Higher Fibrinogen Levels Research Articles

Prognostic significance of fibrinogen levels in sepsis-associated acute kidney injury: unveiling a nonlinear relationship and clinical implications

BackgroundFibrinogen plays a pivotal role in the inflammatory cascade and is intricately linked to the pathogenesis of sepsis. Nevertheless, its significance as a prognostic marker for sepsis-associated acute kidney injury (SA-AKI) remains uncertain. This study aimed to investigate the association between fibrinogen levels and 28-day mortality with sepsis-associated acute kidney injury.MethodThe fibrinogen levels of patients admitted to the intensive care unit of Beth Israel Deaconess Medical Center between 2008 and 2019 were retrospectively assessed, and those diagnosed with SA-AKI were divided into low, middle and high fibrinogen level groups according to tertiles. Multivariate Cox proportional hazards model was used to assess the 28-day mortality risk of the SA-AKI patients.ResultsA total of 3,479 patients with SA-AKI were included in the study. Fibrinogen demonstrated an independent association with 28-day mortality, yielding a hazard ratio (HR) of 0.961 (95% confidence interval [CI]: 0.923-0.999, P = 0.0471). Notably, a non-linear relationship between fibrinogen levels and 28-day mortality was observed, with the threshold observed at approximately 1.6 g/l. The effect sizes and corresponding CIs below and above this threshold were 0.509 (0.367, 0.707) and 1.011 (0.961, 1.064), respectively. Specifically, the risk of mortality among SA-AKI patients decreased by 49.1% for every 1 g/l increment in fibrinogen, provided that fibrinogen levels were less than 1.6 g/l.ConclusionIn patients with SA-AKI, a non-linear relationship was identified between fibrinogen levels and 28-day mortality. Particularly, when their fibrinogen levels were less than 1.6 g/l, a concomitant decrease in 28-day mortality was observed as fibrinogen levels increased.

Time-Dependent Association of Preinjury Anticoagulation on Traumatic Brain Injury-Induced Coagulopathy: A Retrospective, Multicenter Cohort Study

BACKGROUND AND OBJECTIVES: The impact of preinjury anticoagulation on coagulation parameters over time after traumatic brain injury (TBI) has remained unclear. Based on the hypothesis that preinjury anticoagulation significantly influences the progression and persistence of TBI-induced coagulopathy, we retrospectively examined the association of preinjury anticoagulation with various coagulation parameters during the first 24 hours postinjury in 5 periods. METHODS: Data from the Japanese registry of patients with TBI aged ≥65 years admitted between 2019 and 2021 were used. Time since injury was classified into 5 categories through a graphical analysis of coagulation parameters. We examined the association between preinjury anticoagulation and the platelet count, prothrombin time-international normalized ratio (PT-INR), activated partial thromboplastin time (APTT), D-dimer level, and fibrinogen level during each period by analysis of covariance using 10 clinical factors as confounding factors. RESULTS: Data from 545 patients and 795 blood tests were analyzed. The patients' mean age was 78.9 years, and 87 (16%) received anticoagulation therapy. The preinjury anticoagulation group had significantly greater Rotterdam computed tomography scores and poorer outcomes at discharge than the control group, with significantly lower D-dimer levels and higher fibrinogen levels. Analysis of covariance revealed significant associations between the D-dimer level and preinjury anticoagulation within 2 to 24 hours postinjury, APTT and preinjury anticoagulation within 1 to 24 hours, and PT-INR and preinjury anticoagulation throughout all periods up to 24 hours postinjury. CONCLUSION: Despite more severe TBI signs and poorer outcomes, the preinjury anticoagulation group had significantly lower D-dimer levels, especially within 2 to 24 hours postinjury. Thus, D-dimer levels during this period may not reliably represent TBI severity in patients receiving anticoagulation therapy before injury. Preinjury anticoagulation was also associated with an elevated PT-INR and prolonged APTT from early to 24 hours postinjury, highlighting the importance of aggressive anticoagulant reversal early after injury.

Heparin-binding protein and sepsis-induced coagulopathy: Modulation of coagulation and fibrinolysis via the TGF-β signalling pathway

BackgroundHeparin-binding protein (HBP) levels have been linked to organ failure and may represent an inflammatory biomarker of sepsis. We found disseminated intravascular coagulation (DIC) is associated with higher HBP levels in patients and in in vivo and in vitro models. This prospective, single-center observational study investigated the effects and underlying mechanisms of HBP on the coagulation cascade in sepsis. Methods538 patients with sepsis from June 2016 to December 2019 were enrolled. Mechanisms underlying HBP and the coagulation system were investigated in human umbilical vein endothelial cells (HUVEC) and C57 mice. ResultsIncreased HBP was associated with sepsis-induced DIC. The optimal cutoff value was 37.5 ng/mL (sensitivity: 56 %, specificity: 65 %). Antithrombin-III (AT-III) activity, plasmin-a2 plasmin inhibitor complex (PIC), procalcitonin (PCT), hemoglobin, and HBP ≥37.5 ng/mL were associated with of DIC occurrence. In HUVECs &C57 mice models, Western blotting, qPCR, and immunohistochemistry analysis showed that the binding between HBP and TGF-β receptor 2 (TGFBR2) caused elevation of plasminogen activator inhibitor-1 (PAI-1) levels. Furthermore, we found that mice stimulated with HBP had higher levels of fibrinogen and D-dimer in the blood. HBP treatment caused the accumulation of fibrinogen in mice lung tissue. Treatment with TGFBR2-small interfering RNAs inhibited the effects. ConclusionPatients with sepsis having HBP ≥37.5 ng/mL at admission were more likely to develop DIC. HBP upregulates the expression of fibrinogen and PAI-1 via TGFBR2 and the TGF-β signalling pathway.

High rates of hepatic involvement associated with new epidemic measles strains in Romania.

Similar to other European countries, a measles epidemic dominated by D8 genotype strains is ongoing since 2022 in our country. Recent reports of liver involvement associated with new measles virus (MeV) strains are scarce. The aim of the study was to compare the clinical characteristics between hospitalized patients with measles from the current epidemic and those from the previous outbreak and to analyze the risk factors associated with hepatic involvement. Data were collected retrospectively for all consecutive adult ( ≥18 years old) patients admitted between October 2022-April 2024 and January 2018-December 2019. A number of 228 patients from the current and 130 from the previous MeV epidemic were included. The main statistically significant differences were those regarding hepatic involvement (77.2% vs. 45.4%, p < 0.001) and significant hepatocellular injury (23.6% vs. 10.7%, p = 0.003). Compared to cases without liver involvement (123), patients with hepatocytolysis (235) had a higher prevalence of keratoconjunctivitis (42.5% vs. 28.4%, p = 0.01), thrombocytopenia (47.6% vs. 34.9%, p = 0.02), severe lymphopenia (51% vs. 35.7%, p = 0.007) and high fibrinogen levels (58.7% vs. 47.1%, p = 0.04). MeV strains from the 2022-2024 epidemic were the strongest predictors of hepatic involvement in the multivariable analysis (odds ratio = 4.3, 95% confidence interval: 2.5-7.4, p < 0.001). The mortality rate of patients with hepatocellular injury was 1.2%. The current measles epidemic is dominated by high rates of hepatic involvement compared to the previous outbreak. Although not associated with a significant mortality, the potential change in MeV hepatotropism could have important clinical implications and warrants further monitoring.

Preoperative fibrinogen level predicts the risk and prognosis of patients with native valve infective endocarditis undergoing valve surgery.

The aim of this study was to assess the clinical significance and prognostic value of the preoperative fibrinogen (FBG) level in patients with native valve infective endocarditis (NVIE) who underwent valve surgery. This retrospective study included a total of 163 consecutive patients who were diagnosed with NVIE and underwent valve surgery from January 2019 to January 2022 in our hospital. The primary endpoint was all-cause mortality. All-cause mortality was observed in 9.2% of the patients (n = 15). Body mass index (BMI) was lower in the survival group (p = 0.025), whereas FBG (p = 0.008) and platelet count (p = 0.044) were significantly greater in the survival group than in the death group. Multivariate Cox proportional hazards analysis revealed that FBG (HR, 0.55; 95% CI, [0.32-0.94]; p = 0.029) was an independent prognostic factor for all-cause mortality. Furthermore, Kaplan‒Meier survival curve analysis revealed that patients with low FBG levels (<3.28 g/L) had a significantly greater mortality rate (p = 0.034) than did those with high FBG levels (>3.99 g/L). In the trend analysis, the FBG tertiles were significantly related to all-cause mortality in all three adjusted models, and the p values for trend were 0.017, 0.016, and 0.028, respectively. Preoperative FBG may serve as a prognostic factor for all-cause mortality, and an FBG concentration less than 3.28 g/L was associated with a greater risk of all-cause mortality in NVIE patients undergoing valve surgery.

Biochemical Markers in the Prediction of Pregnancy Outcome in Gestational Diabetes Mellitus.

Background and Objectives: Gestational diabetes mellitus (GDM) may impact both maternal and fetal/neonatal health. The identification of prognostic indicators for GDM may improve risk assessment and selection of patient for intensive monitoring. The aim of this study was to find potential predictors of adverse pregnancy outcome in GDM and normoglycemic patients by comparing the levels of different biochemical parameters and the values of blood cell count (BCC) between GDM and normoglycemic patients and between patients with adverse and good outcome. Materials and Methods: Prospective clinical study included 49 patients with GDM (study group) and 44 healthy pregnant women (control group) who underwent oral glucose tolerance test (OGTT) at gestational age of 24-28 weeks. At the time of OGTT peripheral blood was taken for the determination of glucose levels, insulin, glycated hemoglobin, lipid status, homeostatic model assessment, BCC, iron and zinc metabolism, liver function, kidney function and inflammatory status. Each group was divided into two subgroups-normal and poor pregnancy outcome. Results: Higher RBC, hemoglobin concentration, hematocrit value, fasting glucose, uric acid and fibrinogen were found in GDM patients compared to control group. In GDM patients with poor pregnancy outcome values of fibrinogen, ALT, sedimentation rate, granulocyte and total leukocyte counts were elevated, while the serum level of zinc was significantly lower. Higher level of fibrinogen was found in normoglycemic patients with adverse pregnancy outcomes. ROC curve was constructed in order to assess fibrinogen's biomarker potential. The established AUC value for diagnostic ROC was 0.816 (p < 0.001, 95% CI 0.691-0.941), while the AUC value for assessing fibrinogen's potential to predict poor pregnancy outcome in GDM was 0.751 (p = 0.0096, 95% CI 0.561-0.941). Conclusions: The results of our study demonstrated that the best prognostic potential in GDM showed inflammation related parameters, identifying fibrinogen as a parameter with both diagnostic and prognostic ability.

Correlation between plasma fibrinogen levels and microvascular complications in type 2 diabetes.

To determine how plasma fibrinogen levels impact the severity of microvascular complications in people with type 2 diabetes while focussing on the molecular mechanisms of fibrinogen's role in such complications. The analytical, cross-sectional study was conducted from September 2022 to March 2023 at the Department of Medicine, Mardan Medical Complex and Teaching Hospital, Khyber Pakhtunkhwa, Pakistan, and comprised adult patients of either gender who had been diagnosed with type 2 diabetes and microvascular complications. Each patient was subjected to an evaluation of microvascular complications, including diabetic retinopathy, nephropathy and neuropathy, using validated diagnostic criteria and clinical examinations. Data was analysed using SPSS 26. Of the 174 patients 97(%) were males and 77(%) were females. Retinopathy was found in 57(32.7) patients with median age 53 years (interquartile range: 46-63 years). Nephropathy was found in 55(31.6%) subjects with median age 54 years (interquartile range: 50-61 years). Neuropathy was found in 62(35.6%) patients with median age 53 years (interquartile range: 48-58 years). Diabetic neuropathy was significantly associated with elevated plasma fibrinogen levels and various biomarkers, such as creatinine, urea, fasting blood glucose, glycated haemoglobin and estimated average glucose (p<0.05). Diabetic retinopathy was significantly linked with higher levels of fibrinogen, which manifested through symptoms, like floaters or dark spots, impaired colour vision, difficulty seeing at night, blurred or fluctuating vision and vision loss (p<0.05). Diabetic nephropathy and the progression of its severity was significantly associated with increased fibrinogen levels, as well as markers, like albuminuria, creatinine, urea, fasting blood glucose, glycated haemoglobin and estimated average glucose (p<0.05). Elevated plasma fibrinogen levels in patients with type 2 diabetes significantly correlated with increased microvascular complications, underscoring the importance of monitoring and managing fibrinogen levels to mitigate diabetes-associated vascular pathologies.

Effect of impaired myocardial contractility on coronary flow reserve and inflammatory processes in chronic coronary syndrome

Aim. To study the relationship between myocardial contractility impairment in chronic coronary syndrome and the state of coronary flow reserve, the degree of systemic inflammation and endothelial dysfunction. Materials and methods. We examined 120 patients with stable angina pectoris (SAP) of functional class (FC) II–III, who were assigned into two groups: group 1 comprised 65 patients with left ventricular ejection fraction (LVEF) ≥55 %, and group 2 was composed of 55 patients with LVEF &lt;55 %. Diagnostic methods included clinical and instrumental examination data, analyses of lipid profile, inflammation biomarkers, endothelial functional state, hemogram data, leukocyte inflammation markers, and questionnaires. Results. Compared to group 1, group 2 patients showed an increase in the left atrium (p &lt; 0.001) and right ventricle (p = 0.027) sizes; significantly lower LVEF (50.16 ± 0.42 % vs 58.77 ± 0.41 %; p &lt; 0.001); thickening of the intima-media complex in the right (p = 0.003) and left (p = 0.017) common carotid arteries; significantly lower load threshold values (p = 0.008), exercise tolerance (p = 0.004) and heart rate variability indicators – SDNN (standard deviation of normal-to-normal intervals over 24 hours; p = 0.046). Group 2 patients were characterized by more active low-grade chronic inflammation, as indicated by increased levels of leukocytes (p = 0.024), neutrophils (p &lt; 0.001), and decreased lymphocyte levels (p = 0.021); significantly higher levels of leukocyte inflammation markers, in particular, the neutrophil-to-lymphocyte ratio (p &lt; 0.001), platelet-to-lymphocyte ratio (p = 0.004), systemic immune-inflammation index (p &lt; 0.001), systemic inflammation response index (p &lt; 0.001), and aggregate index of systemic inflammation (p &lt; 0.001) as compared to group 1 individuals. Patients with LVEF &lt;55 % had higher levels of fibrinogen (p &lt; 0.001), uric acid (p = 0.002), high-sensitivity C-reactive protein (p = 0.007), and endothelin-1 (p &lt; 0.001) compared to those with LVEF ≥55 %. Conclusions. Group 2 patients need a more thorough monitoring and a more intensive treatment aimed at reducing the inflammatory process.

Serum Biomarkers to Dynamically Predict the Risk of Cardiovascular Events in Patients under Oncologic Therapy. A Multicenter Observational Study.

Serum biomarkers have been investigated as predictive risk factors for cancer-related cardiovascular (CV) risk, but their analysis is limited to their baseline level rather than their overtime change. Besides historically validated causal factors, inflammatory and oxidative stress (OS) related markers seem to be correlated to CV events but this association needs to be further explored. We conducted an observational study to determine the predictive role of the longitudinal changes of commonly used and OS-related biomarkers during the cancer treatment period. Patients undergoing anticancer therapies, either aged 75+ years old or younger with an increased CV risk according to European Society of Cardiology guidelines, were enrolled. We assessed the predictive value of biomarkers for the onset of CV events at baseline and during therapy using Cox model, Subpopulation Treatment-Effect Pattern Plot (STEPP) method and repeated measures analysis of longitudinal data. From April 2018 to August 2021, 182 subjects were enrolled, of whom 168 were evaluable. Twenty-eight CV events were recorded after a median follow up of 9.2 months (Interquartile range, IQR: 5.1-14.7). Fibrinogen and troponin levels were independent risk factors for CV events. Specifically, patients with higher than the median levels of fibrinogen and troponin at baseline had higher risk compared with patients with values below the medians, hazard ratio (HR) = 3.95, 95% CI, 1.25-12.45 and HR = 2.48, 0.67-9.25, respectively. STEPP analysis applied to Cox model showed that cumulative event-free survival at 18 and 24 months worsened almost linearly as median values of fibrinogen increased. Repeated measure analysis showed an increase over time of D-Dimer (p-interaction event*time = 0.08), systolic (p = 0.07) and diastolic (p = 0.05) blood pressure and a decrease of left ventricular ejection fraction (p = 0.15) for subjects who experienced a CV event. Higher levels of fibrinogen and troponin at baseline and an increase over time of D-Dimer and blood pressure are associated to a higher risk of CV events in patients undergoing anticancer therapies. The role of OS in fibrinogen increase and the longitudinal monitoring of D-dimer and blood pressure levels should be further assessed.

CRP, Fibrinogen, White Blood Cells, and Blood Cell Indices as Prognostic Biomarkers of Future COPD Exacerbation Frequency: The TIE Cohort Study.

Background/Objective: Systemic inflammation is common in chronic obstructive pulmonary disease (COPD), and evidence suggests that inflammatory biomarkers can predict acute exacerbations (AECOPDs). The aim of this study was to analyse whether C-reactive protein (CRP), fibrinogen, white blood cell count (WBC), or the blood cell indices PLR (platelet-to-lymphocyte ratio), SII (systemic immune inflammation index), SIRI (systemic inflammation response index), and AISI (aggregate index of systemic inflammation) can predict future AECOPDs. Methods: In the Tools Identifying Exacerbations (TIE) cohort study, participants with spirometry-confirmed COPD were recruited from primary and secondary care in three Swedish regions and assessed during a stable phase of COPD. AECOPD frequency during the three-year follow-up was reviewed in medical records. Associations were analysed via ordinal logistic regressions. Results: Of the 571 participants, 46% had ≥1 AECOPD during follow-up, and the mean ± SD AECOPD frequency was 0.63 ± 1.2/year. In unadjusted analyses, high levels of CRP (odds ratio 1.86, 95% CI 1.29-2.67), fibrinogen (2.09, 1.38-3.16), WBCs (2.18, 1.52-3.13), SII (1.52, 1.05-2.19), SIRI (1.76, 1.23-2.52), and AISI (1.99, 1.38-2.87) were associated with a higher AECOPD frequency. After adjustment for AECOPD history, age, sex, smoking, body mass index, COPD Assessment Test score, lung function, and inhaled corticosteroid use, associations remained for high levels of CRP (adjusted odds ratio of 1.64; 95% CI of 1.08-2.49), fibrinogen (1.55; 1.07-2.24), and WBC (1.65; 1.10-2.47). Conclusions: CRP, fibrinogen, and WBC, assessed during stable-phase COPD, enhanced AECOPD prediction, whereas PLR, SII, SIRI, and AISI did not.

Perioperative Hyper-coagulation and Thrombosis: Cost Analysis After Congenital Heart Surgery.

Thrombosis, a major adverse event of congenital heart surgery, has been associated with poor outcomes. We hypothesized that in CHD patients undergoing cardiac surgery, increased perioperative use of pro-coagulant products may be associated with postoperative thrombosis in the setting of hyperfibrinogenemia, leading to greater hospital and blood product costs. Single-center retrospective study. Data from Boston Children's Hospital's electronic health record database was used in this study. All patients undergoing congenital heart surgery between 2015 and 2018 with postoperative fibrinogen levels above 400mg/dl were reviewed. Of 334 patients with high plasma fibrinogen levels, 28 (8.4%) developed postoperative thrombosis (median age: one year, 59% male). In our cohort, 25 (7%) demonstrated evidence of baseline hypercoagulability by one or more panel test results. Thrombosis was associated with greater hospital and blood product costs, longer ventilation times, and longer hospital and ICU length of stays. Preoperative hypercoagulable state (odds ratio: 2.58, 95% CI [1.07, 9.99], p = 0.002), postoperative red blood cell transfusion (odds ratio: 1.007, 95% CI [1.000, 1.015], p = 0.04), and single ventricle physiology (univariate odds ratio: 2.94, 95% CI [1.09, 7.89], p = 0.03) were predictors of postoperative thrombosis. Preoperative hypercoagulable state and intraoperative platelet transfusion were predictors of hospital cost. Thrombosis was associated with worse in-hospital outcomes and higher costs. Preoperative hypercoagulable state and postoperative red blood cell transfusion were significant predictors of thrombosis. Risk prediction models that can guide thrombosis prevention are needed to improve outcomes of patients undergoing congenital heart surgery.

Systemic Inflammation, the Peripheral Blood Transcriptome, and Primary Melanoma

Peripheral blood transcriptomes from 383 newly-diagnosed melanoma patients were subjected to differential gene expression analysis. The hypotheses were that impaired systemic immunity is associated with poorer prognosis (thicker tumors and fewer tumor infiltrating lymphocytes (TILs)) and evidence of systemic inflammation (high-sensitivity C-reactive protein (hsCRP) and fibrinogen levels). Higher fibrinogen levels were associated with thicker primaries. In single gene analysis hsCRP levels were significantly associated with higher blood CD274 expression, (coding for PD-L1), but each was independently prognostic, with hsCRP associated with increased mortality, and higher CD274 protective, independent of age. Pathway analysis identified downregulation of immune cell signalling pathways in the blood of people with thicker tumors and notable upregulation of STAT1 in people with brisk TILs. Transcriptomic data provided evidence for increased NFB signalling with higher inflammatory markers but with reduction in expression of HLA class II molecules and higher CD274 suggesting that aberrant systemic inflammation is a significant mediator of reduced immune function in melanoma. In summary, transcriptomic data revealed evidence of reduced immune function in patients with thicker tumors and fewer TILs, at diagnosis. Inflammatory markers were associated with thicker primaries and independently with death from melanoma suggesting that systemic inflammation contributes to that reduced immune function.

Study of clinical profile of patients with acute coronary syndrome and the correlation of serum fibrinogen and grace score as a prognostic marker for predicting 3-month mortality

Introduction. Acute coronary syndrome (ACS), encompassing unstable angina, non-ST-segment eleva­tion myocardial infarction (NSTEMI), and ST-segment elevation myocardial infarction (STEMI), is a major global health concern due to its high morbidity and mortality. Research highlights a link between ACS and elevated acute phase reactants like C-reactive protein, emphasizing the role of inflammation and atherosclerosis. Serum fibrinogen, crucial in thrombus formation and an inflammatory marker, is significant in the coagu­lation process. This study investigates the predictive value of serum fibrinogen levels and the GRACE score for 3-month mortality in ACS patients. Aim. To examine the clinical profile of ACS patients and evaluate serum fibrinogen and GRACE score as prognostic markers for 3-month mortality. Methodology. A prospective observational study was conducted on 50 patients diagnosed with ACS at Saveetha Medical College Hospital. The study included adults over 18 with ACS, excluding those with severe comorbid conditions like end-stage liver disease or malignancy. Serum fibrinogen levels were measured at presentation and at 3 months using an automated coagulation analyzer. GRACE scores were calculated, and clinical assessments including ECG, cardiac markers, and ECHO were conducted. Data analysis involved IBM SPSS Statistics, utilizing descriptive statistics, t-tests, ANOVA, and Pearson's Correlation. Results. The study group had diverse demographics and a high prevalence of cardiovascular symptoms and comorbidities. The clinical profile of ACS showed a higher incidence of STEMI. Serum fibrinogen levels varied significantly across different Killip classes at presentation and at 3 months, with the highest levels in the more severe classes. Higher serum fibrinogen was linked to recurrent heart failure admissions and higher KILIPS class. However, there was no significant difference in fibrinogen levels between patients with and without interventions. The GRACE score was higher in STEMI patients, those with LV dysfunction, and correlated with higher serum fibrinogen. Lower FACIT F scores, indicating higher fatigue, were associated with higher fibrinogen levels and readmissions for heart failure. Conclusion. Higher serum fibrinogen levels and GRACE scores at presentation and at three months are indicators of severe myocardial infarction, increased heart failure readmission rates, and greater fatigue in ACS patients. These markers are valuable for evaluating morbidity in ACS and can aid in enhancing patient management strategies.

The Influence of Hyperthyroidism on the Coagulation and on the Risk of Thrombosis.

Introduction: Apart from the well-known fact that hyperthyroidism induces multiple prothrombotic disorders, there is no consensus in clinical practice as to the impact of hyperthyroidism on the risk of thrombosis. The aim of this study was to examine the various hemostatic and immunologic parameters in patients with hyperthyroidism. Methods: Our study consists of a total of 200 patients comprised of 64 hyperthyroid patients, 68 hypothyroid patients, and 68 euthyroid controls. Patient thyroid status was determined with standard tests. Detailed hemostatic parameters and cardiolipin antibodies of each patient were determined. Results: The values of factor VIII (FVIII), the Von Willebrand factor (vWF), fibrinogen, plasminogen activator inhibitor-1 (PAI-1), and anticardiolipin antibodies of the IgM class were significantly higher in the hyperthyroid patients than in the hypothyroid patients and euthyroid controls. The rate of thromboembolic manifestations was much higher in hyperthyroid patients (6.25%) than in hypo-thyroid patients (2.9%) and euthyroid controls (1.4%). Among hyperthyroid patients with an FVIII value of ≥1.50 U/mL, thrombosis was recorded in 8.3%, while in hyperthyroid patients with FVIII value ≤ 1.50 U/mL the occurrence of thrombosis was not recorded. The incidence of atrial fibrillation (AF) was significantly higher (8.3%) in the hyperthyroid patients compared to the hypothyroid patients (1.5%) and euthyroid controls (0%). Conclusions: High levels of FVIII, vWF, fibrinogen, PAI-1, and anticardiolipin antibodies along with other hemostatic factors contribute to the presence of a hypercoaguable state in patients with hyperthyroidism. The risk of occurrence of thrombotic complications is especially pronounced in patients with a level of FVIII exceeding 150% and positive anticardiolipin antibodies of the IgM class. Patients with AF are at particularly high risk of thrombotic complications due to a hyperthyroid prothrombotic milieu.

The influence of triglyceride and low-density-lipoprotein target levels on microcirculation: Is there a difference?

Background and aimsThis study aimed to validate the role of high low-density lipoprotein cholesterol [LDL-C] and triglyceride [TG] treatment target levels on the microcirculation in a very high and high cardiovascular risk group. Methods119 patients with high or very high cardiovascular [CV] risk were included. We have registered the main co-morbidities, smoking habits, body mass index [BMI] and the lipid lowering medication. Hematocrit, whole blood viscosity [WBV] and plasma viscosity [PV], red blood cell [RBC] aggregation and deformability and fibrinogen, total cholesterol [TC], high-density lipoprotein cholesterol [HDL-C], LDL-C and TG levels were determined. ResultsThe investigation found significantly higher PV values in patients with non-target LDL-C, associated with higher fibrinogen level. Non-target TG was related to deteriorated microcirculatory parameters, as significantly higher RBC aggregation, lower RBC deformability, and higher WBV and PV. The main microcirculatory benefit in diabetes could be gained from target level of TG, in chronic coronary syndrome [CCS] patients it is more advantageous to reach both LDL-C and TG target. ConclusionThe results could highlight, that TG should play a role in failing microcirculation and cause potentially life-threatening complications, which would worsen the survival and quality of life of high or very high risk CV patients.

Effect of low fibrinogen level on in-hospital mortality and 6-month functional outcome of TBI patients, a single center experience.

In patients affected by traumatic brain injury (TBI), hypofibrinogenemia within the initial hours of trauma can be expected due to vascular and inflammatory changes. In this study, we aimed to evaluate the effect of hypofibrinogenemia on the in-hospital mortality and 6-month functional outcomes of TBI patients, admitted to Rajaee Hospital, a referral trauma center in Shiraz, Iran. This study included all TBI patients admitted to our center who had no prior history of coagulopathy or any systemic disease, were alive on arrival, and had not received any blood product before admission. On admission, hospitalization, imaging, and 6-month follow-up information of included patients were extracted from the TBI registry database. The baseline characteristics of patients with fibrinogen levels of less than 150mg/dL were compared with the cases with higher levels. To assess the effect of low fibrinogen levels on in-hospital mortality, a uni- and multivariate was conducted between those who died in hospital and survivors. Based on the 6-month GOSE score of patients, those with GOSE < 4 (unfavorable outcome) were compared with those with a favorable outcome. A total of 3049 patients (84.3% male, 15.7% female), with a mean age of 39.25 ± 18.87, met the eligibility criteria of this study. 494 patients had fibrinogen levels < 150mg/dl, who were mostly younger and had lower average GCS scores in comparison to cases with higher fibrinogen levels. By comparison of the patients who died during hospitalization and survivors, it was shown that fibrinogen < 150mg/dl is among the prognostic factors for in-hospital mortality (OR:1.75, CI: 1.32:2.34, P-value < 0.001), while the comparison between patients with the favorable and unfavorable functional outcome at 6-month follow-up, was not in favor of prognostic effect of low fibrinogen level (OR: 0.80, CI: 0.58: 1.11, P-value: 0.19). Hypofibrinogenemia is associated with in-hospital mortality of TBI patients, along with known factors such as higher age and lower initial GCS score. However, it is not among the prognostic factors of midterm functional outcome.

Prediction of Survival in the Elderly Patients with Glioblastoma using Cumulative Inflammatory Markers Score

Abstract Objectives This retrospective study aimed to explore the prognostic effect of cumulative score based on neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), and fibrinogen in older adults diagnosed with glioblastoma (GBM). Design Retrospective study. Setting Huashan Hospital. Participants Patients aged over 60 years and diagnosed with GBM between 2010 and 2017. Main Outcome Measures Results of preoperative routine biochemistry and coagulation blood examinations were reviewed from medical records. Overall survival (OS) was considered a period from first resection surgery until death. Progression-free survival (PFS) was considered a period from initial operation until the date of tumor progression demonstrated in brain magnetic resonance imaging or death from any cause. If no event occurred, the last follow-up appointment was the end of the observation for OS or PFS. The Kaplan–Meier method was used to evaluate survival curves, and prognostic factors were analyzed by the Cox proportional hazards model. Results A total of 289 patients were included. Patients with higher levels of fibrinogen, NLR, and PLR had significantly shorter median OS (p = 0.001, p = 0.016, and p = 0.002, respectively) and PFS (p = 0.004, p = 0.022, and p = 0.009, respectively) compared with those with lower levels. Multivariate analyses showed a significant association between higher F-NLR-PLR score and reduced OS (adjusted hazard ratios [aHRs]: 1.356, 95% confidence interval [CI] 1.009–1.822 for scores 1–2 compared with 0; 5.974, 95% CI 2.811–12.698 for score 3 compared with 0). Similarly, a significant association between higher F-NLR-PLR score and reduced PFS was observed (aHR: 1.428, 95% CI 1.066–1.912 for scores 1–2 compared with 0; aHR: 2.860, 95% CI 1.315–6.223 for score 3 compared with 0). Conclusion Higher F-NLR-PLR score is associated with reduced OS and PFS in older adults with GBM, which helps identify patients at high risk and guide the individualized treatment in clinical practice.

Coagulation assessment of severe acute respiratory syndrome coronavirus 2 (SARS-CoV2) infected pregnant women and their offspring by using rotational thromboelastometry (ROTEM).

During pregnancy, severe acute respiratory syndrome coronavirus 2 (SARS-CoV2) infection may intensify the gestational procoagulant state. Coronavirus disease 2019 (COVID-19) associated coagulopathy (CAC) constitutes an exacerbated immunothrombosis response. There islimited data regarding the coagulation profile of SARS-CoV2-infected pregnant women, especially those with CAC, and the effect on their offspring. This prospective study aimed to compare the hemostatic profile of those women and their neonates with healthy mother-neonate pairs. Conventional coagulation tests (CCTs) and rotational thromboelastometry (ROTEM) were employed to evaluate the hemostatic profiles. Neonates were assessed at birth and on the fourth day of life. We enrolled 46 SARS-CoV2-infected pregnant women and 22 healthy controls who gave birth to 47 and 22 neonates, respectively. CAC was present in 10 participants. SARS-CoV2-infected pregnant women manifested slightly prolonged APTT and higher fibrinogen levels. Regarding ROTEM, we noted decreased FIBTEM CFT, with higher A10, A-angle, and MCF. The CAC group presented lower platelet count, increased fibrinogen levels, and higher FIBTEM A10 and MCF. PT was slightly prolonged at birth in neonates bornto SARS-CoV2-infected mothers. During the fourth day of life, D-dimers were significantly increased. Concerning ROTEM, neonates born to SARS-CoV2-infected mothers showed lower FIBTEM CT at birth. SARS-CoV2-infected pregnant women present a hypercoagulable profile. Hypercoagulability with elevated fibrinolysis and lower platelet count is observed in participants with CAC. The coagulation profile of neonates born to SARS-CoV2 mothers seems unaffected. Elevated D-dimers on the fourth day may reflect a neonatal inflammatory response to maternal SARS-CoV2.

COVID-19: Not a thrombotic disease but a thromboinflammatory disease.

While Coronavirus Disease in 2019 (COVID-19) may no longer be classified as a global public health emergency, it still poses a significant risk at least due to its association with thrombotic events. This study aims to reaffirm our previous hypothesis that COVID-19 is fundamentally a thrombotic disease. To accomplish this, we have undertaken an extensive literature review focused on assessing the comprehensive impact of COVID-19 on the entire hemostatic system. Our analysis revealed that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection significantly enhances the initiation of thrombin generation. However, it is noteworthy that the thrombin generation may be modulated by specific anticoagulants present in patients' plasma. Consequently, higher levels of fibrinogen appear to play a more pivotal role in promoting coagulation in COVID-19, as opposed to thrombin generation. Furthermore, the viral infection can stimulate platelet activation either through widespread dissemination from the lungs to other organs or localized effects on platelets themselves. An imbalance between Von Willebrand Factor (VWF) and ADAMTS-13 also contributes to an exaggerated platelet response in this disease, in addition to elevated D-dimer levels, coupled with a significant increase in fibrin viscoelasticity. This paradoxical phenotype has been identified as 'fibrinolysis shutdown'. To clarify the pathogenesis underlying these hemostatic disorders in COVID-19, we also examined published data, tracing the reaction process of relevant proteins and cells, from ACE2-dependent viral invasion, through induced tissue inflammation, endothelial injury, and innate immune responses, to occurrence of thrombotic events. We therefrom understand that COVID-19 should no longer be viewed as a thrombotic disease solely based on abnormalities in fibrin clot formation and proteolysis. Instead, it should be regarded as a thromboinflammatory disorder, incorporating both classical elements of cellular inflammation and their intricate interactions with the specific coagulopathy.

COVID-19 HASTALARINDA PSİKİYATRİK BELİRTİLER VE BU BELİRTİLERLE İLİŞKİLİ FAKTÖRLER: PERİFERİK İNFLAMASYON BELİRTEÇLERİ BUNLARDAN BİRİ OLABİLİR Mİ ?

OBJECTIVE: In addition to respiratory symptoms, there have been reports of increased psychiatric symptoms in COVID-19 patients. In this study, it is aimed to reveal the psychiatric symptoms seen in COVID-19 patients. We also investigated the relationship between these psychiatric symptoms and peripheral inflammatory markers. MATERIAL AND METHODS: The patients were evaluated with "Interview Forms" specially created by the researchers for the study. DSM-V Acute Stress Disorder Scale (ASDS); Perceived Stress Scale-10 (PSS-10); State-Trait Anxiety Inventory (STAI-T/S); and finally Hospital Anxiety and Depression Scale (HADS) were used to determine patients' acute and perceived stress levels, depression and anxiety symptoms, state and generalized anxiety levels, and how these psychiatric symptoms were affected by different social conditions. D-dimer, fibrinogen, lymphocytes, CRP (C-reactive protein) and ferritin levels were taken into account as inflammatory markers. RESULTS: Our study included 108 inpatients and 31 outpatients with COVID-19. The ASDS, STAI State Scale, and HADS depression scale scores of inpatients patients were found to be higher compared to outpatient patients. Increased fibrinogen levels in blood tests were found to predict higher acute stress disorder scores. HAD-Depression subscale and fibrinogen levels were also found to be positively correlated with each other. CONCLUSIONS: Stress, depression and anxiety symptoms accompany COVID-19. In addition, high fibrinogen levels may be associated with psychiatric symptoms. Psychiatric symptoms are indirectly affected by physical illnesses. We can say that a pandemic that causes fear and anxiety all over the world may suppress the immune system in individuals and the suppressed immune system may indirectly make the infection more complicated.