Fibrinogen-to-Albumin Ratio in Neonatal Sepsis.

Background: Previous studies have established an association between fibrinogen-to-albumin ratio (FAR) and cancer, cardiovascular disease, and coronavirus disease 2019. However, no studies have investigated the relationship between FAR and neonatal sepsis. This study aims to evaluate the association of fibrinogen-to-albumin ratio with the presence and severity of sepsis in neonates. Methods: A total of 1292 neonates with suspected sepsis were enrolled in this study. Clinical and laboratory data were collected from electronic medical records. Neonates with final diagnosis with sepsis were divided into the sepsis group, The remaining neonates were divided into the control group. Neonates with sepsis were further categorized into mild (n = 312) and severe (n = 425) groups based on the severity of their condition. FAR was determined by dividing the plasma fibrinogen concentration (g/L) by the serum albumin concentration (g/L). The statistical analyses were conducted using the SPSS 26.0 statistical software package, as deemed appropriate. Results: FAR levels were significantly higher in neonates with sepsis compared to the control group. Additionally, a significant gradual increase in FAR was observed in the control, mild sepsis, and severe sepsis groups (P < 0.001). Correlation analysis showed that FAR had a positive correlation with PCT, CRP, and the length of hospital stay. Multiple logistic regression analysis showed that FAR was independently associated with the presence and severity of neonatal sepsis. Specifically, FAR was identified as an independent risk factor for both the presence of sepsis (OR = 8.641, 95% CI 5.708-13.080, P < 0.001) and severe sepsis (OR = 2.817, 95% CI 1.701-4.666, P < 0.001). Conclusion: FAR is significantly increased in neonates with sepsis and had a correlation with the severity of sepsis. Increased FAR was an independent predictor for the presence and severity of neonatal sepsis.

Clinical value of procalcitonin-to-albumin ratio for identifying sepsis in neonates with pneumonia.

BACKGROUND: It is possible that neonates with pneumonia also have unrecognized sepsis. Identifying sepsis in neonates with pneumonia may cause some trouble for clinicians. This study aimed to evaluate the clinical value of the procalcitonin-to-albumin ratio (PAR) in identifying sepsis in neonates with pneumonia. METHODS: We retrospectively included 912 neonates with pneumonia from January 2016 to July 2021. Clinical and laboratory data were collected from electronic medical records. Among neonates with pneumonia, 561 neonates were diagnosed with sepsis, according to the International Pediatric Sepsis Consensus. Neonates were divided into a sepsis group and a pneumonia group. A multivariate logistic regression analysis was used to evaluate whether PAR was a potential independent indicator for identifying sepsis in neonates with pneumonia. Receiver operating characteristic (ROC) curve analysis was performed to evaluate the diagnostic value of PAR in sepsis. RESULTS: Neonates with sepsis have a higher PAR (p < 0.001). Correlation analysis showed that PAR was positively correlated with the level of C-reactive protein (r = 0.446, p < 0.001). Multiple logistic regression analysis showed that PAR was an independent predictor of the presence of sepsis in neonates with pneumonia. ROC curve analysis revealed that PAR had good power in identifying sepsis in neonates with pneumonia (area under curve (AUC) = 0.72, 95% confidence interval (CI), 0.68-0.75, p < 0.001). CONCLUSION: PAR can be used as a new biomarker to identify sepsis in neonates with pneumonia.

Compared with neonates with pneumonia, neonates with both pneumonia and sepsis had a higher PAR.PAR was a useful biomarker in distinguishing septic neonates from neonates with pneumonia.

Clinical Value of Prognostic Nutritional Index in Prediction of the Presence and Severity of Neonatal Sepsis.

PURPOSE: The prognostic nutritional index (PNI) is a common indicator of nutritional and inflammatory status and is associated with various diseases such as cancer, cardiovascular diseases and infectious diseases. However, to date, no study has concentrated on the role of PNI in assessing and predicting the presence and severity of neonatal sepsis. Therefore, the present study aimed to explore the association of the PNI with the presence and severity of neonatal sepsis. MATERIALS AND METHODS: A total of 1196 neonates with suspected sepsis were enrolled in this study and their complete clinical and laboratory data were collected. PNI was calculated as serum albumin (g/L) + 5 × total lymphocyte count (109/L). Multivariate logistic regression analysis was performed to identify the risk factors for the presence and severity of neonatal sepsis. Receiver operating characteristic (ROC) curve analysis was performed to evaluate the predictive value of PNI. All statistical analyses were performed using the statistical package SPSS 24.0. RESULTS: PNI was lower in neonates with sepsis and decreased significantly with the severity of sepsis. The correlation analysis demonstrated that the PNI was negatively correlated with the levels of the inflammatory marker procalcitonin (PCT) and C-reactive protein (CRP), and the length of hospital stay. Multivariate logistic regression analysis revealed that the PNI was independently and inversely associated with the presence and severity of neonatal sepsis. The area under the ROC curve of the PNI was 0.64 (95% confidence interval (CI): 0.61-0.67, P < 0.001) for severe sepsis and 0.69 (95% CI: 0.60-0.78, P < 0.001) for septic shock. In addition, our data revealed that PNI was also independently correlated with the length of hospital stay. CONCLUSION: PNI is an independent predictor for the presence and severity of neonatal sepsis.

Sex-related differences in the association between plasma fibrinogen and non-calcified or mixed coronary atherosclerotic plaques.

BACKGROUND: Plasma fibrinogen (FIB) has been demonstrated to be a risk factor for cardiovascular disease. Patients with non-calcified plaque (NCP) or mix plaque (MP) have a higher risk of poor outcomes. However, the association between FIB and the presence of NCP or MP (NCP/MP) remains unclear, and if present, whether sex has any impact on this association remains unknown. The aim of this study was to investigate the role of FIB in predicting the presence of NCP/MP and evaluate whether sex has any impact on this association. METHODS: A total of 329 subjects were recruited, and the clinical and laboratory data were collected. Plasma FIB was detected by enzyme-linked immunosorbent assay. According to whether they had coronary atherosclerotic plaques and the characteristics of the most stenotic plaque, we divided them into three groups: no plaque (NP), calcified plaque (CP), and NCP/MP. RESULTS: Patients with NCP/MP had significantly higher FIB level in females, but not in males. Multiple logistic regression analysis showed that FIB was an independent risk factor for the presence of NCP/MP (odds ratio [OR] = 3.677, 95% CI 1.539-8.785, P = 0.003) in females. Receiver operating characteristic (ROC) curve analysis showed that the optimal cut-off value FIB for predicting the presence of NCP/MP was 3.41 g/L (area under curve [AUC] = 0.73, 95% CI 0.63-0.82, P <  0.001) in females. CONCLUSIONS: FIB is independently associated with the presence of NCP/MP in females, but not in males. These results suggest that the potential significance of FIB-lowering regimens in females with NCP/MP.

Protective Role for LPA3 in Cardiac Hypertrophy Induced by Myocardial Infarction but Not by Isoproterenol.

Background: We previously reported that lysophosphatidic acid (LPA) promoted cardiomyocyte hypertrophy in vitro via one of its G protein-coupled receptor subtypes, LPA3. In this study, we examined the role of LPA3 in cardiac hypertrophy induced by isoproterenol (ISO) and myocardial infarction. Methods:In vitro, neonatal rat cardiomyocytes (NRCMs) were subjected to LPA3 knocked-down, or pretreated with a ß-adrenergic receptor (ß-AR) antagonist (propranolol) before LPA/ISO treatment. Cardiomyocyte size and hypertrophic gene (ANP, BNP) mRNA levels were determined. In vivo, [Formula: see text] and wild-type mice were implanted subcutaneously with an osmotic mini-pump containing ISO or vehicle for 2 weeks; echocardiography was performed to determine the heart weight/body weight ratio, cardiomyocyte cross-sectional area, and level of ANP mRNA expression. [Formula: see text] and wild-type mice were subjected to permanent coronary artery ligation or sham surgery for 4 weeks; cardiac function, including the degree of hypertrophy and infarction size, was determined. Results:In vitro, we found that knocked-down LPA3 in NRCMs did not attenuate ISO-induced hypertrophy, and propranolol was unable to abolish LPA-induced hypertrophy. In vivo, chronic ISO infusion caused cardiac hypertrophy in wild-type mice, while hypertrophic responses to ISO infusion were not attenuated in [Formula: see text] mice. However, in a myocardial infarction (MI) model, [Formula: see text] mice exhibited reduced cardiac hypertrophy compared to wild-type mice at 4 weeks post-MI, which was associated with reduced cardiac function and increased infarct size. Conclusions: Our data show that LPA3 appears to play a protective role in myocardial hypertrophy post-MI, but does not appear to be involved in the hypertrophy that occurs in response to ß-AR stimulation in vivo and in vitro. These results implicate LPA-LPA3 lipid signaling in cardiac hypertrophy occurring after pathological insults like MI, which presents a new variable in ß-AR-independent hypertrophy. Thus, modulation of LPA3 signaling might represent a new strategy for preventing the stressed myocardium from ischemia injury.