Higher Levels Of Inflammatory Markers Research Articles

A Prospective Study of Incidence, Risk Factors, and Outcomes of Acute Kidney Injury in Coronavirus Disease 2019

Background: Acute kidney injury (AKI) is common after coronavirus 2 infection (COVID-19), leading to higher morbidity and mortality. There is little prospective data from India regarding the incidence, risk factors, and outcome of AKI in COVID-19. Materials and Methods: This study was conducted prospectively in adult patients between September and December 2020 in a tertiary care hospital in the national capital region of Delhi. A total of 856 patients with COVID-19 infection were enrolled in the study. Survivors were followed for 3 months after discharge. Results: Out of 856 patients, 207 (24%) developed AKI. AKI was significantly higher in those with severe disease as compared to mild-moderate disease (88% vs. 12%, P = 0.04). Out of all AKI, 3.4% had stage 1, 9.2% had stage 2, and the rest 87.4% had stage 3 AKI. 183/207 (88%) patients were on mechanical ventilators, 133 (64%) required inotropic support, and 137/207 (83.6%) patients required kidney replacement therapy. Out of 207 AKI patients, 74% (153) died as compared to 4% (27) in non-AKI group (P = 0.0001). After 3 months, chronic kidney disease (CKD) developed in 10/54 (18.5%) patients. On multivariable analysis, the presence of diabetes mellitus, severe COVID-19 disease, high levels of C reactive protein, lactate dehydrogenase, D-Dimer, and use of intravenous steroids, tocilizumab and remdesivir, were found to be significant predictors of AKI. Conclusion: AKI is common after COVID-19 infection and it is a significant risk factor for mortality in COVID-19. Patients with diabetes and high levels of inflammatory markers have higher mortality. CKD may develop in many patients after discharge.

Vitamin D level in COVID-19 patients has positive correlations with autophagy and negative correlations with disease severity

Background and ObjectivesThere is still incomplete understanding of the pathogenesis of COVID-19. Calcitriol, the main form of vitamin D in serum, regulates immune responses and increases resistance to pathogens, but the mechanism by which it protects against COVID-19 is uncertain. Autophagy has antiviral effects and helps to maintain homeostasis, but its specific role in COVID-19 is also uncertain. Both vitamin D and autophagy have important functions in the lung microenvironment. This study examined the relationship of serum vitamin D and autophagy-related proteins in patients with COVID-19 and evaluated their potential use as biomarkers.MethodsBlood samples from COVID-19 patients at the Second Hospital of Jilin University were collected. The levels of vitamin D, autophagy-related proteins (Becline 1 [BECN1] and autophagy-related 7 [ATG7]), and inflammatory markers (TNF-α and IL-1β) were measured using enzyme-linked immunosorbent assays.ResultsWe examined 25 patients with mild/moderate COVID-19 and 27 patients with severe/critical COVID-19. The group with severe/critical COVID-19 had more abnormalities in many laboratory indicators, including lower levels of autophagy markers (BECN1 and ATG7) and vitamin D, and higher levels of inflammatory markers (TNF-α and IL-1β). Partial correlation analysis showed that vitamin D had strong positive correlations with ATG7 (r = 0.819, p < 0.001) and BECN1 (r = 0.900, p < 0.001).ConclusionOur results demonstrated that the vitamin D level had significant negative correlations with COVID-19 severity and strong positive correlations with autophagy. These findings enhance our understanding of the pathogenesis of COVID-19, and provide a theoretical basis for clinical interventions that target autophagy and vitamin D.

Beta-amyloid plaque deposits and increased tau protein in the early diagnosis of alzheimer’s disease: the importance of physical activity in the prevention and evolution of the patient

In recent years, it has become clear that the β-amyloid (Aβ) component of senile plaques may be the key molecule in the pathology of Alzheimer's disease (AD). However, the origin and site of Aβ's neurotoxic action are still the subject of controversy. The precursor of the β-amyloid peptide is the β-amyloid precursor protein, which is predominantly neuronal. The hypothesis is that intraneuronal dysregulation of Amyloid Precursor Protein (APP) leads to the accumulation of Aβ peptides in intracellular compartments. This accumulation impairs the trafficking of APP, which initiates a cascade of pathological changes and causes the degeneration of pyramidal neurons. The increased secretion of Aβ as a function of stressed neurons and degenerated neuron remnants provides seeds for extracellular Aβ aggregates, which induce secondary degenerative events involving neighboring cells such as neurons, astroglia and macrophages/microglia. The benefits of physical exercise to reduce low-grade inflammation and improve cognitive function have become a growing field of interest. Epidemiological research has shown that a sedentary lifestyle intensifies the processes of disability and dependence, and also increases the incidence of chronic diseases. Physical exercise has been inversely associated with high levels of different inflammatory markers. It plays a neurotrophic role, capable of promoting a reduction in the accumulation of β-amyloid peptide and the hyperphosphorylation of tau protein, being an important alternative pathway for reducing the degenerative process, which does not result in the release of pro-inflammatory factors, as well as helping to reduce the levels of pro-inflammatory cytokines and improve peripheral concentrations.

Analysis of Factors Influencing Trauma Healing in Children with Second-Degree Burns: A Single-Center Retrospective Study

Background: The complexity of studying secondary burn wound healing in children arises from the varying ability of skin tissue regeneration across different ages. Despite advancements, there are still gaps in our understanding. Objectives: This study aimed to explore factors influencing wound healing in children with second-degree burns to guide clinical treatment and nursing practices. Methods: We conducted a retrospective analysis of children with second-degree burns treated in our burn surgery department from January 2020 to December 2022. Based on the events per variable (EPV) rule, 220 children were included. They were categorized based on the quality of wound healing 14 days post-admission (good or poor), evaluated by the healing rate and scar formation. Children's clinical data were extracted from medical records for analysis. Binary logistic regression identified factors associated with poor healing outcomes in second-degree burns. Results: Among 220 patients with secondary burns, 166 (75.46%) experienced good wound healing, while 54 (24.54%) had poor outcomes. The Hosmer-Lemeshow test indicated a good model fit (χ2 = 9.739, P = 0.28). Significant variables included burn area (odds ratio [OR] = 1.217, 95% confidence interval [CI] = 1.109 - 1.335, P < 0.05), number of drug changes (OR = 1.902, 95%CI = 1.392 - 2.599, P < 0.05), white blood cell count (OR = 1.076, 95%CI = 1.008 - 1.150, P < 0.05), neutrophil count (OR = 1.080, 95%CI = 1.018 - 1.146, P < 0.05), and neutrophil ratio (OR = 1.040, 95%CI = 1.002 - 1.081, P < 0.05). Conclusions: Effective treatment and nursing of children with second-degree burns should prioritize managing large burn areas and high levels of inflammatory markers. Additionally, minimizing drug changes during the nursing process can enhance wound healing in children.

Inflammatory depression is associated with selective glomerular hypofiltration

BackgroundSystemic low-grade inflammation may be a pathophysiological mechanism in a subtype of depression. In this study we investigate a novel candidate mechanism of inflammatory depression - Selective Glomerular Hypofiltration Syndromes (SGHS) - which are characterized by a reduced estimated glomerular filtration rate (eGFR) based on cystatin C (cysC) relative to eGFR based on creatinine (crea). SGHS have been associated with increased blood levels of pro-inflammatory markers but have never been investigated in a sample of depressed individuals. MethodThe prevalence of SGHS was compared between 313 patients with difficult-to-treat depression and 73 controls. Since there is no single established eGFRcysC/eGFRcrea-ratio cut-off to define SGHS, several cut-offs were investigated in relation to a depression diagnosis, inflammation, and symptom severity. Plasma inflammatory markers tumor necrosis factor alpha (TNF-α), interferon gamma (IFN-γ), interleukin (IL)-6, IL-8, and IL-10 were available from 276 depressed patients. We examined mediation effects of IL-6 on the relationship between SGHS and depression. ResultsDepressed patients were more likely to have SGHS compared to controls defining SGHS as either eGFRcysC/eGFRcrea-ratio < 0.9 (33.2 % vs 20.5 %, p = 0.035) or < 0.8 (15.7 % vs 5.5 %, p = 0.023). Lower eGFRcysC/eGFRcrea-ratio was associated with higher levels of inflammatory markers in depressed patients. IL-6 partly mediated the relationship between SGHS and depression. ConclusionThis is the first study to demonstrate a link between SGHS and inflammatory depression. If replicated in independent and longitudinal cohorts, this may prove to be a relevant pathophysiological mechanism in some cases of depression that could be targeted in future intervention and prevention studies.

Predictors of in-hospital death in children with myocardial injury related to COVID-19.

Myocardial injury due to COVID-19 infection is associated with higher mortality rates, higher intensive care unit admissions, and greater levels of inflammatory and cardiac markers. However, given the smaller number of papers regarding pediatric patients, there is still scarce data about mortality predictors in this population. This study aims to identify independent predictors of in-hospital death among pediatric patients hospitalized with myocardial injury related to COVID-19. This is an observational, prospective, and longitudinal study of pediatric patients who were hospitalized between March 2020 and June 2021 in a tertiary pediatric hospital. A total of 1,103 consecutive pediatric patients tested positive for COVID-19, and 232 were admitted. All patients underwent cardiac evaluation with electrocardiogram, echocardiogram, and cardiac markers. Of these patients, 88 were diagnosed with myocardial injury but 1 patient refused to participate, therefore 87 patients were included in the study. The median age at the time of diagnosis was 2 years (0-18), 38% had pre-existing comorbidities, and the mortality was 12% (n = 11). Cardiac evaluation has revealed high levels of troponin I in 63%, and electrocardiogram and echocardiogram abnormalities in 81% and 22% respectively. We found that high levels of inflammatory markers had higher mortality, but they didn't emerge as significant predictors of mortality when adjusted for other variables. Patients without pre-existing comorbidities were less likely to die in both univariate and multivariate analysis. Our findings may help healthcare providers better understand the cardiac implications of COVID-19 and define the necessity of cardiac surveillance amongst hospitalized pediatric patients.

Proteomics on human cerebral cavernous malformations reveals novel biomarkers in neurovascular dysfunction for the disease pathology

BackgroundCerebral cavernous malformation (CCM) is a disease associated with an elevated risk of focal neurological deficits, seizures, and hemorrhagic stroke. The disease has an inflammatory profile and improved knowledge of CCM pathology mechanisms and exploration of candidate biomarkers will enable new non-invasive treatments. MethodsWe analyzed protein signatures in human CCM tissue samples by using a highly specific and sensitive multiplexing technique, proximity extension assay. FindingsData analysis revealed CCM specific proteins involved in endothelial dysfunction/inflammation/activation, leukocyte infiltration/chemotaxis, hemostasis, extracellular matrix dysfunction, astrocyte and microglial cell activation. Biomarker expression profiles matched bleeding status, especially with higher levels of inflammatory markers and activated astrocytes in ruptured than non-ruptured samples, some of these biomarkers are secreted into blood or urine. Furthermore, analysis was also done in a spatially resolving manner by separating the lesion area from the surrounding brain tissue. Our spatial studies revealed that although appearing histologically normal, the CCM border areas were pathological when compared to control brain tissues. Moreover, the functional relevance of CD93, ICAM-1 and MMP9, markers related to endothelial cell activation and extracellular matrix was validated by a murine pre-clinical CCM model. InterpretationHere we present a novel strategy for proteomics analysis on human CCMs, offering a possibility for high-throughput protein screening acquiring data on the local environment in the brain. Our data presented here describe CCM relevant brain proteins and specifically those which are secreted can serve the need of circulating CCM biomarkers to predict cavernoma's risk of bleeding.

Interplay of inflammatory markers and anti-SARS-CoV-2 antibodies in COVID-19 mortality: A prospective cohort study

ObjectivesDespite high global vaccination coverage, it remains unclear how vaccination and anti-SARS-CoV-2 antibodies affect immune responses and inflammation levels in patients with COVID-19. It is further unclear whether the inflammatory response differs depending on antibody levels and whether the combination of antibody and inflammation levels in COVID-19 patients affects mortality rates. MethodsWe conducted a prospective multicenter cohort study that included 1031 hospitalized COVID-19 patients from five hospitals. Anti-SARS-CoV-2-spike antibodies, interleukin-6 (IL6), and CRP were measured on hospital admission. The prespecified endpoint was all-cause in-hospital mortality. ResultsWe observed significantly lower levels of CRP (P<0.001) and IL6 (P<0.001) in patients with antibody levels above 1200 BAU/ml. After adjusting for potential confounders, patients with high levels of inflammatory markers (CRP>6 mg/dl or IL6>100 pg/ml) combined with low levels of anti-SARS-CoV-2-spike antibodies (<1200 BAU/ml) were approximately 8 times more likely to die than patients with low inflammatory responses and high antibody levels (CRP: aHR 7.973, 95% CI 2.744-23.169, P<0.001; IL6: aHR 8.973, 95% CI 3.549-22.688, P<0.001). ConclusionHospitalized COVID-19 patients presenting with high inflammatory markers and low antibody levels exhibited the highest mortality risks. Higher antibody levels are associated with lower levels of inflammation in hospitalized COVID-19 patients.

Exploring the Link between Chronic Inflammation and Atherosclerosis-Endometriosis Association

Background: Atherosclerotic cardiovascular disease (ASCVD) and endometriosis are both inflammatory diseases with significant implications for clinical practice and public health. Evidence Acquisition: To examine the clinical question regarding the relationship between ASCVD and endometriosis, we gathered data from various sources, including research studies and subsequent reference searches of retrieved articles. Our research strategies focused on identifying high-quality evidence through comprehensive study time periods and rigorous methods for quality assessment and article inclusion. Results: Our review of the literature reveals significant findings regarding the interplay between ASCVD and endometriosis. Both conditions share inflammation as a key factor in their pathophysiology. Inflammation not only contributes to the initiation and progression of vascular damage in ASCVD but also plays a role in the development and persistence of endometriosis. Women with endometriosis demonstrate higher levels of inflammatory markers and endothelial activation. Conclusions: Based on the available evidence, we conclude that there is a likely genetic link between ASCVD and the development of endometriosis. Additionally, the influence of estrogen on ASCVD varies depending on the stage of atherosclerosis. While estrogen may be protective in women with early artery blockages, it can pose a potential risk to those with established atherosclerosis. Clinicians should consider these factors when managing patients with ASCVD and endometriosis to optimize care.

Possible risk factors for atrial fibrillation in patients with heart failure with mildly reduced ejection fraction

Aim. To study possible risk factors (RFs) for the development of paroxysmal and persistent atrial fibrillation (AF) in patients with heart failure with mildly reduced ejection fraction (HFmrHF).Material and methods. The study included 193 patients with chronic HFmrHF and non-valvular paroxysmal/persistent AF. Seventy-six comparable patients, but without AF, were studied as a control group. All patients underwent a detailed physical examination, including electrocardiography (ECG), echocardiography, ambulatory blood pressure monitoring, and Holter ECG monitoring. Levels of inflammatory markers, namely high-sensitivity C-reactive protein, interleukin-6, tumor necrosis factor-a and fibrotic marker, transforming growth factor-b1 (TGF-b1) were measured using ELISA. The results obtained were analyzed using the method of binary logistic regression and odds ratio (OR), which allows us to assess the relationship of a specific outcome with possible risk factors and compare study groups according to the detection rate of risk factors.Results. A higher level of diastolic blood pressure (DBP) (OR=1,09, confidence interval (CI)=1,01-1,17, p=0,017) is a possible risk factor for paroxysmal AF in patients with CHF. Possible risk factors for paroxysmal and persistent AF in such patients are an increase in episodes of hypertensive crisis (OR=1,17, CI=1,071,43, p=0,001) and an increase in body mass index (BMI) (OR=1,13, CI=0,931,27, p=0,031). An increase in the OR index of left ventricular diastolic and systolic parameters was associated with significant atrial and ventricular remodeling, which contributes to AF progression from paroxysmal to persistent. Higher levels of inflammatory markers were observed in patients with AF compared with patients with HFmrHF without AF. The increase in the OR level of TGF-b1 (OR=3,84, CI=2,106,23, p=0,005) was significant in patients with persistent AF.Conclusion. Using the OR method, an increase in DBP, the prevalence of hypertensive crisis, BMI, left atrial and ventricular remodeling, an increase in markers of systemic inflammation and fibrosis are possible risk factors for AF in patients with HFmrHF.

Association between Controlling Nutritional Status (CONUT) Score and Body Composition, Inflammation and Frailty in Hospitalized Elderly Patients.

a total of 361 patients were retrospectively recruited and divided into three groups based on the CONUT score. patients with a score ≥5 exhibited significantly higher levels of inflammatory markers, such as erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), Neutrophil/Lymphocytes ratio (NLR), main platelet volume (MPV), and ferritin, compared to those with a lower score. Furthermore, these patients showed unfavorable changes in body composition, including a lower percentage of skeletal muscle mass (MM) and fat-free mass (FFM) and a higher percentage of fatty mass (FM). A positive correlation was found between the CONUT score and inflammatory markers, Geriatric Depression Scale Short Form (GDS-SF), and FM. Conversely, the Mini Nutritional Assessment (MNA), Mini-Mental Status Examination, activity daily living (ADL), instrumental activity daily living (IADL), Barthel index, FFM, and MM showed a negative correlation. Frailty was highly prevalent among patients with a higher CONUT score. The receiver operating characteristic (ROC) curve demonstrated high accuracy in identifying frail patients (sensitivity). a high CONUT score is associated with a pro-inflammatory status as well as with unfavorable body composition. Additionally, it is a good tool to identify frailty among hospitalized elderly patients.

Endothelial dysfunction and cardiovascular risk in post-COVID-19 patients after 6- and 12-months SARS-CoV-2 infection.

SARS-CoV-2 infection causes severe endothelial damage, an essential step for cardiovascular complications. Endothelial-colony forming cells (ECFCs) act as a biomarker of vascular damage but their role in SARS-CoV-2 remain unclear. The aim of this study was to assess whether the number of ECFCs and angiogenic biomarkers remained altered after 6 and 12-months post-infection and whether this imbalance correlated with the presence of long-COVID syndrome and other biological parameters measured. Seventy-two patients were recruited at different time-points after overcoming COVID-19 and thirty-one healthy controls. All subjects were matched for age, gender, BMI, and comorbidities. ECFCs were obtained from peripheral blood and cultured with specific conditions. The results confirm the presence of a long-term sequela in post-COVID-19 patients, with an abnormal increase in ECFC production compared to controls (82.8% vs. 48.4%, P < 0.01) that is maintained up to 6-months (87.0% vs. 48.4%, P < 0.01) and 12-months post-infection (85.0% vs. 48.4%, P < 0.01). Interestingly, post-COVID-19 patients showed a significant downregulation of angiogenesis-related proteins compared to controls indicating a clear endothelial injury. Troponin, NT-proBNP and ferritin levels, markers of cardiovascular risk and inflammation, remained elevated up to 12-months post-infection. Patients with lower numbers of ECFC exhibited higher levels of inflammatory markers, such as ferritin, suggesting that ECFCs may play a protective role. Additionally, long-COVID syndrome was associated with higher ferritin levels and with female gender. These findings highlight the presence of vascular sequela that last up to 6- and 12-months post-infection and point out the need for preventive measures and patient follow-up.

A dose-response meta-analysis of randomized clinical trials investigating the effects of omega-3 supplementation on body weight in patients with cancer cachexia

BackgroundCachexia is one of the side effects of cancer diseases that can be reduced weight, and lower overall survival. Weight loss has been associated with adverse outcomes in both cancer patients and patients with benign diseases. There is no definitive treatment for fully reverse cachexia. studies showed higher levels of inflammatory markers in patient with cachectic cancer. Therefore, this study aimed to investigate the dose-response effects of omega-3 as an anti-inflammatory supplement on body weight in patients with cancer cachexia. MethodsOnline databases including PubMed, Scopus, and Web of Science were systematically searched by relevant keywords up to January 2022. Random effect analysis was applied to perform meta-analysis. Subgroup analyses were performed to find heterogeneity sources. Quality assessment was conducted using Revised Cochrane Collaboration’s tool II. Trim and fill analysis were also carried out in case of the presence of publication bias. The certainty in the evaluations was assessed by the GRADE approach. ResultsOmega-3 supplementation resulted in a significant increase of body weight in patients with cancer cachexia when the age of study participants was ≥ 67 years and the baseline weight of them was ≤ 60 kg (WMD= 0.99; 95% CI: 0.06, 1.92 and WMD= 1.22; 95% CI: 0.14, 2.30, respectively). Also, there was a non-significant linear relationship between the dosage of omega-3 supplementation and body weight in patients with cancer cachexia. ConclusionOmega-3 supplementation may be a promising agent to increase body weight in patients with cancer cachexia. Also, a non-significant linear relationship between the dosage of omega-3 supplementation and body weight was found in these patients.

Patellar and quadriceps tendon rupture are associated with hip fracture in hemodialysis patients with severe hyperparathyroidism.

Spontaneous rupture of the patellar (PTR) and quadriceps (QTR) tendon is infrequent. Systemic diseases such as diabetes mellitus, CKD, and secondary hyperparathyroidism (SHPT) are risk factors. The present cohort study aimed to evaluate risk factors associated with tendon rupture in hemodialysis (HD) patients with SHPT, as well as outcomes including surgical complications, re-ruptures, and fracture. Baseline clinical, laboratorial data, and radiographs were analyzed. Patients were followed up from March 2012 to March 2020. One-hundred thirty-one patients (≥18yr of age, on HD ≥ 6mo, with SHPT) were included. Incidence rates of PTR and QTR were 2.3 and 1.7/10000 HD patients/yr, respectively. The mean age of patients with tendon rupture was 44.0 ± 11.2yr. These patients exhibited higher serum levels of phosphorus (6.3 ± 1.5mg/dL vs 5.6 ± 1.1mg/dL; P = .005), PTH (2025.7 ± 667.6pg/mL vs 1728.4 ± 684.8pg/mL; P = .035), and C-reactive-protein (35.4 ± 32.9mg/dL vs 17 ± 24.5mg/dL; P = .002) compared to the group without tendon rupture. The mean follow-up was 56.7 ± 27.1mo. No patient required a new surgical approach or experienced re-rupture. Of all patients, 31% experienced hip fracture: 50% in the group with rupture (29.5 ± 17.4mo after the tendon rupture) vs 26% without tendon rupture (P = .015). After adjustment, the hazard ratio for hip fracture was 2.87 (95% CI, 1.27-6.49; P = .012). Patients with SHPT and high levels of phosphorus, PTH, and inflammatory markers were at greater risk for tendon rupture. Surgical complication rates were low. However, results suggest that tendon rupture of knee extensor mechanism in HD patient with SHPT should be regarded as a "red flag" for future hip fracture.

Coronary atherosclerosis and periodontitis have similarities in their clinical presentation.

Periodontitis (PE) and coronary heart disease (CHD) possess multiple mechanisms for a putative association. This case-control study compared the periodontal status among CHD subjects to controls without CHD, while also investigating atheroma invasion by known periodontal pathogens. 161 subjects participated in this study were divided into three CHD groups: No CHD, chronic CHD, acute CHD. Additional analysis involved grouping subjects according to number of atheromas: no atheroma, 1-4 atheromas, 5-18 atheromas. Data were collected from medical records, periodontal examinations, and questionnaires that included demographic, behavioral, and oral health variables. Angiographic catheterizations were analyzed according to the number of atheroma lesions, lesion size, lesion location, and atheroma lesion stability. Lipoprotein profile, inflammatory markers and cells were analyzed. The microbiological branch added 30 individuals who had their atheroma lesion and subgingival plaque analyzed using polymerase chain reaction probes against the 16 s region, red complex and Aggregatibacter actinomycetemcomitans' DNA. Subjects with CHD had high levels of systemic inflammatory markers and low levels of high-density lipoproteins compared to subjects without CHD. Subjects without CHD and clear coronaries had a prevalence of mild CAL, while individuals with more atheroma lesions had advanced CAL and more active PE. Subjects with more advanced CAL were 4 times more likely to have CHD compared to subjects with less, which is comparable to smoking. Only 4 subjects had the screened pathogens detected in atheroma, although these subjects also have the screened pathogens in subgingival plaque. However, 80% of atheromas had bacteria. CHD and PE showed similarities in progression while active PE led to more atheroma lesions that also tended to be larger in size.

Patient global assessment and inflammatory markers in patients with idiopathic inflammatory myopathies – A longitudinal study

AimTo explore if patient global assessment (PGA) is associated with inflammation over time and if associations are explained by other measures of disease activity and function in patients with idiopathic inflammatory myopathies (IIM). MethodsPGA and systemic inflammatory markers prospectively collected over five years were retrieved from the International MyoNet registry for 1200 patients with IIM. Associations between PGA, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP) and creatine kinase (CK) were analyzed using mixed models. Mediation analysis was used to test if the association between PGA and inflammatory markers during the first year of observation could be explained by measures of disease activity and function. ResultsPGA improved, and inflammatory markers decreased during the first year of observation. In the mixed models, high levels of inflammatory markers were associated with worse PGA in both men and women across time points during five years of observation. In men, but not in women, the association between elevated ESR, CRP and poorer PGA was explained by measures of function and disease activity. With a few exceptions, the association between improved PGA and reduced inflammatory markers was partially mediated by improvements in all measures of function and disease activity. ConclusionIncreased levels of systemic inflammation are associated with poorer PGA in patients with IIM. In addition to known benefits of lowered inflammation, these findings emphasize the need to reduce systemic inflammation to improve subjective health in patients with IIM. Furthermore, the results demonstrate the importance of incorporating PGA as an outcome measure in clinical practice and clinical trials.

Baseline NT-proBNP levels as a predictor of short-and long-term prognosis in COVID-19 patients: a prospective observational study

BackgroundUp to 20% of COVID-19 patients can suffer COVID-19-related myocardial injury. Elevated cardiac biomarkers, such as hs-cTnT and NT-proBNP, have been related to worse short-term prognosis. However, data on NT-proBNP and long-term prognosis are scarce. We have evaluated the potential association of baseline age-adjusted NT-proBNP levels and outcomes at one-year follow-up in COVID-19 patients.MethodsThis was a single-center prospective study of 499 COVID-19 patients in whom NT-proBNP was assessed at hospital admission. NT-proBNP levels were age-adjusted and patients were classified as high or low NT-proBNP. Clinical and demographic characteristics, comorbidities, laboratory results, and in-hospital complications and mortality were compared between the two groups. Survivors of the acute phase of COVID-19 were followed up for one year from admission to detect readmissions and mortality.ResultsThe 68 patients with high NT-proBNP levels at hospital admission were older, with more cardiovascular risk factors, cardiovascular disease, comorbidities, myocardial injury, and higher levels of inflammatory markers than patients with low NT-proBNP levels. They also had more in-hospital complications and a higher acute-phase mortality rate (60.3% vs. 10.2%, p < 0.001). High NT-proBNP levels were an independent marker of death during hospitalization (HR 1.95; CI 1.07–3.52). At one-year follow-up, high NT-proBNP levels were independently associated with mortality (HR 2.69; CI 1.47–4.89). Among survivors of the acute phase of COVID-19, there were no differences in hospital readmissions between those with high vs. low NT-proBNP levels, but survivors with high baseline NT-proBNP levels showed a higher 1-year mortality rate (7.4% vs. 1.3%, p = 0.018).ConclusionsHigh age-adjusted NT-proBNP levels at the time of hospital admission for COVID-19 are associated with poor short and long-term prognosis. High NT-proBNP seems also to be related to worse prognosis in survivors of the acute phase of COVID-19. A closer follow-up on these patients may be crucial.

Investigating the relationship between muscle mass and nasal Methicillin-Resistant Staphylococcus aureus (MRSA) colonization: Analysis of the National Health and Nutrition Examination Survey (NHANES).

Methicillin-resistant Staphylococcus aureus (MRSA) nasal colonization is associated with an increased risk of infection disease. Low muscle mass has been linked to higher levels of inflammatory markers and weakened immune response, which may impact the susceptibility to nasal MRSA colonization. The relationship between muscle function and immune response to pathogens may be bidirectional. This study investigates the association between muscle mass and nasal MRSA colonization in adults. The present cross-sectional study utilized data from the National Health and Nutrition Examination Survey (NHANES) conducted between 2001 and 2004. Appendicular skeletal muscle mass (ASM) adjusted by body mass index (BMI) (ASM/BMI) was used to evaluate muscle mass. Multivariate logistic regression, adjusted for demographic and infection factors, was used to analyze the association between muscle mass and nasal colonization by MRSA. A subgroup analysis based on age and gender was performed to assess the impact of muscle mass on nasal MRSA colonization. Nasal MRSA colonization was more prevalent in females, those with smaller household sizes, lower income, lower ASM/BMI, those who had stayed in healthcare facilities in the past 12 months, and individuals with diabetes and smoking habits. After adjusting for confounding factors, a dose-dependent association was found between decreasing quartiles of ASM/BMI and the risk of nasal MRSA colonization (p < 0.05). Additionally, per 1 unit increase in ASM/BMI was related to a 64% lower risk of nasal MRSA colonization. This study suggests a significant negative correlation between ASM/BMI and the risk of nasal MRSA colonization. However, more prospective studies are required to investigate the causal relationship between muscle mass and colonization.

Impact of comorbidities and inflammatory markers on mortality of COVID-19 patients.

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus that causes coronavirus disease 2019 (COVID-19) is a serious global health concern. The severity of the disease can be determined by serologic indicators such as C-reactive protein, lactate dehydrogenase, D-dimer, ferritin, and interleukin-6. (IL-6). Patients with preexisting conditions such as respiratory, cardiovascular, and pulmonary disease could be at risk of adverse outcomes. It is crucial to provide adequate medical care to manage these patients and increase their chances of survival. The study examined the impact of comorbidity and inflammatory markers on the severity and mortality of hospitalised COVID-19 patients. This retrospective study included 101 COVID-19 patients who had comorbidities and were hospitalised from April 2021 to April 2022. Patients with a severe COVID-19 infection could be anticipated to have higher levels of inflammatory markers in their blood. Patients with chronic kidney and coronary artery disease have a worse prognosis than those with other comorbidities (P value <0.001). However, tuberculosis had no statistically significant effect on mortality and showed a minimal chance of death (P value = 0.303). In addition, tocilizumab performed poorly and was ineffective against the COVID-19 treatment. However, ivermectin exhibited a statistically significant probability of survival in COVID-19 patients. The inflammatory markers D-dimer, ferritin, and IL-6 were identified as valuable indicators of disease severity. Further, chronic kidney disease and coronary artery disease were identified as risk factors for mortality, while tuberculosis showed potential protective effects. The study showed that higher neutrophil levels were linked to mortality in tocilizumab-treated patients, while ivermectin showed promise in increasing survival rates.

Difficulties in myocarditis diagnosis: a case report

Myocarditis is often difficult to diagnose. The diagnostic difficulties include nonspecific symptoms or a “vague” clinical picture, absence of pathognomonic signs during physical examination, and endomyocardial biopsy, which is the “gold standard” of diagnosis of myocarditis, being an invasive procedure that is performed under strict indications in certain patients. Nevertheless, as radiology is rapidly developing, clinicians are now able to noninvasively diagnose symptoms of inflammatory myocardial damage, including edema and myocardial fibrosis, using cardiac magnetic resonance imaging. This article presents the clinical case of a young patient with symptoms of acute coronary syndrome, who showed no evidence of coronary artery disease. Myocarditis was suspected because of increased activity of cardiospecific enzymes and high levels of inflammatory markers, pronounced electrocardiography changes with positive dynamics, and recent infection. Magnetic resonance imaging was used to confirm myocarditis diagnosis. Thus, this case study demonstrates the role of imaging techniques in the differential diagnosis of ischemic and inflammatory heart diseases.