Death In Patients Research Articles

Genetic Diversity, Virulence Factors and Antibiotic Resistance of Listeria monocytogenes from Food and Clinical Samples in Southern Poland.

Listeriosis is one of the most serious foodborne diseases under surveillance, with an overall mortality rate in the EU currently being high at 18.1%. Therefore, this study aims to investigate Listeria monocytogenes strains isolated from clinical and food samples for susceptibility to antimicrobials, presence of virulence factors, and genetic diversity. Species were identified using the MALDI-TOF, resistance to 11 antibiotics was determined according to EUCAST guidelines, and multiplex PCR was used for serotyping and detecting virulence genes. Strains were genotyped using the PFGE method. Clinical strains showed full sensitivity to all tested antibiotics. In total, 33.3% of strains from food products were found to be resistant to ciprofloxacin and 4.2% to tetracycline. Most of the tested isolates (79.2%) belonged to serotype 1/2a-3a, and the rest (20.8%) belonged to serotype 4ab-4b,4d-4e. Five virulence genes (prfA, hlyA, plcB, inlA, and lmo2672) were detected in all strains studied. The llsX gene was the least common, in 37.5% of clinical strains and 18.75% of strains isolated from food products. Among the analyzed strains, 13 strains displayed unique PFGE profiles. The other 11 strains belong to 3 clusters of pulsotypes: cluster 1 (2 strains), cluster 2 (6 strains), and cluster 3 (2 strains). The percentage of hospitalizations and deaths of Polish patients with listeriosis indicates the seriousness of this disease, especially in an aging society, while the molecular testing of clinical strains has been rarely performed, which makes it difficult to determine the source of infection.

The efficacy and safety of dopamine versus norepinephrine in management of paediatric septic shock

Background: Septic shock is one of most common cause of death in pediatric patients. The optimum septic shock vasopressor support strategy is currently debated. This study was performed to evaluate the efficacy and safety of norepinephrine (NE) and dopamine (DA) as the initial vasopressor in pediatric septic shock patients. Methods: A prospective, randomized, clinical trial was carried out between January 2022 to January 2023 in a pediatric intensive care unit comparing DA with NE as the initial vasopressor in fluid-resuscitated 100 pediatric patients with septic shock. Normalization of blood pressure was taken as end point. If the maximum dose of the initial vasopressor was unable to attain the hemodynamic goal, then another vasopressor agent was added. Patients were monitored for response and side effect. Results: DA had a mortality of 50% as compared to 40% in NE. Arrhythmias occurred in 27.5% cases in DA group and 8.33% cases in NE group. There was a significantly greater incidence of sinus tachycardia with DA (12.5%) than NE (5%). Conclusions: NE showed better efficacy than DA in pediatric patients with septic shock with lesser event of arrhythmias.

Factors Mediating Lung Cancer in Never Smokers Identified from Epidemiologic Analysis

Lung Cancer in Never-Smokers (LCINS) is one of the leading causes of cancer patient deaths in the United States. Unlike lung cancer onset by cigarette smoking, LCINS is not as readily understood and research on the subject has been conflicting. Thus, early diagnosis and prevention are key in reducing mortality among LCINS patients. In this study, the Prostate, Lung, Colorectal, and Ovarian (PLCO) dataset contains more than 155,000 participants and over 36,000 never-smokers. Data from more than 5,000 patients with LCINS were analyzed using R and Excel software to determine risk factors of LCINS. The factors analyzed for predictive power in LCINS incidence were age, height, weight, body mass index, race, income, family history, and secondary smoke exposure. Multiple statistical methods, including t-tests, ANOVA tests, and logistic regression, were implemented to assess each factor. Through comparison and corroboration of results from these statistical methods, age and race were identified as the key factors that had statistically significant evidence as potential influences in LCINS incidence. This was indicated by strong positive correlation between age/race and the predicted probability of LCINS development with a statistically significant p value. Other physical characteristics did not appear to have a significant impact on the likelihood of developing LCINS. In addition, the statistical method that provided the most information regarding a factor’s power was logistical regression due to the binomial outcome of whether or not a patient has LCINS. It enables a deeper elucidation of how individual factors influence the probability of LCINS development. These results provide valuable insights into demographic risk factors for LCINS and lay the groundwork for future investigations, potentially including the application of advanced analytical techniques such as deep learning algorithms to explore additional predictive factors for LCINS and other lung cancer subtypes.

Cardiovascular death risk in patients with solid tumors: a population-based study in the United States.

Previous studies have focused on the risk of cardiovascular disease (CVD)-specific death in hematological cancers and in some single anatomical tumor sites, there remains a paucity of data on systematic analyses in solid tumors. The objective of this study is to evaluate the distribution, risk, and trends of CVD-specific death in patients with solid tumors. A total of 2 679 293 patients with solid tumors diagnosed between 1975 and 2019 were screened from the Surveillance, Epidemiology and End Results (SEER) program across 15 anatomical sites. Standardized mortality ratios (SMRs) and absolute excess risks (AERs) were used to describe the intensity of CVD-specific death, competing risk regression models were used to assess the risk of CVD-specific death, and restricted cubic spline analyses were employed to investigate the potential linear or nonlinear relationship between age and CVD death. CVD-specific death in patients with solid tumors accounted for 48.95% of non-cancer deaths. Compared with the general population, patients with solid tumors had higher SMR and AER of CVD death (SMR: 1.15; AER: 21.12), heart disease-related death (SMR: 1.13; AER: 13.96), and cerebrovascular disease-related death (SMR: 1.20; AER: 4.85). Additionally, the SMR exhibited a decreasing trend with increasing time to diagnosis. Furthermore, a nonlinear relationship was observed between age and CVD-specific death in patients with solid tumors of different systems. CVD-specific death accounted for a large proportion of the cause of non-cancer deaths. Patients with solid tumors exhibit an elevated risk of CVD-specific death. Screening for CVD death and optimizing risk management in patients with solid tumors throughout anticancer treatment may be beneficial in preventing CVD death.

ABCL-134 Warburg-Effect Driven Lactic Acidosis is Associated With Early Death in Patients with Lymphoma

ABCL-134 Warburg-Effect Driven Lactic Acidosis is Associated With Early Death in Patients with Lymphoma

Warburg-Effect Driven Lactic Acidosis is Associated With Early Death in Patients with Lymphoma

Warburg-Effect Driven Lactic Acidosis is Associated With Early Death in Patients with Lymphoma

Underlying Cause of Death in Patients With Multiple Myeloma: A 21-Year Mortality Analysis

Underlying Cause of Death in Patients With Multiple Myeloma: A 21-Year Mortality Analysis

Proportion trends, cancer stage, and survival of patients with cancer diagnosed through emergency and nonemergency departments: a nationwide cohort study.

To reduce mortality, the Taiwan government has vigorously promoted free cancer screening and preventive health screening services. Cancers are usually advanced by the time they are discovered in the emergency department. Through this study, we aimed to understand the characteristics of cancer patients diagnosed through the emergency department and thus identify high-risk populations by comparing cancer staging and survival rates in patients diagnosed in the emergency department and those diagnosed in the non-emergency department. The retrospective study enrolled a total of 389,043 patients over the age of 20 who were newly diagnosed with one of the five major cancers (including lung cancer, colorectal cancer, breast cancer, prostate cancer, and oral cancer) between 2008 and 2017 and analyzed their diagnostic pathway, cancer stage at diagnosis, and survival time. Of the study participants, 59,423 patients (about 15.3%) were diagnosed with cancer through the emergency department. We found that a sizable proportion of older people and patients with low education and low incomes were diagnosed through emergency department visits, and those with a health condition comorbidity severity of 3 had the highest proportion diagnosed by the emergency department, advanced stages at diagnosis, and risk of death. These can be classified as high-risk groups. In addition, 76.4% of patients diagnosed in the emergency department had advanced cancer, and the risk of death was 1.46 times higher than that of patients diagnosed in the non-emergency department. Although cancer screening is available, it does not reduce the proportion of patients with advanced cancer who are diagnosed through or at the time of diagnosis in the emergency department. The present study found that the government's cancer screening did not affect the proportion or number of cancers diagnosed through emergency department visits. Therefore, the government should focus on more cancer screening, health education in high-risk groups, and strengthening the link between emergency and oncology departments to reduce the risk of death for patients diagnosed through emergency department visits.

Effect of post thrombolytic intracerebral hemorrhage volume on 90-day outcomes in acute ischemic stroke patients

Background and PurposePost thrombolytic intracerebral hemorrhage (ICH) is associated with higher rate of death or disability in acute ischemic stroke patients. We investigated the relationship between post thrombolytic ICH volume and change in volume and death or disability at 90 days in acute ischemic stroke patients. MethodsWe analyzed 110 patents recruited in the Safety Evaluation of 3K3A-APC in Ischemic Stroke (RHAPSODY) trial who received intravenous tissue plasminogen activator (tPA) followed by mechanical thrombectomy (if indicated) and 3K3A-APC or placebo. ICH volume was measured at Day 2 and Day 7 using susceptibility weighted sequence (SWI) on magnetic resonance imaging (MRI). We also calculated the post thrombolytic ICH volume change between Day 2 and Day 7. Outcomes were determined by using utility weighted modified Rankin scale (UW-mRs) at 90-days, Outcomes were determined by using utility weighted modified Rankin scale (UW-mRS) at 90 days. To minimize interpretation bias, outcome assessors were blinded to the treatment allocation and clinical data.We adjusted for age, gender, National Institutes of Health Stroke Scale (NIHSS) score (<10,10-19 and ≥20), location of hemorrhage (single basal ganglia hemorrhage, single lobar, single cerebellum, and multiple sites) in multivariate regression analysis. ResultsA total of 88 (80%) of 110 patients had post thrombolytic ICH (mean volume 28.3 ml ± SD 62 ml). The strata of ICH volume were not associated with UW-mRs at 90 days: <20 cc (regression coefficient (RC)-0.05, p= 0.58), 20-39 cc (RC-0.22, p=0.17), or ≥40 cc (RC-0.34, p= 0.083) compared with no ICH after adjusting for potential confounders. Change in ICH mean volume 26.78 ml ±59.68, 52 had increase in volume) between Day 2 and day 7 was not associated with UW-mRS at 90 days (RC -67.71, p= 0.06). ConclusionsWe did not observe any independent effect of post thrombolytic ICH volume on death or disability in acute ischemic stroke patients. Although further studies must be done, our data suggest that strategies to prevent ICH expansion such as antifibrinolytic medications and reduction in ICH volume such as surgical evacuation may not reduce death or disability in acute ischemic stroke patients with post thrombolytic ICH.

Predictive role of hematological indices in patients with acute coronary syndrome in Ethiopia: Intrahospital outcomes

BackgroundApart from troponins, various additional biomarkers that indicate myocardial injury, inflammation, thrombosis, and other routes are being studied to improve the treatment of acute coronary syndrome (ACS). Myeloid activity has been found to be elevated in ACS, and this has sparked a great deal of interest in hematological parameters since they might offer independent insights into pathophysiology and risk assessment. ObjectiveThe purpose of this study was to evaluate the hematological markers' prognostic ability for all intrahospital causes of mortality in individuals with an ACS diagnosis. MethodsA long-term cohort study based at an institution was done. At Jimma Medical Center, patients with an ACS diagnosis were progressively brought in between May 1, 2022, and October 31, 2023. Complete blood counts (CBC) and biochemical analysis were carried out. Multilevel mixed effect logistic regression was computed to evaluate the predictive competence of hematological indices on intrahospital mortality. Prognostic performance of hematological parameters was done using the ROC curve analysis. ResultA total of 110 patients were included, of which 99 (90 %) were diagnosed ST-elevation myocardial infarction, and 74 (67.3 %) were men. The mean age was 56 (±11) years. RDW, platelet count, and MCV were independently associated with intrahospital mortality (AOR = 1.20 with P < 0.001, AOR = 0.995 with P < 0.03, and AOR = 0.897 with P < 0.025, respectively). The predictive power of RDW-SD for intrahospital mortality was evaluated by ROC analysis, the AUC value were 0.737 (95 % CI 0.669–0.805). ConclusionThis study found that red cell distribution width, mean corpuscular volume, and platelets were predictive factors for intrahospital death in patients with ACS. Thus, it is possible to predict the prognosis of an ACS patient using hematological data.

Bone marrow mesenchymal stromal cells attenuate smoke inhalation injury by regulating the M1/M2-Th17/Treg immune homeostasis axis

Smoke inhalation injury (SII) is the leading cause of death in fire burn patients. The inflammatory response induced by smoke inhalation is a significant factor in the development of acute lung injury or acute respiratory distress syndrome (ALI/ARDS). Mesenchymal stem cells (MSCs) can alleviate various inflammatory diseases by regulating the polarization of macrophages from the M1 to the M2 phenotype. Moreover, MSCs can facilitate the inflammatory response by regulating Th17/Treg homeostasis. However, little is known about the associations among MSCs, M1/M2 macrophages and Th17/Treg homeostasis. Therefore, the purpose of this study was to evaluate whether MSCs affect subsequent Th17/Treg differentiation and immune homeostasis by regulating M1/M2 polarization in SII. Our results showed that bone marrow mesenchymal stem cells (BMSCs) ameliorated lung inflammatory injury and fibrosis after SII by affecting the polarization of alveolar macrophages (AMs) from the M1 to the M2 phenotype. Moreover, BMSCs maintain Th17/Treg immune homeostasis by increasing the proportion of Treg cells and decreasing the proportion of Th17 cells. In vitro, we further demonstrated that BMSCs promoted the polarization of AMs from the M1 to the M2 phenotype and decreased IL-23 levels. Reduced IL-23 decreased Th17 differentiation and promoted Th17/Treg balance. Therefore, BMSCs ameliorate the inflammatory response and lung damage after SII through regulating M1/M2 polarization and subsequent Th17/Treg immune homeostasis, which are linked to alveolar macrophage-derived IL-23. These findings provide novel insight into how BMSCs regulate the M1/M2-Th17/Treg immune homeostasis axis and provide new therapeutic targets for more effective control of the inflammatory response after SII.

Factors associated with hospitalization and mortality in adult and pediatric extrapulmonary tuberculosis at a tertiary care hospital in Central India

Background Comorbidities complicate the management of tuberculosis (TB) and have become an essential part of the end TB strategy to eradicate TB. However, pulmonary TB has received the most attention, and little is known about the impact of comorbidities and other factors on outcomes in patients with extrapulmonary tuberculosis (EPTB). Objectives Our aim was to analyze the factors associated with hospitalization and mortality in EPTB at a hospital in Central India, using non-TB patients with similar clinical presentations as a comparison. Methods Patients with presumptive EPTB were prospectively enrolled and followed up until the end of treatment or for at least 6 months. Detailed demographic and clinical information was collected for all participants, and patients were categorized as TB or non-TB using a composite reference standard. Multivariate logistic regression was used to analyze the impact of various clinical findings and risk factors on hospitalization and mortality. Results A total of 276 patients were categorized as TB cases and 175 as non-TB cases. Factors associated with hospitalization in children were younger age and non-adenitis site of disease. In adults, factors associated with mortality were older age, non-adenitis site of disease and HIV infection regardless of TB diagnosis, while diabetes mellitus increased the odds of mortality in EPTB patients. Conclusion Our results show that comorbidities increase the odds of death in both TB and non-TB patients in low-resource settings. This argues for a shift away from the traditional vertical management of diseases in these areas and supports a continued focus on building robust healthcare systems.

Overexpression of microRNA-611 inhibits TGF-β-induced epithelial-mesenchymal transition and migration in lung cancer cells through MAPKAP1

Metastasis is a major cause of death in patients with lung cancer (LC). microRNA-611 (miR-611), a miRNA, has been little studied in cancer. Here, we aimed to further elucidate the roles of miR-611 in epithelial-mesenchymal transition (EMT) and migration induced by transforming growth factor-β (TGF-β) in LC cells and the possible underlying mechanisms. miR-611 and MAPKAP1 expression was first identified in LC tissues from metastatic and nonmetastatic patients, and their expression was associated with overall survival. Gain- and loss-of-function experiments were performed to verify the impacts of miR-611 and MAPKAP1 on pAKT expression, EMT, and migration in LC cells treated with TGF-β. The interaction between miR-611 and MAPKAP1 was also determined with a luciferase reporter assay. In our study, miR-611 was expressed at low levels, and MAPKAP1 was highly expressed in LC tissues, which was associated with metastasis and short overall survival. Functionally, miR-611 inhibition or MAPKAP1 overexpression accelerated EMT and migration and upregulated pAKT in TGF-β-treated A549 and H1299 cells; miR-611 overexpression or MAPKAP1 silencing exerted the opposite effects as miR-611 inhibition or MAPKAP1 overexpression. Mechanistically, miR-611 could target and downregulate MAPKAP1. MAPKAP1 expression was also negatively correlated with miR-611 expression in LC tissues. In addition, miR-611 overexpression reduced the EMT and migration of TGF-β-treated A549 and H1299 cells by targeting MAPKAP1. In conclusion, miR-611 overexpression attenuated EMT and migration by targeting MAPKAP1 in TGF-β-induced LC cells, indicating that miR-611 is a biological target for LC treatment.

Prognostic impact of myosteatosis on survival with immune checkpoint inhibitors: A systematic review and meta-analysis

Myosteatosis has emerged as a promising prognostic biomarker for survival outcomes in patients with advanced cancer. However, recent research has yielded conflicting results on the association between myosteatosis and survival in patients treated with immune checkpoint inhibitors (ICIs). Therefore, we performed this systematic review and meta-analysis to evaluate the association between myosteatosis and survival outcomes in patients treated with ICIs. We conducted a systematic review using Pubmed, Web of Science, and Scopus databases for studies published until June 10, 2024. This protocol was registered in the PROSPERO database (Registration Number: CRD42023466337). We performed the meta-analyses with the generic inverse-variance method with a random effects model. Eleven studies involving 1362 patients were included. The pooled analysis showed that patients with myosteatosis had a significantly higher risk of death compared to patients without myosteatosis (HR: 1.61, 95% CI: 1.23-2.12, p<0.001). Subgroup analysis revealed this association was stronger in melanoma patients (HR: 2.07, 95% CI: 1.09-3.94, p=0.030). Furthermore, patients with myosteatosis had an increased risk of progression or death than those without myosteatosis (HR: 1.31, 95% CI: 1.05-1.64, p=0.020). Myosteatosis is associated with a higher risk of death in ICI-treated patients. Further research in larger cohorts is needed to standardize the definition of myosteatosis as well as the true mechanistic association between myosteatosis and survival in patients treated with ICIs.

FNDC4 reduces hepatocyte inflammatory cell death via AMPKα in metabolic dysfunction-associated steatotic liver disease

The molecular mediators responsible for the progression of metabolic dysfunction-associated steatotic liver disease (MASLD) to steatohepatitis (MASH) have not yet been completely disentangled. We sought to analyze whether FNDC4, an hepatokine and adipokine with anti-inflammatory properties, is involved in TNF-α-induced inflammatory cell death in patients with MASLD. Plasma FNDC4 (n=168) and hepatic FNDC4 and inflammatory cell death (n=65) were measured in samples from patients with severe obesity with available liver biopsy-proven MASLD diagnosis. The effect of FNDC4 on TNF-α-induced pyroptosis, apoptosis and necroptosis (PANoptosis) and mitochondrial dysfunction was studied invitro using human HepG2 hepatocytes. Compared with individuals with normal liver, patients with type 2 diabetes and MASLD exhibited decreased hepatic FNDC4 mRNA and protein levels, which were related to liver inflammation. An overexpression of TNF-α, its receptor TNF-R1 and factors involved in inflammatory cell death was also found in the liver of these patients. FNDC4-knockdown in HepG2 hepatocytes increased apoptotic cell death, while FNDC4 treatment blunted NLRP3 inflammasome-induced pyroptosis, apoptosis and necroptosis in TNF-α-stimulated hepatocytes. Moreover, FNDC4 improved TNF-α-induced hepatocyte mitochondrial dysfunction by enhancing mitochondrial DNA (mtDNA) copy number and OXPHOS complex subunits I, II, III and V protein expression. Mechanistically, AMP-activated protein kinase α (AMPKα) was required for the FNDC4-mediated inhibition of cell death and increase in mtDNA content. FNDC4 acts as a hepatocyte survival factor favouring mitochondrial homeostasis and decreasing inflammatory cell death via AMPKα. Collectively, our study identifies FNDC4 as an attractive target to prevent hepatocellular damage in patients with MASLD.

The different paradigms of NK cell death in patients with severe trauma

Lymphocyte decline, particularly the depletion of NK cells, is a prominent feature of immunosuppression following severe tissue injury, heightening the susceptibility of severe trauma patients to life-threatening infections. Previous research indicates that the reduction in the number of NK cells is closely associated with the process of cell death. Nonetheless, the precise mechanism of NK cell death remains unknown. Here, we discovered that following severe traumatic injury, NK cells undergo several cell death pathways, dominated by apoptosis and pyroptosis with coexistence of necrotic cell death, immunogenic cell death, ferroptosis, and autophagy. These NK cells with different paradigms of death have diverse cytokine expression profiles and diverse interactions with other immune cells. Further exploration revealed that hypoxia was strongly associated with this diverse paradigm of NK cell death. Detailed investigation of paradigms of cell death may help to enhance comprehension of lymphopenia post-severe trauma, to develop new strategy in preventing immunosuppression, and then to improve outcome for severe trauma population.

SGLT2 inhibitors for patients with type 2 diabetes mellitus after myocardial infarction: a nationwide observation registry study from SWEDEHEART

Sodium-glucose co-transporter 2 (SGLT2) inhibitors have been shown to reduce rates of heart failure hospitalisations and cardiovascular death in patients with type 2 diabetes and prior cardiovascular disease. We hypothesised that SGLT2 inhibitors could provide cardiovascular benefits in the post-myocardial infarction setting. We aimed to investigate cardiovascular outcomes of SGLT2 inhibitor therapy in patients with type 2 diabetes mellitus after myocardial infarction in a Swedish nationwide registry. We included all patients with type 2 diabetes surviving a type 1 acute myocardial infarction from January 1, 2018 to December 31, 2021. Patients were included if they were discharged with an estimated glomerular filtration rate (eGFR)>30mL/min/1.73 m2 in the nationwide Swedish Web-system for Enhancement and Development of Evidence-based care in Heart disease Evaluated According to Recommended Therapies (SWEDEHEART) registry. We identified all patients discharged with or without an SGLT2 inhibitor prescription 120 days before or within three days after discharge from the cardiac care unit. The primary outcome measure was a composite of death and first hospitalisation for heart failure after one year analysed using an adjusted Cox regression. A total of 11,271 patients were included. Of these, 2498 (22.2%) received SGLT2 inhibitor treatment. Patients who were prescribed SGLT2 inhibitors were younger, more often presented with a STEMI and had worse left ventricular ejection fraction at index hospitalisation. SGLT2 inhibitor use was associated with lower rates of the composite outcome (hazard ratio (HR) of 0.70 (95% confidence interval (CI) 0.59-0.82). Treatment with SGLT2 inhibitors after myocardial infarction in patients with type 2 diabetes was associated with a lower rate of cardiovascular events. This work was supported by Hjärt-Lungfonden, Vetenskapsrådet, Knut and Alice Wallenberg Foundation, ALF, the Bundy Academy, and Skåne University Hospital funds.

Retrospective Longitudinal Observational Study on the Long-Term Effects of Sodium-Glucose Cotransporter-2 Inhibitors on the Development of Metabolic Dysfunction-Associated Steatotic Liver Disease in Type 2 Diabetic Japanese Patients.

Background/Objectives: The health burden of metabolic dysfunction-associated fatty liver disease (MASLD) has been increasing lately. Cardiovascular disease (CVD) is the main cause of death in MASLD patients; therefore, the treatments for MASLD should improve both CV risk factors such as obesity, diabetes, and dyslipidemia, in addition to an improvement in liver function. The evidence on the long-term effects of sodium-glucose cotransporter 2 inhibitors (SGLT2is) on the progression of MASLD in Asian populations is very limited. Methods: The retrospective longitudinal study was performed by using the medical records at our institute. We picked up patients with type 2 diabetes who had taken SGLT2is for at least 3 years or longer between 1 April 2014 and 31 March 2018. We collected the data on metabolic parameters, including laboratory data and anthropometric parameters, and compared the data before and after the initiation of SGLT2is treatment. Results: During the observation period, 324 patients had taken SGLT2is for 3 years. Three-year SGLT2is treatment significantly reduced body weight, hemoglobin A1c, low-density lipoprotein cholesterol, triglyceride, and non-high-density lipoprotein cholesterol (non-HDL-C). Such favorable changes in serum lipids were remarkable in patients with statins. Furthermore, this treatment significantly improved liver function and the markers for hepatic steatosis and hepatic fibrosis. Conclusions: Considering that the development of CVD determines the prognosis of MASLD patients, long-term SGLT2is treatment may be an ideal therapy for MASLD patients.

High myoglobin level as an independent risk factor for death in elderly patients with critical COVID-19 infection: a retrospective case-control study

AimThis study aimed to discover risk factors for death in patients with critical COVID-19 infection in order to identify patients with a higher risk of death at an early stage.MethodsWe retrospectively analyzed the clinical data of patients with critical COVID-19 infection from April 2022 to June 2022. Data were collected from the electronic medical records. Propensity matching scores were used to reduce the effect of confounding factors, such as patient baseline variables. Independent risk factors affecting patient prognosis were assessed using univariate logistic regression and multivariate logistic regression analysis. Restricted cubic spline curves were used to assess the relationship between independent and dependent variables.ResultsThe data of 132 patients with critical COVID-19 infection were included in the study. Of the 132 patients, 79 survived and 53 died. Among laboratory indicators, patients who died had higher proportions of abnormalities in procalcitonin, aspartate aminotransferase (AST), creatinine, cardiac troponin I, and myoglobin. Univariate and multivariate logistic regression analyses suggested that abnormal AST (OR = 4.98, P = 0.02), creatinine (OR = 7.93, P = 0.021), and myoglobin (OR = 103.08, P = 0.002) were independent risk factors for death. After correction for AST and creatinine, a linear relationship between myoglobin and risk of death in patients was found using restricted cubic splines.ConclusionHigh myoglobin level is an independent risk factor for death and is therefore a prognostic marker in elderly patients with severe COVID-19 infection.

Predictors for cause-specific and timing of deaths in patients with COVID-19: a cohort study in Taiwan

BackgroundThis cohort study determines the predictors for cause-specific and timing of deaths in patients with COVID-19 in Taiwan.MethodsPatients with laboratory-confirmed COVID-19 admitted to Taipei City Hospital from January 1 to July 31, 2022, were recruited in this cohort. All patients were followed up until death, discharge from the hospital, or August 31, 2022. Early deaths within the first 2 weeks were recorded, and the cause of death was confirmed by the death certificate database of Taiwan. Predictors of cause-specific and timing of deaths of patients with COVID-19 were determined using multinomial Cox proportional hazards regression analysis.ResultsOf the 195 (8.0%) patients who died during hospitalization, 147 (84.0%) had COVID-19-specific deaths. Moreover, 54.9% of the deceased patients had early death. After controlling for other covariates, patients aged ≥ 65 years had a higher risk of COVID-19-specific, non-COVID-19-specific, early, and late deaths [adjusted hazards ratio (AHR): 3.85, 6.45, 3.33, and 6.57; 95% confidence interval (CI): 1.91–7.78, 1.17–35.68, 1.51–7.36, and 2.18–19.76, respectively]. Fully vaccinated patients had a lower risk of COVID-19-specific (AHR: 0.68; 95% CI: 0.47–0.98) and early deaths (AHR: 0.54; 95% CI: 0.35–0.84), whereas comorbid patients with chronic obstructive pulmonary disease had a higher risk of non-COVID-19-specific deaths (AHR: 5.43; 95% CI: 1.73–17.03).ConclusionsThis study suggests that prioritizing COVID-19 vaccination and carefully monitoring comorbid patients during hospitalization can reduce the risk of COVID-19-specific and early deaths and non-COVID-19-specific mortalities, respectively.