Clinical biochemistry最新文献

Background

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.

Methods

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.

Results

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.

Conclusions

These findings suggest that blood redox balance is disrupted in AD.

Objectives

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.

Methods

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.

Results

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.

Conclusions

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.

Introduction

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.

Methods

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.

Results

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.

Conclusions

CA-125 correlates with early LV remodeling and LVEF deterioration in ACS patients.

Background

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.

Methods

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.

Results

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).

Conclusion

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.

Objectives and aim

This study aimed to identify precise biomarkers and develop targeted therapeutic strategies for preventing premature atherosclerotic cardiovascular disease in patients with familial hypercholesterolemia (FH) by investigating the quantitative and qualitative abnormalities in the metabolic network of lipids in these patients using an advanced lipidomics platform.

Design & Methods

The study population comprised 18 homozygous (HoFH), 18 heterozygous (HeFH) FH patients, and 20 healthy controls. Cholesterol oxidation products (oxysterol, COPs) and main lipid classes were determined using gas chromatography–mass spectrometry. Results were expressed as percentages of total fat matter for lipid classes and percentages of total COPs for oxysterols. The principal component analysis (PCA) was also carried out, to highlight the correlation between studied parameters and groups investigated.

Results

Patients (both HoFH and HeFH) showed lower content of free fatty acids (FFAs) and greater values of triacylglycerols (TAGs) in comparison to controls. HoFH showed lower monoacylglycerols (P<0.01) and higher free cholesterol (FC) (P<0.05) when compared to HeFH and controls. The total content of COPs ranged from 1.96 to 4.25 mg/dL, from 2.27 to 4.05 mg/dL, and from 0.79 to 4.12 mg/dL in healthy controls, HoFH and HeFH groups, respectively, with no significant differences between patients and controls. In general, the 7α-hydroxycholesterol (7α-HC) was greater than other COPs. However, no significant differences were found between the three studied groups. Moreover, an opposite trend was observed between 7α-HC and 7-ketocholesterol (7-KC). Additionally, when PCA was carried out, the first two PCs explained 92.13 % of the total variance, of which the PC1 describes 53.94 % of variance mainly correlated to TAGs, diacylglycerols (DAGs), and 7-KC. On the other hand, the PC2 was correlated primarily for FFAs, FC and esterified sterols (E-STE).

Conclusions

In conclusion, abnormal levels of TAGs, DAGs and 7-KC were associated with HeFH while HoFH was associated with the abnormal amount of E-STE.

Introduction

Identifying controllable risk factors for large-artery atherosclerosis (LAA) stroke is crucial due to its significant role as a leading cause of ischemic stroke. We aimed to validate the correlation of serum vitamin B₁₂ with LAA stroke.

Methods

Inpatients with LAA stroke and healthy controls were retrospectively collected for a case-control study from January 2020 to May 2022. Serum vitamin B₁₂ concentration and other blood indicators, demographic, lifestyle factors and comorbidities were investigated. Logistic regression analysis was used to identify the correlation of serum vitamin B₁₂ concentrations with LAA stroke, meanwhile adjusted for confounding factors.

Results

Patients with LAA stroke had significantly lower serum vitamin B₁₂ concentrations in comparison to those of controls. In the fully adjusted model, vitamin B₁₂ (per 1 interquartile range increase, odds ratio [OR] = 0.84, 95 % confidence interval [CI]: 0.77–0.91), vitamin B₁₂ < 200 pg/mL (OR=7.70, 95 %CI: 2.19–27.03) and vitamin B₁₂ < 300 pg/mL (OR=4.19, 95 %CI: 1.82–9.66) were independently factors for LAA stroke. Furthermore, the optimal cut-off values for vitamin B₁₂ to predict LAA stroke were 305.25 pg/mL (area under the curve [AUC] = 0.71) when unadjusted and 308.25 pg/mL when adjusted for age and sex (AUC=0.68). Lower vitamin B₁₂ concentrations were significantly associated with male sex, smoking, older age, higher neutrophil count, higher creatinine, lower folate and higher total homocysteine.

Conclusion

Results indicate that low concentration of serum vitamin B₁₂ may be a strong predictor for the risk of LAA stroke.

Exocrine pancreatic insufficiency (EPI) is a condition caused by a deficiency of exocrine pancreatic enzymes, resulting in malabsorption of nutrients. Clinical manifestations of EPI may include steatorrhea, weight loss, diarrhea, and abdominal pain. Although direct testing is the most sensitive and specific for EPI, these tests are invasive, time consuming, expensive, and not well standardized. Fecal elastase (FE-1) has been shown to be an indirect marker of the exocrine secretory capacity of the pancreas and has become the most commonly employed indirect test for diagnosis of EPI. Measurement of fecal elastase consists of two main phases, a preanalytical phase and analytical phase. The preanalytical phase involves stool collection, storage and handling. The second phase is the analytical phase, which includes the actual assay processes and products used to produce a result. For FE-1 this includes sample extraction and measurement on an immunoassay. Each step in the process can influence the result and contribute to heterogeneity in FE-1 measurement, potentially impacting clinical diagnosis and management. Thus, this paper provides an overview of the preanalytical and analytical factors that can affect measurement and interpretation of FE-1 results.

Aim

In various experimental animal studies, it has been proven that solanine, a subtype of glycoalkaloids, is responsible for neural tube defects. However, there have not been any human studies yet in this area. Our aim is to investigate whether there are any connections between blood glycoalkaloid levels and anencephaly in humans.

Methods

Blood and amniotic fluid samples were taken from patients diagnosed with fetal anencephaly during pregnancy. The samples from patients with normal pregnancies were taken as well and was compared to the patients with fetal anencephaly during pregnancy. We searched the levels of three glycoalkaloids: solanine, chaconine and solamargine in the collected samples.

Results

Solanine, which is one of the glycoalkaloids, could not be detected in both serum and amniotic fluid in the anencephaly as well as the control groups. However, alpha-solamargine levels were observed to be significantly higher in the blood and amniotic fluid samples of the control group than in the study group (p = 0.04). Alpha-chaconine levels were also significantly higher in the control group (p < 0.001) as well.

Conclusion

Based on our tests, we can conclude that no connections were found between blood solanine levels and anencephaly during pregnancy. Alpha-chaconine and alpha-solamargine levels were observed to be higher in blood and amniotic fluid in pregnancies without anencephaly. The relationship between glycoalkaloids and congenital anomalies needs to be further investigated in tissues other than blood.

Introduction

Serum is the International Federation of Clinical Chemistry (IFCC)-recommended matrix for the measurement of lactate dehydrogenase (LD); however, many laboratories opt for lithium heparin plasma to achieve quicker turnaround times and minimize tube usage.

When introducing the new Sigma-Strong IFCC-recommended LDH2 assay from Abbott Laboratories on lithium-heparin collected samples, we observed a rise in the patient median LD activity as well as several samples exhibiting falsely elevated values.

Materials and methods

120 + serum and plasma samples from consenting patients were collected and evaluated for complete blood count and lactate dehydrogenase using two different assays. Aggregated patient results before and after introduction of the LDH2 assay were compared.

Results

Mean LD was 14% higher in plasma than in serum when using the LDH2 assay but only 5% higher when using the previous LDH legacy assay from Abbott Laboratories. Similarly, platelets and leukocytes were 10–30 times higher in plasma than in serum. Aggregated lactate dehydrogenase patient results demonstrated a dramatic increase in patient median following introduction of the LDH2 assay. Various experiments were tried to reduce cellular interference, but the only viable solution we found, apart from reverting to the LDH legacy assay, was to utilize serum tubes.

Conclusion

We conclude that lithium-heparin plasma leads to falsely elevated lactate dehydrogenase activity when using the LDH2 assay. These errors can be prevented by using serum collected in gel separator tubes.