Pseudomyxoma peritonei (PMP) is a rare malignancy that lacks a highly sensitive and specific biomarker for its diagnosis. Identifying reliable serum markers is crucial for improving the diagnostic accuracy and management of PMP. This study aims to explore the diagnostic value of serum growth differentiation factor 15 (GDF-15) in patients with PMP.
We carried on a 1:1 matched case-control study. 44 patients with PMP hospitalized in Aerospace Center Hospital were recruited as cases, and 44 sex- and age-matched apparently healthy participants were selected as controls. The serum GDF-15 concentrations were tested using an ELISA method. The diagnostic value of GDF-15 in PMP patients was assessed by receiver operating characteristic (ROC) curve analysis.
The median serum GDF-15 level in PMP patients was 1192.77 (843.03–1879.06) pg/mL, notably higher than that in healthy controls [533.27 (410.46–641.47) pg/mL] (P<0.001). The area under the curve (AUC) of serum GDF-15 for PMP diagnosis was 0.907, the optimal diagnostic threshold value was 644.58 pg/mL, the sensitivity was 93.18 %, and the specificity was 77.27 %. The AUC of GDF-15 combined with carbohydrate antigen 125 (CA125) was larger than that of GDF-15 alone (P=0.027), and the sensitivity and specificity achieved 86.36 % and 95.45 %. GDF-15 levels showed a significant correlation with age (P=0.042), with younger PMP patients exhibiting notably lower concentrations of GDF-15 compared to older patients.
Serum GDF-15 could become a new marker for the PMP diagnosis. The combination of GDF-15 and CA125 demonstrated superior diagnostic performance for PMP compared to GDF-15 alone, achieving a sensitivity of 86.36% and a specificity of 95.45%.
Increased albuminuria is associated with elevated mortality. Urine albumin (U-ALB) above 20 mg/L or albumin-to-creatinine ratio (U-ACR) of 3 g/mol are indicative of moderately increased albuminuria. Due to limited standardization among U-ALB methods, diagnosis of increased albuminuria might prove difficult.
Data from Equalis’s external quality assessment scheme for low U-ALB levels during 2005–2023 were categorized according to manufacturer and divided into central laboratory (CLAB) and point-of-care testing (POCT) methods. Manufacturer median values were compared to total group mean consensus values and manufacturer CV% was compared at different U-ALB levels.
CLAB was generally closer to consensus values and had lower CV% than POCT at U-ALB levels around 20 mg/L. For CLAB, Roche methods were approximately equal to consensus U-ALB, Abbott 4 % above, and Siemens 5 % below. For POCT, HemoCue was 1 % below, Siemens 7 % above, and Abbott 8 % below. For U-Creatinine, all manufacturers generally had a good agreement differing on average by 1–4 % from consensus.
Although U-ALB methods generally meet The National Kidney Disease Education Program (NKDEP) recommendations of method bias less than 13 % and imprecision less than 30 %, differences among manufacturers have increased over the last years, with 2023 showing the largest differences between methods. This highlights the need for guidelines for albuminuria and ACR to take method differences into consideration, but also for implementation of suitable urine reference materials.
Alzheimer’s disease (AD) is a steadily advancing neurodegenerative condition, the occurrence and prevalence of which are on the rise in various populations. Suspected factors contributing to its development encompass the buildup of amyloid β (Aβ) plaques, the formation of neurofibrillary tangles induced by tau proteins, and heightened oxidative stress. In this study, we aimed to evaluate intra-cellular glutathione status and extracellular thiol-disulphide status in patients with AD.
Adult patients (>60 years old) diagnosed with AD based on DSM-IV diagnostic criteria were included in the study. Patients were divided into 3 groups as mild, moderate and severe according to Mini Mental Status Examination (MMSE) and clinical findings. Extracellular thiol-disulfide and intracellular oxidized-reduced glutathione status parameters for patient and control groups were analyzed before and after reduction procedures by using reaction of thiol groups with DTNB.
The reduced forms of both balances (native thiol (NT) and reduced glutathione (GSH)) were significantly lower in the patient group than the control group (p = 0.031 and <0.001, respectively), while oxidized forms (disulphide (SS) and oxidized glutathione (GSSG)) and SS/NT and GSSG/GSH percent ratios were significantly higher (p < 0.05 for all). The disease duration and oxidative stress were significantly higher in the severe group of AD. There was a shift in intracellular and extracellular thiol balances towards the oxidized side, along with correlations between MMSE and these balances (rho = −0.412 for SS/NT and rho = −0.488 for GSSG/GSH), with GSSG/GSH identified as a significant predictive factor (odds ratio (95 % confidence interval): 1.352 (1.136–1.610) for the moderate group and 1.829 (1.451–2.305) for the severe group.
These findings suggest that blood redox balance is disrupted in AD.
The objective of this study was to determine the in vivo correlation of ionized magnesium (iMg) with ionized calcium (iCa), total calcium, albumin and pH. In addition, the analytical interference of iCa on iMg measurement on the Stat Profile Prime Plus (Nova Biomedical) and vice versa was defined.
In vivo correlation of iCa, iMg and pH was studied in 238 paired blood gas samples of 109 different patients admitted to the intensive care unit. Albumin and total magnesium (tMg) were measured in heparinized plasma samples. Measurement of iMg was performed with the ion selective magnesium electrode (ISE) of the Stat Profile Prime Plus (Nova Biomedical) and iCa and pH were measured with a Rapid Point 500 blood gas analyzer (Siemens). Albumin, total calcium and total magnesium were analyzed with a Siemens Atellica CH. Analytical interference of iCa with iMg and vice versa was investigated using unbuffered saline solutions.
In the studied patient population, no significant correlations were observed between iMg and iCa, albumin, and pH. An inverse relationship was observed between iCa and Mg-ISE. For every 0.1 mmol/L change in iCa concentration, the iMg concentration deviated by 0.01 mmol/L at an iMg concentration of 0.5 mmol/L and by 0.013 mmol/L at an iMg concentration of 1.0 mmol/L. The measurement of iCa was not affected by iMg.
In vivo, no correlation was observed between iMg with iCa, albumin and pH. Interference of iCa on iMg measurement was noted, with a maximum deviation of ±0.02 mmol/L iMg across the reference range of iCa (1.15–1.32 mmol/L). Additionally, the iCa measurement was not affected by the iMg concentration.
Several biomarkers are characteristically elevated in patients with acute heart failure (AHF). Our hypothesis was they could predict early changes in left ventricular (LV) characteristics in acute coronary syndrome (ACS) patients. The objective of this study was two-fold: a) compare circulating concentrations of NT-pro BNP, CA-125, ST2, galectin-3 and pro-adrenomedullin among 4 groups of individuals (healthy controls; patients with ACS without AHF; patients with ACS and AHF and patients admitted for AHF); and b) evaluate whether these biomarkers predict adverse LV remodeling and ejection fraction changes in ACS.
6 biomarkers (NT-pro BNP, CA-125, ST2, galectin-3, pro-adrenomedullin and C-reactive) were measured within the first 48 h of admission. Echocardiograms were performed during admission and at 3 months. Variables associated with LV end-diastolic volume (EDV) and ejection fraction (LVEF) change were assessed by multivariate linear regression.
We analyzed 51 patients with ACS, 16 with AHF and, 20 healthy controls. NT-pro BNP and ST2 concentrations were elevated at similar values in patients admitted for AHF and ACS complicated with HF but CA-125 concentrations were higher in AHF patients. NT-pro BNP concentrations were positively correlated with CA-125 (rho = 0.58; p < 0.001), ST2 (rho = 0.58; p < 0.001) and galectin-3 (rho = 0.37; p < 0.001)
Median change (median days was 83 days after) in EDV and LVEF was 5 %. CA-125 concentrations were positively associated to LV EDV change (β-coefficient 1.56) and negatively with LVEF trend (β-coefficient = −0.86). No other biomarker predicted changes in EDV or LVEF.
CA-125 correlates with early LV remodeling and LVEF deterioration in ACS patients.
The serum lactate level has been confirmed to be an independent risk factor for the occurrence of acute kidney injury (AKI) in many diseases. However, the correlation between serum lactate level and AKI in critical patients with acute ischemic stroke (AIS) has not been clear. Moreover, limited studies have examined the mediating effect of serum glucose on the association between serum lactate and AKI.
We identified 1,435 AIS patients from the Medical Information Mart for Intensive Care (MIMIC-III) database and divided them into AKI or No-AKI groups. We used a propensity score matching method to reduce confounding factors. Linear regression, logistic regression, and restricted cubic splines (RCS) plots were used to evaluate relationships between serum lactate levels and AKI. Finally, the mediating role of serum glucose on the relationship between serum lactate and AKI was investigated utilizing the mediation analysis.
In the present study, a total of 634 critical patients aged ≥ 18 years with AIS were included after propensity score matching (1:1). We used RCS plotting to reveal a linear association between serum lactate levels and AKI (P for nonlinearity < 0.001). After full adjustment for potential confounders (Model 3), high lactate levels increased the risk of AKI (odds ratio, 2.216; 95 % confidence interval, 1.559–3.271; P-value < 0.001). Serum glucose explained 14.9 % of the association between serum lactate and AKI among critical patients with AIS (P-value < 0.001), 16.4 % among patients with AIS and diabetes mellitus (DM) (P-value = 0.24), and 19.5 % among patients with AIS and without DM (P-value < 0.001).
Serum lactate was independently associated with increased risk-adjusted AKI in critical patients with AIS. The increase in serum glucose may have mediated this effect, especially in patients without DM.