCR technique. Frequency of mutations for FVL was 11.7%, whereas for PTG was 3.5%. The frequency of FVL and PTG's mutations in our patient group was found to be significantly higher than the normal population ( P < 0.0001, 0.004, respectively). There was no difference in the frequency of mutations of FVL and PTG between the patients ventilated - invasively and noninvasively. There was also no difference in D-dimer, ferritin, fibrinogen, ex status, and entubational status between the groups of FVL and PTG mutated and wild-type. To the best of our knowledge, it is the first time that we have examined the frequencies of FVL and PGM's mutations in severe COVID-19 disease on such a large scale. The frequencies of both mutations in severe COVID-19 patients were higher than in the healthy population. We believe that studies prospectively designed, including asymptomatic and mild COVID-19 patients, will provide more comprehensive information on the subject.

Characteristics and outcomes of COVID-19 in heart transplantation recipients in the Netherlands.

BackgroundImmunocompromised patients are at high risk of complicated severe acute respiratory coronavirus 2 infection. The aim of this retrospective study was to describe the characteristics and outcomes of heart transplantation (HTx) recipients with coronavirus disease 2019 (COVID-19) in the Netherlands.MethodsHTx patients from one of the three HTx centres in the Netherlands with COVID-19 (proven by positive reverse-transcription polymerase chain reaction or serology test result) between February 2020 and June 2021 were included. The primary endpoint was all-cause mortality and the secondary endpoint was disease severity.ResultsCOVID-19 was diagnosed in 54/665 HTx patients (8%), with a mean (± standard deviation (SD)) time after HTx of 11 ± 8 years. Mean (± SD) age was 53 ± 14 years and 39% were female. Immunosuppressive therapy dosage was reduced in 37% patients (20/54). Hospitalisation was required in 39% patients (21/54), and 13% patients (7/54) had severe COVID-19 (leading to intensive care unit (ICU) admission or death). In-hospital mortality was 14% (3/21), and all-cause mortality was 6%. Compared with patients with moderate COVID-19 (hospitalised without ICU indication), severe COVID-19 patients tended to be transplanted earlier and had a significantly higher mean (± SD) body mass index (26 ± 3 vs 30 ± 3 kg/m2, p = 0.01). Myocardial infarction, cellular rejection and pulmonary embolism were observed once in three different HTx patients.ConclusionHTx patients were at increased risk of complicated COVID-19 with frequent hospitalisation, but the all-cause mortality was substantially lower than previously described (7–33%).Supplementary InformationThe online version of this article (10.1007/s12471-022-01720-9) contains supplementary material, which is available to authorized users.

Leukocyte glucose index as a novel biomarker for COVID-19 severity

The severity of coronavirus disease 2019 (COVID-19) quickly progresses with unfavorable outcomes due to the host immune response and metabolism alteration. Hence, we hypothesized that leukocyte glucose index (LGI) is a biomarker for severe COVID-19. This study involved 109 patients and the usefulness of LGI was evaluated and compared with other risk factors to predict COVID 19 severity. LGI was identified as an independent risk factor (odds ratio [OR] = 1.727, 95% confidence interval [CI]: 1.026–3.048, P = 0.041), with an area under the curve (AUC) of 0.749 (95% CI: 0.642–0.857, P < 0.0001). Interestingly, LGI was a potential risk factor (OR = 2.694, 95% CI: 1.575–5.283, Pcorrected < 0.05) for severe COVID-19 in female but not in male patients. In addition, LGI proved to be a strong predictor of the severity in patients with diabetes (AUC = 0.915 (95% CI: 0.830–1), sensitivity = 0.833, and specificity = 0.931). The AUC of LGI, together with the respiratory rate (LGI + RR), showed a considerable improvement (AUC = 0.894, 95% CI: 0.835–0.954) compared to the other biochemical and respiratory parameters analyzed. Together, these findings indicate that LGI could potentially be used as a biomarker of severity in COVID-19 patients.

Effect of COVID-19 on Serum Activity of Liver Enzymes: Is This Associated with Severity and Mortality Rate?

Abstract Introduction Coronavirus disease 2019 (COVID-19) is a viral infection caused by a novel coronavirus known as the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The disease raises an enormous public health challenge for the international community. Liver enzymes have been reported to be frequently elevated in hospitalized patients with severe COVID-19 disease. Materials and Methods This article is a narrative review of abnormal liver tests and liver injury as a manifestation of progression to severe pneumonia. We collected data from the PubMed database (National Library of Medicine, Bethesda, Maryland, United States). We used the search term “abnormal liver test” and relevant records were measured. The review article was organized thematically. Results This narrative review aims to summarize the available clinical data on abnormal liver enzymes in coronavirus infection and its association with the risk of mortality, severer pneumonia, and systemic inflammation. Some clinical studies refer to abnormal liver tests and liver injury as a manifestation of progression to severe pneumonia. Recent research verified the relationship between hepatic liver enzyme activities and liver damage in patients with COVID-19, which suggested that it might reflect the infection severity and the mortality risk. Thus, this review investigated the correlation between liver serum enzymes level and the severity of COVID-19 patients, by reviewing investigating the relationship between the illness severity in COVID-19 patients with abnormal liver tests, liver pathology, and markers of inflammation. Conclusion In the current pandemic of SARS-CoV-2, abnormalities of liver enzyme tests were commonly observed in patients with COVID-19. However, because of multiorgan damages that observed in COVID-19 patients, various issues should be considered such as the pathology and pathophysiology of the liver tissue, especially on the activation process of the immune response and cytokine storm to prevent the severity of the disease.

Intensive care unit-acquired weakness: A review from molecular mechanisms to its impact in COVID-2019.

Intensive Care Unit-Acquired Weakness (ICU-AW) is a generalized and symmetric neuromuscular dysfunction associated with critical illness and its treatments. Its incidence is approximately 80% in intensive care unit patients, and it manifests as critical illness polyneuropathy, critical illness myopathy, and muscle atrophy. Intensive care unit patients can lose an elevated percentage of their muscle mass in the first days after admission, producing short- and long-term sequelae that affect patients’ quality of life, physical health, and mental health. In 2019, the world was faced with coronavirus disease 2019 (COVID-19), caused by the acute respiratory syndrome coronavirus 2. COVID-19 produces severe respiratory disorders, such as acute respiratory distress syndrome, which increases the risk of developing ICU-AW. COVID-19 patients treated in intensive care units have shown early diffuse and symmetrical muscle weakness, polyneuropathy, and myalgia, coinciding with the clinical presentation of ICU-AW. Besides, these patients require prolonged intensive care unit stays, invasive mechanical ventilation, and intensive care unit pharmacological therapy, which are risk factors for ICU-AW. Thus, the purposes of this review are to discuss the features of ICU-AW and its effects on skeletal muscle. Further, we will describe the mechanisms involved in the probable development of ICU-AW in severe COVID-19 patients.