Admission Levels Research Articles

Factors associated with 30-day mortality in patients receiving mechanical circulatory support for cardiogenic shock

Abstract Introduction Mechanical circulatory support (MCS) is often deployed in patients with refractory cardiogenic shock complicating acute myocardial infarction (AMI-CS). Nevertheless, the mortality rate in these patients remains utterly high, around 50%. Purpose The aim of this study was to identify patient characteristics associated with 30-day mortality in patients receiving MCS for AMI-CS. Methods In the Netherlands, all patients undergoing percutaneous coronary intervention (PCI) are prospectively entered in the Netherlands Heart Registration (NHR). Additional data were retrieved for all CS patients between 2017-2021 in 14 Dutch hospitals, including MCS usage. Survivors and non-survivors amongst MCS treated patients were compared to identify patient characteristics associated with 30-day mortality. In addition, multivariate logistic regression analysis on imputed data was performed to quantify these associations in adjustment for confounders. Results MCS was deployed in 516 (23.3%) of all AMI-CS patients. MCS patients had a mean age of 64.2 (± 12.5) years and 74.6% were male. An intra-aortic balloon pump (IABP) was used in 49.0% of the patients. Impella, extracorporeal membrane oxygenation (ECMO) and multiple devices were used in 18.2%, 13.2% and 18.4% respectively. The overall 30-day mortality rate was 55.0%. At baseline, MCS survivors were younger (62.8 vs 65.2, p=0.03), had diabetes less often (18.4 vs. 28.0, p=0.02), and presented with a higher mean arterial pressure (MAP) (77.9 vs. 71.7, p<0.01). An out-of-hospital cardiac arrest (OHCA) preceded in 34.3% of the survivors versus 42.0% of the non-survivors (p=0.09). Survivors also had lower admission levels of lactate (5.0 vs. 7.8, p<0.01), glucose (12.1 vs. 15.2, p<0.01) and creatinine (94 vs. 115, p<0.01). Multivessel disease (MVD) was present less frequently in survivors compared to non-survivors (62.1% vs. 74.2%, p<0.01). In-hospital cardiac arrest (IHCA) occurred less often in survivors both prior to PCI (8.2% vs. 18.0%, p<0.01) and during PCI (22.8% vs. 34.6%, p<0.01). After multivariate logistic regression, higher age (OR 1.04, 95%CI: 1.02-1.05), resuscitation prior to (OR 2.11, 95 %CI: 1.09-4.09) or during PCI (OR 1.58, 95% CI: 1.01-2.47) and the presence of MVD (OR 2.07, 95% CI: 1.32-3.25) were independently associated with 30-day mortality in AMI-CS patients who received MCS. Conclusion In AMI-CS patients who received MCS, older age, the occurrence of an IHCA prior to or during PCI, and the presence of MVD were independently associated with an increased 30-day mortality.Figure 1.Table 1.

Timing of intravenous immunoglobulin treatment and outcome in Guillain-Barré syndrome: Is time nerve?

Despite treatment, a considerable proportion of patients with Guillain-Barré syndrome (GBS) experience poor recovery, highlighting a therapeutic need. There is a lack of evidence that treatment timing affects recovery. This study aims to investigate the effects of intravenous immunoglobulin (IVIg) timing on disability and speed of recovery in GBS. We performed a retrospective study of 136 IVIg-treated GBS patients admitted to two Korean centers between 2010 and 2021. We analyzed the effect of time to IVIg on the GBS disability scale (GBS-DS) and the degree of improvement from nadir (∆GBS-DS) at 1, 3, 6, and 12 months, as well as the time to regain the ability to walk or run unaided. Time to IVIg was treated either as a continuous variable or categorized into 1-week intervals to explore critical time windows. Known prognostic factors, the modified Erasmus GBS Outcome Scores on admission and pre-treatment serum albumin levels were adjusted as covariates. Shorter time to IVIg was independently associated with better GBS-DS, greater ∆GBS-DS, and shorter time to walk or run unaided at all time points. The therapeutic effect of IVIg was notably diminished when administered beyond the first 2 weeks of onset. Our study highlights the timing of IVIg as a modifiable prognostic factor in GBS. The earlier IVIg is initiated, the better the outcomes, with the ideal time window being within the first 2 weeks. These findings underscore the importance of prompt diagnosis and early intervention to optimize recovery in GBS patients.

Atrial fibrillation versus non-atrial fibrillation coronary embolism.

Coronary embolism (CE) is an uncommon cause of non-atherosclerotic acute myocardial infarction (AMI). Although atrial fibrillation (AF) is the main cause of CE, evidence of clinical, biochemical, echocardiographic, angiographic findings and outcomes of AF CE is lacking. We retrospectively analyzed 85 consecutive patients with CE that was diagnosed based on criteria encompassing clinical, angiographic and diagnostic imaging findings. We classified patients according to AF CE or non-AF CE. Forty-five patients presented with AF CE (53%). Patients with AF CE were older (76 ± 12 vs. 63 ± 14 years; p < 0.001) and had more often chronic kidney disease (24% vs. 5%; p = 0.01). AF CE had lower estimated glomerular filtration rate at admission (59 ± 18 vs. 77 ± 16 ml/min/1.73 m2; p < 0.001) and higher brain natriuretic peptide levels (512 ± 417 vs. 210 ± 479 pg/ml; p = 0.02). Coronary arteriography revealed a higher incidence of coronary artery obstruction in the AF CE group (73% vs. 38%; p = 0.001) without differences in interventional management. The AF CE group showed higher left atrial volume index (LAVI) (42 ± 15 vs. 25 ± 12 ml/m2; p < 0.001) and showed lower left atrium ejection fraction (LAEF) (32 ± 17 vs. 49 ± 17%; p = 0.001). In the multivariable analysis AF CE (OR 10 [95% CI 1.04-95; p = 0.046]) and LAEF (OR 0.94 [95% CI 0.88-0.99; p = 0.02]) were associated with worse in-hospital outcomes. Moreover, in the multivariable analysis, prior stroke (OR 12.5 [95% CI 1.1-137; p = 0.04]) and LAVI (OR 1.1 [95% CI 1.03-1.14; p = 0.003]) were independently associated with worse long-term outcomes. AF CE has specific characteristics compared to non-AF-CE and it is associated with more in-hospital events. Furthermore, atrial cardiopathy is associated with worse in-hospital and long-term outcomes in this setting.

Red Blood Cell Distribution Width (RDW) During Admission and Anxiety Following Acute Myocardial Infarction

Background: Myocardial infarction (MI), a life-threatening event, is often accompanied by an increased risk of anxiety. There is a growing association between anxiety and cardiovascular disease (CVD). Recent studies have shown that anxiety is associated with blood inflammatory markers, such as red blood cell distribution width (RDW). Objectives: We aimed to evaluate RDW levels during admission and anxiety levels after acute myocardial infarction (AMI). Methods: In this cross-sectional study, 250 patients with AMI participated during 2023-2024. Demographic information and RDW levels were obtained within 24 hours after admission. The intensity of anxiety was evaluated using the Hamilton Anxiety Rating Scale (HRSA) two weeks after the occurrence of AMI. All data analyses were performed using SPSS version 24. Results: Of the total participants, 51.6% experienced anxiety two weeks after AMI. The mean age of patients in the anxiety and non-anxiety groups was 59.77 ± 10.10 and 62.68 ± 12.20 years, respectively. Among the laboratory parameters, only blood urea nitrogen was statistically different between the two groups (P &lt; 0.027). The RDW level was 13.63 ± 1.20 in the anxiety group and 13.59 ± 1.51 in the non-anxiety group (P &gt; 0.174). There was no statistically significant difference between RDW levels and post-AMI anxiety (P &gt; 0.001). Conclusions: This study is the first to investigate the predictive value of RDW for post-AMI anxiety. Based on our findings, no significant relationship was observed between RDW and anxiety following AMI. Therefore, further studies in this field are needed to determine whether this cost-effective and readily available marker should be used for anxiety prediction after AMI.

Association between admission inflammatory indicators and 3-year mortality risk in geriatric patients after hip fracture surgery: a retrospective cohort study.

Recent research indicates that the monocyte lymphocyte ratio (MLR), neutrophil lymphocyte ratio (NLR), platelet lymphocyte ratio (PLR), C-reactive protein (CRP), and systemic immune-inflammation index (SII) may serve as valuable predictors of early postoperative mortality in elderly individuals with hip fractures. The primary objective of the study was to examine the association between preoperative MLR, NLR, PLR, CRP, and SII levels and 3-year mortality risk in geriatric patients after hip fracture surgery. The study included patients aged 65 years or older who underwent hip fracture surgery between November 2018 and November 2019. Admission levels of MLR, NLR, PLR, CRP, and SII were measured. The median follow-up period was 3.1 years. Cox proportional hazards models were used to calculate the hazard ratio (HR) for mortality with adjusting for potential covariates. Time-dependent receiver operating characteristic (ROC) curves were employed to assess the predictive capability of inflammatory indicators for mortality. A total of 760 patients completed the follow-up (79.4 ± 7.8 years, 71.1% female). A higher preoperative MLR was found to be significantly associated with an increased 3-year postoperative mortality risk (HR 1.811, 95% CI 1.047-3.132, P = 0.034). However, no significant correlations were observed between preoperative NLR, PLR, CRP, SII and 3-year mortality. The areas under the ROC curve (AUCs) of MLR for predicting 30-day, 120-day, 1-year, and 3-year mortality were 0.74 (95% CI 0.53-0.95), 0.70 (95% CI 0.57-0.83), 0.67 (95% CI 0.60-0.74), and 0.61 (95% CI 0.56-0.66), respectively. Preoperative MLR is a useful inflammatory marker for predicting 3-year mortality in elderly hip fracture patients, but its predictive ability diminishes over time.

Contribution of ethnicity, area level deprivation and air pollution to paediatric intensive care unit admissions in the United Kingdom 2008–2021

There is emerging evidence on the impact of social and environmental determinants of health on paediatric intensive care unit (PICU) admissions and outcomes. We analysed UK paediatric intensive care data to explore disparities in the incidence of admission according to a child's ethnicity and the degree of deprivation and pollution in the child's residential area. Data were extracted on children <16 years admitted to UK PICUs between 1st January 2008 and 31st December 2021 from the Paediatric Intensive Care Audit Network (PICANet) database. Ethnicity was categorised as White, Asian, Black, Mixed or Other. Deprivation was quantified using the 'children in low-income families' measure and outdoor air pollution was characterised using mean annual PM2.5 level at local authority level, both divided into population-weighted quintiles. UK population estimates were used to calculate crude incidence of PICU admission. Incidence rate ratios were calculated using Poisson regression models. There were 245,099 admissions, of which 60.7% were unplanned. After adjusting for age and sex, Asian and Black children had higher relative incidence of unplanned PICU admission compared to White (IRR 1.29 [95% CI: 1.25-1.33] and 1.50 [95% CI: 1.44-1.56] respectively), but there was no evidence of increased incidence of planned admission. Children living in the most deprived quintile had 1.50 times the incidence of admission in the least deprived quintile (95% CI: 1.46-1.54). There were higher crude admission levels of children living in the most polluted quintile compared to the least (157.8 vs 113.6 admissions per 100,000 child years), but after adjustment for ethnicity, deprivation, age and sex there was no association between pollution and PICU admission (IRR 1.00 [95% CI: 1.00-1.00] per 1μg/m3 increase). Ethnicity and deprivation impact the incidence of PICU admission. When restricting to unplanned respiratory admissions and ventilated patients only, increasing pollution level was associated with increased incidence of PICU admission. It is essential to act to reduce these observed disparities, further work is needed to understand mechanisms behind these findings and how they relate to outcomes. There was no direct funding for this project. HM was funded by an NIHR Academic Clinical Fellowship (ACF-2022-18-017).

Total Antioxidant Status and Oxidative Stress in Patients with COVID-19 Infection.

Oxidative stress (OS) may have a role in the pathogenesis and severity of the coronavirus disease 2019 (COVID-19) disease. The present study was conducted to estimate the association of inflammatory markers, total antioxidant status (TAS), and malondialdehyde (MDA) levels with the severity of the disease and to identify their trends after recovery. Adult patients admitted with moderate or severe COVID-19 were included after obtaining written informed consent from patient or next of kin. Patients who were critically ill, on ventilator, or in sepsis/septic shock were excluded. Levels of inflammatory markers, TAS, and OS as measured by MDA were estimated within 24 hours of admission and reevaluated at 12 weeks following discharge. The mean age of the 40 patients (42.5% females) was 55 ± 15 years. TAS values (in trolox equivalents/L) were significantly reduced in severe compared to moderate COVID-19 patients at admission (7.2 ± 4.19 vs 12.3 ± 5.21). These increased at 12 weeks after discharge. The MDA levels (in nmol/mL) were significantly higher in severe in comparison to moderate disease (7.1 ± 2.68 vs 4.1 ± 1.81). These values showed a downward trend 12 weeks after discharge in severe disease group. Admission levels of interleukin-6 (IL-6), D-dimer, and lactate dehydrogenase (LDH) were statistically higher in severe COVID-19 patients in contrast to moderate disease. Moderate and severe COVID-19 are associated with a state of high OS and a low total antioxidant levels which tend to recover at 3 months following discharge.

Trauma promotes heparan sulfate modifications and cleavage that disrupt homeostatic gene expression in microvascular endothelial cells.

Introduction: Heparan sulfate (HS) in the vascular endothelial glycocalyx (eGC) is a critical regulator of blood vessel homeostasis. Trauma results in HS shedding from the eGC, but the impact of trauma on HS structural modifications that could influence mechanisms of vascular injury and repair has not been evaluated. Moreover, the effect of eGC HS shedding on endothelial cell (EC) homeostasis has not been fully elucidated. The objectives of this work were to characterize the impact of trauma on HS sulfation and determine the effect of eGC HS shedding on the transcriptional landscape of vascular ECs. Methods: Plasma was collected from 25 controls and 49 adults admitted to a level 1 trauma center at arrival and 24h after hospitalization. Total levels of HS and angiopoietin-2, a marker of pathologic EC activation, were measured at each time point. Enzymatic activity of heparanase, the enzyme responsible for HS shedding, was determined in plasma from hospital arrival. Liquid chromatography-tandem mass spectrometry was used to characterize HS di-/tetrasaccharides in plasma. In vitro work was performed using flow conditioned primary human lung microvascular ECs treated with vehicle or heparinase III to simulate human heparanase activity. Bulk RNA sequencing was performed to determine differentially expressed gene-enriched pathways following heparinase III treatment. Results: We found that heparanase activity was increased in trauma plasma relative to controls, and HS levels at arrival were elevated in a manner proportional to injury severity. Di-/tetrasaccharide analysis revealed lower levels of 3-O-sulfated tetramers with a concomitant increase in ΔIIIS and ΔIIS disaccharides following trauma. Admission levels of total HS and specific HS sulfation motifs correlated with 24-h angiopoietin-2 levels, suggesting an association between HS shedding and persistent, pathological EC activation. In vitro pathway analysis demonstrated downregulation of genes that support cell junction integrity, EC polarity, and EC senescence while upregulating genes that promote cell differentiation and proliferation following HS shedding. Discussion: Taken together, our findings suggest that HS cleavage associated with eGC injury may disrupt homeostatic EC signaling and influence biosynthetic mechanisms governing eGC repair. These results require validation in larger, multicenter trauma populations coupled with in vivo EC-targeted transcriptomic and proteomic analyses.

High viral loads combined with inflammatory markers predict disease severity in hospitalized COVID-19 patients: Results from the NOR-Solidarity trial.

To investigate temporal changes in the association between SARS-CoV2 viral load (VL) and markers of inflammation during hospitalization, as well as the ability of these markers alone or in combination to predict severe outcomes. Serial oropharyngeal and blood samples were obtained from hospitalized COVID-19 patients (n=160). Levels of inflammatory markers and oropharyngeal VL were measured during hospitalization (admission, days 3-5, and days 7-10) and related to severe outcomes (respiratory failure/intensive care unit admission). Elevated admission levels of IL (interleukin)-6, IL-33, IL-8, monocyte chemoattractant protein-1 (MCP-1), interferon-γ-induced protein 10 (IP-10), IL-1β, and IL-1Ra were associated with severe outcomes during hospitalization. Although no inflammatory markers correlated with VL at baseline, there was a significant correlation between VL and levels of IP-10 and MCP-1 at days 3-5, accompanied by IL-8 and IL-6 at days 7-10. Finally, there was a seemingly additive effect of IP-10, MCP-1, and IL-6 in predicting severe outcomes when combined with high VL at baseline. An increasing number of inflammatory markers were associated with VL during the first 10 days of hospitalization, and several of these markers were associated with severe outcomes, in particular when combined with elevated VL. Future studies should assess the potential for combining antiviral and immunomodulatory treatment, preferably guided by viral and inflammatory biomarkers, for the selection of high-risk patients.

Unraveling PTSD: Symptom cluster change during and 1 year after veterans' residential PTSD treatment.

Although treatment of posttraumatic stress disorder (PTSD) is effective in reducing symptom severity, remission rates are low. One potential underlying reason for treatment ineffectiveness is differential response of specific PTSD symptom clusters. Using data from a national Veterans Affairs (VA) residential PTSD treatment cohort, we conducted a longitudinal study to examine changes in Diagnostic and Statistical Manual of Mental Disorders, fifth edition PTSD symptom clusters from admission to 1-year follow-up. PTSD symptom data were analyzed from a national cohort of veterans who completed VA PTSD residential treatment between October 2019 and September 2020 (n = 1,648; 13% women; median age 44.2 years). Endorsement (%) and severity (M[SD]) of PTSD clusters and individual symptoms were compared at admission, discharge, 4-month and 1-year follow-ups. Large magnitude reductions in all four PTSD symptom clusters were observed from admission to discharge and both follow-ups; however, endorsement of all symptom clusters remained high. Intrusions (Cluster B) were the most highly endorsed at discharge and follow-up, whereas avoidance symptoms (Cluster C) were the least highly endorsed. Differential patterns of change were observed among the 20 individual PTSD symptoms; for example, flashbacks decreased during treatment, but increased to near admission levels by 1-year postdischarge. Results suggest that intrusive symptoms may be more resistant to residential treatment for PTSD and contribute to lower likelihood of treatment success. Future work is needed to examine differential treatment response for PTSD clusters, to inform the improvement of current and creation of novel treatment interventions, and to better address intrusive symptoms to maximize PTSD treatment gains. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

Circulating soluble CD163 is associated with reduced Glasgow Coma Scale Score and 1-year all-cause mortality in traumatized patients

Soluble CD163 (sCD163) is a biomarker of macrophage activation, not previously investigated in the circulation of traumatized patients. A biobank of 398 adult trauma patients was analyzed. Patients with an Injury Severity Score (ISS) >8 served as trauma patients (n = 195) and those with ISS ≤ 8 as trauma controls (n = 203). Serum samples obtained upon admission, 15h and 72h after were analyzed for sCD163 using an in-house ELISA. Multiple linear regression was used to analyze the association between admission levels of sCD163 with, 1: overall trauma severity (ISS), and 2: severity of injury to specified organs using Abbreviated Injury Score (AIS) and Glasgow Coma Scale (GCS). The association between the peak level of sCD163 with 1-year all-cause mortality was analyzed by logistic regression analysis. Median admission levels of sCD163 were higher in trauma patients than trauma controls [2.32 (IQR 1.73 to 2.86) vs. 1.92 (IQR 1.41 to 2.51) mg/L, p < 0.01]. Worsening GCS score was associated with a 10.3% (95% CI: 17.0 to 3.1, p < 0.01) increase in sCD163. Increasing Head-AIS score was associated with a 5.1% (95% CI: −0.5 to 11.0, p = 0.07) increase in sCD163. The remaining AIS scores and ISS were not consistently associated with sCD163 admission levels. Each mg/L increase in sCD163 peak level had an odds ratio 1.34 (95%CI: 0.98 to 1.83), p = 0.06) after adjustment for age, sex, and GCS. Circulating sCD163 is increased in traumatized patients and associated with worsening GCS. Our findings suggest an association between circulating sCD163 levels with 1-year all-cause mortality.

Impact of Human IFITM3 Polymorphism rs12252 on COVID-19 Severity and Mortality in an Egyptian Cohort

Abstract Background Coronavirus disease 2019 (COVID-19) is a pandemic respiratory disease with a high mortality rate, caused by infection with severe acute respiratory syndrome coronavirus 2. Variants of the gene encoding the interferon-induced membrane protein IFITM3 have been linked to severe viral illnesses. We investigated whether the COVID-19 clinical outcomes caused by SARS-CoV-2 infection in a cohort of COVID-19 Egyptian patients were inconsistent and could have been caused by the IFITM3-SNP rs12252 polymorphism. Aim of the Work The purpose of this study is to determine the frequency of the IFITM3 rs12252 SNP in a cohort of COVID-19 Egyptian patients, and its impact on illness severity and outcome, as well as its influence on IL-6 serum levels. Patients and Methods This cross-sectional study included 100 patients diagnosed as positive for COVID-19. They were enrolled in AL-Obour Quarantine Hospital. They were categorized into three groups, mild cases, who attended AL-Obour outpatient clinic, moderate and severe cases who were admitted to the hospital ward and ICU, respectively. All subjects of this study were subjected to full medical history, clinical evaluation, laboratory investigations, serum IL-6 levels by ELISA and IFITM3 gene polymorphism by real-time PCR. Results The results of the current study demonstrated a significant difference between mortality and the minor G allele of rs12252 within IFITM3 in COVID-19 patients (OR = 4.5 [95% CI; 1.4–14.30], P = 0.006). IL-6 showed no association either to disease severity or IFITM3 rs12252 genotype frequency. Conclusion The present study has shown a significant association between G allele variant of IFITM3 rs12252 and COVID-19 mortality. However, results failed to demonstrate any significant association between rs12252 polymorphism and disease severity, ICU admission or serum IL-6 levels. Therefore, understanding the interaction between SARS-CoV-2 and the IFITM3-rs12252 allele could help identify novel therapeutic targets, leading to precise biological and immune therapy for SARS-CoV-2 infection.

Relation of Total Antioxidant Capacity to Clinical Severity of COVID-19 Infection in Paediatric Patients

Abstract Objectives The pathogenesis of COVID-19 infection is still not well clarified. In this regard oxidative stress and its relation to disease severity is one of the topics that need to be investigated. Aim This study was carried out to investigate the relationship between the oxidant stress and antioxidant system represented by total antioxidant capacity and clinical severity of COVID19 infection in pediatric age group. Methods The current cross-sectional study included 45 patients with COVID 19 PCR-proven infection admitted at the Children’s Hospital, Faculty of Medicine, Ain Shams University compared to 45 healthy age and sex matched control group. Detailed medical history, thorough examination and recording of all infection related laboratory parameters were done for each enrolled case. Measurement of total antioxidant capacity (TAC) in the serum of all studied patients and controls was done by ELISA. Results TAC levels were considerably lower in pediatric patients (median 24u/l, IQR 9-37u/l) compared to healthy individuals (median 90u/l, IQR 77-100u/l, p &amp;lt; 0.001) and the levels were statistically lower in severe cases compared to those with mild disease (p = 0.008). In this regard, 100% of controls showed normal TAC while only 31.1% from cases exhibited normal TAC levels and 68.9% of cases had low TAC levels. There was strong statistical significance between PICU admission and low TAC levels (p = 0.035). Additionally, the TAC showed negative correlation with the initial CRP of patients (r= -0.433, p = 0.003). There was also a significant inverse correlation between TAC and time needed for viral clearance (r=- 0.418, p = 0.004) as well as a significant positive correlation between body mass index z-score and TAC levels (r = 0.423, p value 0.004). Conclusion Total antioxidant capacity could serve as a novel prognostic marker of COVID -19 infection severity in pediatric patients.

Serum Uric Acid Levels as a Risk Stratification Tool in Hypertensive Disorders of Pregnancy: A Retrospective Study.

Worldwide, hypertensive disorders of pregnancy (HDP) are among the leading causes of maternal and fetal morbidity and mortality. Serum uric acid is a test that can evaluate the severity of HDP and the associated maternal and fetal morbidity and mortality. To examine the relationship between maternal serum uric acid levels and the severity of HDP and overall pregnancy outcomes. A retrospective study was conducted on women with a gestational age > 20 weeks and BP >140/90 mmHg over three years. A total of 134 patients were included in the study. Patients with chronic hypertension, hyperuricemia without hypertension, and other major illnesses were excluded. Data were collected from medical records, including age, gravida, parity, weight, height, gestational age, blood pressure at admission, urine albumin, and serum uric acid levels. Of the 134 enrolled women with HDP, 76 had gestational hypertension, 41 had preeclampsia, and 17 had eclampsia. Mean uric acid levels in mg/dL were 6.06±1.651, 6.20±0.824, and 7.38±1.26 in gestational hypertension, preeclampsia, and eclampsia, respectively, which was a significant association (p=0.002). Mean uric acid in mg/dL was 5.86±1.27 in intensive care unit (ICU) patients compared to 6.45±1.39 in ward patients (p=0.015). There was a significantly increased risk of ICU admission and preterm delivery (r=-0.401, p<0.001) in patients with elevated uric acid levels. There was a significantly increased risk of low-birth-weight babies with elevated uric acid levels (r=-0.278, p=0.001). However, there was no statistically significant increased risk of newborn intensive care unit admissions (p=0.264) with elevated uric acid levels. Serum uric acid levels vary significantly in HDP and were found to be elevated in severe preeclampsia and eclampsia. It can be considered for risk stratification in HDP based on disease severity; however, its role in determining outcomes is debatable. Using serum uric acid levels in predictive models along with known biomarkers may determine its possible additional value in disease prediction and severity.

Understanding the Correlation between Blood Profile and the Duration of Hospitalization in Pediatric Bronchopneumonia Patients: A Cross-Sectional Original Article.

Pediatric bronchopneumonia is a prevalent life-threatening disease, particularly in developing countries. Affordable and accessible blood biomarkers are needed to predict disease severity which can be based on the Duration of Hospitalization (DOH). To assess the significance and correlation between differential blood profiles, especially the Neutrophil-Lymphocyte Ratio (NLR), and the DOH in bronchopneumonia children. A record-based study was conducted at a secondary care hospital in Indonesia. After due ethical permission, following inclusion and exclusion criteria, 284 children with confirmed diagnoses of bronchopneumonia were included in the study. Blood cell counts and ratios were assessed with the DOH as the main criterion of severity. Mann-Whitney test and correlation coefficient were used to draw an analysis. Study samples were grouped into DOH of ≤ 4 days and > 4 days, focusing on NLR values, neutrophils, lymphocytes, and leukocytes. The NLR median was higher (3.98) in patients hospitalized over 4 days (P<0.0001). Lymphocyte medians were significantly higher in the opposite group (P<0.0001). Thrombocyte medians were similar in both groups (P=0.44481). The overall NLR and DOH were weakly positively correlated, with a moderate positive correlation in total neutrophils and DOH, and a moderate negative correlation in total lymphocytes and DOH. The correlation between the DOH ≤ 4 days group with each biomarker was stronger, except for leukocyte and thrombocyte. Analysis of the longer DOH group did not yield enough correlation across all blood counts. Admission levels of leukocyte count, neutrophil, lymphocyte, and NLR significantly correlate with the DOH, with NLR predicting severity and positively correlated with the DOH.

CD66b+/CD68+ circulating extracellular vesicles, lactate dehydrogenase and neutrophil-to-lymphocyte ratio can differentiate coronavirus disease 2019 severity during and after infection.

Coronavirus disease 2019 (COVID-19) has been a major public health burden. We hypothesised that circulating extracellular vesicles (cEVs), key players in health and disease, could trace the cell changes during COVID-19 infection and recovery. Therefore, we studied the temporal trend of cEV and inflammatory marker levels in plasma samples of COVID-19 patients that were collected within 24h of patient admission (baseline, n=80) and after hospital discharge at day-90 post-admission (n=59). Inflammatory markers were measured by standard biochemical methods. cEVs were quantitatively and phenotypically characterized by high-sensitivity nano flow cytometry. In patients recovered from COVID-19 lower levels of inflammatory markers were detected. cEVs from vascular (endothelial cells) and blood (platelets, distinct immune subsets) cells were significantly reduced at day-90 compared to admission levels, a pattern also observed for cEVs from progenitor, perivascular and epithelial cells. The best discriminatory power for COVID-19 severity was found for inflammatory markers lactate dehydrogenase and neutrophil-to-lymphocyte ratio and for granulocyte/macrophage-released CD66b+/CD68+-cEVs. Albeit inflammatory markers were good indicators of systemic inflammatory response and discriminators of COVID-19 remission, they do not completely reveal cell stress and organ damage states. cEVs reaching baseline pre-infection levels at 90 days post-infection in recovered patients discriminate parental cells affected by disease.

The Protective Role of IL-17 and IL-22 in COVID-19 Infection.

The development of a cytokine storm in Coronavirus Disease 2019 (COVID-19) infection can make the disease fatal. We hypothesize that this excessive cytokine production impairs mucosal healing. IL-17 and IL-22 are cytokines that play a key role in protecting and regenerating mucosal tissues.IL-17 and IL-22 support each other and the imbalance between them plays a role in the pathogenesis of many rheumatologic diseases. To investigate whether COVID-19 severity is related to IL17, IL-22, and the IL-17/IL-22 ratio. The study was planned prospectively and included 69 patients with active COVID-19 infection.Three groups were created: patients with upper respiratory tract infection, pneumonia, and cytokine storm. Blood samples were taken from the patients upon their first admission and serum levels of IL-17 and IL-22 were measured using the enzyme-linked immunosorbent assay (ELISA). We assessed the relationship between IL17, IL22, IL17/IL22 ratio, clinical and lung involvement by comparing them with the healthy group. The levels of IL-17 were significantly higher in COVID-19 patients with upper respiratory tract infection compared to the control group (p=0.027). IL17/IL-22 ratio significantly increased in patients with cytokine storm compared to the healthy controls (p=0.027). Serum levels of IL-22 were negatively correlated with the CO-RADS score (r=-0.31, p=0.004), while IL-17/IL-22 ratio was positively correlated with the CO-RADS score (r= 0.29, p=0.008). Levels of IL-17, IL-22 and IL-17/IL-22 may provide valuable insights into the progression of COVID-19.

Admission levels of serum biomarkers have additive and cumulative prognostic value in traumatic brain injury

Elevated levels of CNS-derived serum proteins are associated with poor outcome in traumatic brain injury (TBI), but the value of adding acute serum biomarker levels to common clinical outcome predictors lacks evaluation. We analyzed admission serum samples for Total-Tau (T-Tau), Neurofilament light chain (Nfl), Glial fibrillary acidic protein (GFAP), and Ubiquitin C-terminal hydrolase L1 (UCHL1) in a cohort of 396 trauma patients including 240 patients with TBI. We assessed the independent association of biomarkers with 1-year mortality and 6–12 months Glasgow Outcome Scale Extended (GOSE) score, as well as the additive and cumulative value of biomarkers on Glasgow Coma Scale (GCS) and Marshall Score for outcome prediction. Nfl and T-Tau levels were independently associated with outcome (OR: Nfl = 1.65, p = 0.01; T-Tau = 1.99, p < 0.01). Nfl or T-Tau improved outcome prediction by GCS (Wald Chi, Nfl = 6.8–8.8, p < 0.01; T-Tau 7.2–11.3, p < 0.01) and the Marshall score (Wald Chi, Nfl = 16.2–17.5, p < 0.01; T-Tau 8.7–12.4, p < 0.01). Adding T-Tau atop Nfl further improved outcome prediction in majority of tested models (Wald Chi range 3.8–9.4, p ≤ 0.05). Our data suggest that acute levels of serum biomarkers are independently associated with outcome after TBI and add outcome predictive value to commonly used clinical scores.

Retrospective study of 189 cases of acute perforated peptic ulcer: safety and efficacy of over-the-scope-clip based endoscopic closure.

To compare the clinical outcomes in patients with acute perforated peptic ulcer (PPU) treated with over-the-scope clip (OTSC), non-surgical, and surgical interventions, and to explore the effectiveness and safety of OTSC closure. Hospital stay, antibiotic use, diet resumption time, and mortality rate were analyzed retrospectively. Binary Logistic regression analysis was used to identify the risk factors influencing PPU complicated with sepsis. Patients were divided into three treatment groups: OTSC (n = 62), non-surgical (n = 72), and surgical (n = 55) groups. The median time (IQR) from symptom onset to admission was 9.0 (4-23) h. 88.71% (55/62) of the patients in In the OTSC group underwent OTSC closure within 24h (median [IQR] time: 14.5 [7.00-30.25] h). The perforation diameters in the OTSC and surgical groups were 9.87mm ± 5.97mm and 8.55mm ± 6.17mm, respectively. The median (IQR) hospital stays in the OTSC (9.50 [7.00-12.25] days) and non-surgical group (9.00[7.00-13.00]days) were similar (p > 0.05), but shorter than that in surgical group (12.00[10.00-16.00]days), (p < 0.05). The median duration of antibiotic use was shorter in the OTSC group (7.00[3.00-10.00]) than in the non-surgical group (9.00[7.00-11.00]) and surgical group (11.00[9.00-13.00]) ( p < 0.05); and the time to resume oral feeding was shorter in the OTSC group (4.00[2.00-5.25]) than in the non-surgical group (7.00[6.13-9.00]) and surgical group (8.00[6.53-10.00]), respectively ( p < 0.05). No mortality difference among groups (p = 0.109) was found. Lower albumin level at admission, older age, and elevated creatinine levels were associated with increased sepsis risk, with OR(95%CI) of 0.826 (0.687-0.993), 1.077 (1.005-1.154), and 1.025 (1.006-1.043), respectively (all p < 0.05). OTSC closure improves clinical outcomes of acute PPU patients without sepsis. Age, hypoalbuminemia, and baseline renal dysfunction increase the risk of sepsis, while mortality was associated with sepsis and multiorgan dysfunction.

Type 1 Myocardial Infarction in Patients With Acute Ischemic Stroke

Elevated values of high-sensitivity cardiac troponin (hs-cTn) are common in patients with acute ischemic stroke and are associated with poor prognosis. However, diagnostic and therapeutic implications in patients with ischemic stroke remain unclear. To identify factors indicative of myocardial infarction (MI) in patients with acute ischemic stroke and hs-cTn elevation. The primary hypothesis was that a dynamic change of hs-cTn values (>50% change) in patients with acute ischemic stroke indicates MI. This cross-sectional study was a prospective, observational study with blinded end-point assessment conducted across 26 sites in Germany. Patients were included if they had acute ischemic stroke within 72 hours and either (1) highly elevated hs-cTn values on admission (>52 ng/L) or (2) hs-cTn levels above the upper limit of normal and a greater than 20% change at repeated measurements. Patients were enrolled between August 2018 and October 2020 and had 1 year of follow-up. Statistical analysis was performed between April 2022 and August 2023. Standardized electrocardiography, echocardiography, and coronary angiography. Diagnosis of MI as adjudicated by an independent end-point committee based on the findings of electrocardiography, echocardiography, and coronary angiography. In total, 254 patients were included. End points were adjudicated in 247 patients (median [IQR] age, 75 [66-82] years; 117 were female [47%] and 130 male [53%]). MI was present in 126 of 247 patients (51%) and classified as type 1 MI in 50 patients (20%). Dynamic change in hs-cTn value was not associated with MI in univariable (32% vs 38%; χ2 P = .30) or adjusted comparison (odds ratio, 1.05; 95% CI, 0.31-3.33). The baseline absolute hs-cTn value was independently associated with type 1 MI. The best cutoffs for predicting type 1 MI were at hs-cTn values 5 to 10 times the upper limit normal. This study found that in patients with acute ischemic stroke, a dynamic change in hs-cTn values did not identify MI, underscoring that dynamic changes do not identify the underlying pathophysiological mechanism. In exploratory analyses, very high absolute hs-cTn values were associated with a diagnosis of type 1 MI. Further studies are needed how to best identify patients with stroke who should undergo coronary angiography.