Serum Neuron-specific Enolase Levels Research Articles

Changes of serum NSE, lactate and CRP in patients with postoperative infection after acute craniocerebral injury and their predictive value for prognosis

ABSTRACT To investigate the changes of serum neuron-specific enolase (NSE), lactate and C-reactive protein (CRP) in patients with postoperative infection after acute craniocerebral injury and their predictive value for prognosis. 71 patients with postoperative infection after acute craniocerebral injury were selected as infection group, and 56 patients without postoperative infection were selected as non-infection group. NSE, CRP and blood lactic acid levels were detected in all patients. The relationship between each index and thecondition and prognosis of patients was analyzed. The levels of serum NSE, lactic acid and CRP in infected group were higher than those in non-infection group (P<0.05). The levels of serum NSE, lactic acid and CRP in severe group were higher than those in mild group (P<0.05). Serum levels of NSE, lactic acid and CRP were positively correlated with the severity of infection (P<0.05), the area under the curve (AUC) of the receiver operating characteristic curve (ROC) was greater than that of the NSE level (P<0.05). The levels of serum NSE, lactate and CRP in the good prognosis group were lower than those in the poor prognosis group (P<0.05). The area under the curve (AUC) of receiver operating characteristic curve (ROC) of lactate level in predicting the prognosis of patients with infection was higher than that of NSE and CRP (P<0.05). Serum NSE, lactic acid and CRP have predictive value in patients with acute craniocerebral injury.

Co administration of oxiracetam and monosialotetrahexosylganglioside for the treatment of patients with craniocerebral injury, and their effect on serum S100 proteins and neuron specific enolase

Purpose: To determine the efficacy of oxiracetam plus monosialotetrahexosylganglioside (GM1) in the treatment of craniocerebral injury, and its effect on serum S100 proteins and neuron-specific enolase (NSE).&#x0D; Methods: A total of eighty patients with severe craniocerebral injury admitted to Shengli Oilfield Central Hospital between January 2020 and December 2021 were selected for the study, and assigned 1:1 to control group (GM1 only, 2 mL daily through intravenous drip) and study group (GM1, 2 mL daily through intravenous drip, in combination with oxiracetam, and 4 g dissolved in 100ml of saline daily through intravenous drip). The treatment duration was two months.&#x0D; Results: Baseline patient characteristics were comparable between the two groups (p &gt; 0.05). GM1 plus oxiracetam produced better restoration of cranial functions of patients after craniocerebral injury when compared with GM1 alone, as evidenced by the significantly lower S100 proteins and NSE levels of the study group than the corresponding parameters of the control group after 1, 2, 3, and 7 days of treatment (p &lt; 0.05). More significant mitigation of inflammatory reactions was observed in patients co-administered GM1 and oxiracetam than in those who received GM1 only, as shown by the lower serum concentrations of inflammatory factors {(c-reactive protein (CRP), tumor necrosis factor α (TNF-α), interleukin-6 (IL-6), and neuropeptide Y (NPY)} in the study group as compared with the control group (p &lt; 0.05). A few patients experienced minor adverse reactions such as gastrointestinal discomfort, nausea and vomiting, dizziness and headache, and rash during treatment (p &gt; 0.05).&#x0D; Conclusion: Co-administration of oxiracetam and GM1 is a viable strategy for the treatment of patients with craniocerebral injury, as it significantly lowers the levels of serum S100 proteins and NSE, mitigates inflammatory reactions, and ameliorates cerebral hemodynamics in patients. The combined therapy also has a good safety profile.

Predictive value of soluble CD59 for poor 28-day neurological prognosis and all-cause mortality in patients after cardiopulmonary resuscitation: a prospective observatory study

BackgroundsCD59, as a soluble form of CD59, is observed in multiple types of body fluids and correlated with the cell damage after ischemia/reperfusion injury. This study aims to observe the dynamic changes of serum sCD59 in patients after restoration of spontaneous circulation (ROSC) and explore the association of serum sCD59 with neurological prognosis and all-cause mortality in patients after ROSC.MethodsA total of 68 patients after ROSC were prospectively recruited and divided into survivors (n = 23) and non-survivors (n = 45) groups on the basis of 28-day survival. Twenty healthy volunteers were enrolled as controls. Serum sCD59 and other serum complement components, including sC5b-9, C5a, C3a, C3b, C1q, MBL, Bb, and pro-inflammatory mediators tumor necrosis factor (TNF)-α, interleukin-6 (IL-6), neurological damage biomarkers neuron-specific enolase (NSE) and soluble protein 100β (S100β) were measured by enzyme linked immunosorbent assay on day 1, 3, and 7 after ROSC. Neurologic outcome was assessed using cerebral performance category scores, with poor neurologic outcome defined as 3–5 points.ResultsIn the first week after ROSC, serum levels of sCD59, sC5b-9, C5a, C3a, C3b, C1q, MBL, Bb, TNF-α, IL-6, NSE and S100β were significantly elevated in patients after ROSC compared to healthy volunteers, with a significant elevation in the non-survivors compared to survivors except serum C1q and MBL. Serum sCD59 levels were positively correlated with serum sC5b-9, TNF-α, IL-6, NSE, S100β, SOFA score and APACHE II score. Moreover, serum sCD59 on day 1, 3, and 7 after ROSC could be used for predicting poor 28-day neurological prognosis and all-cause mortality. Serum sCD59 on day 3 had highest AUCs for predicting poor 28-day neurological prognosis [0.862 (95% CI 0.678–0.960)] and 28-day all-cause mortality [0.891 (95% CI 0.769–0.962)]. In multivariate logistic regression analysis, the serum level of sCD59D1 was independently associated with poor 28-day neurological prognosis and all-cause mortality.ConclusionsThe elevated serum level of sCD59 was positively correlated with disease severity after ROSC. Moreover, serum sCD59 could have good predictive values for the poor 28-day neurological prognosis and all-cause mortality in patients after ROSC.

Brain damage serum biomarkers induced by COVID-19 in patients from northeast Brazil.

Neurological symptoms have been often reported in COVID-19 disease. In the present study, we evaluated brain damage associated with the increase of serum levels of neurological biomarkers S100B and neuron-specific enolase (NSE) induced by SARS-CoV-2 infection, in a population from Northeastern Brazil. Thirty-six healthy control (G1) individuals and 141 patients with confirmed COVID-19 were enrolled in this study. Positive-COVID-19 patients were divided into two groups according to the severity of illness by the National Institute of Health (NIH) criteria, 76 patients with mild symptoms for COVID-19 and (G2) and 65 with acute respiratory conditions requiring supplemental oxygenation via intensive care unit (ICU) admission (G3). A follow-up study was conducted with 23 patients from G2 14 (D14) and 21 (D21) days after the onset of symptoms. Serum levels of NSE and S100B were measured using the enzyme-linked immunoassay method (ELISA). Results revealed a significant positive association between G3 patients and S100B serum expression (p = 0.0403). The serum levels of NSE were also significantly enhanced in the G3 group compared to the control (p < 0.0001) and G2 group (p < 0.0001). In addition, clinical features such as symptoms and oxygenation status were not correlated with NSE or S100B serum expression. The follow-up study demonstrated a decrease over time (21days) in NSE serum expression (p < 0.0001). These results suggest that brain damage is followed by acute virus exposure, with no long-term effects. Future work examining COVID-19 recovery will shed light on chronic neurological damage of SARS-CoV-2 infection.

Evaluation of Serum Biomarkers and Electroencephalogram to Determine Survival Outcomes in Pediatric Post-Cardiac-Arrest Patients

Cardiac arrest causes primary and secondary brain injuries. We evaluated the association between neuron-specific enolase (NSE), serum S-100B (S100B), electroencephalogram (EEG) patterns, and post-cardiac arrest outcomes in pediatric patients. A prospective observational study was conducted in the pediatric intensive care unit and included 41 post-cardiac arrest patients who underwent EEG and serum sampling for NSE and S100B. The participants were aged 1 month to 18 years who experienced cardiac arrest and underwent CPR after a sustained return of spontaneous circulation for ≥48 h. Approximately 19.5% (n = 8) of patients survived until ICU discharge. Convulsions and sepsis were significantly associated with higher mortality (relative risk: 1.33 [95% CI = 1.09-1.6] and 1.99 [95% CI = 0.8-4.7], respectively). Serum NSE and S100B levels were not statistically associated with the outcome (p = 0.278 and 0.693, respectively). NSE levels were positively correlated with the duration of CPR. EEG patterns were significantly associated with the outcome (p = 0.01). Non-epileptogenic EEG activity was associated with the highest survival rate. Post-cardiac arrest syndrome is a serious condition with a high mortality rate. Management of sepsis and convulsions affects prognosis. We believe that NSE and S100B may have no benefit in survival evaluation. EEG can be considered for post-cardiac arrest patients.

Expression changes and clinical significance of serum neuron-specific enolase and squamous cell carcinoma antigen in lung cancer patients after radiotherapy

To explore the changes and clinical significance of serum Neuron-Specific Enolase (NSE) and Squamous Cell Carcinoma antigen (SCC) in patients with lung cancer before and after radiotherapy. 82patients with lung cancer were treated with radiotherapy, and effective clinical intervention was given during the radiotherapy process. The patients were followed up for1year after radiotherapy and were divided into a recurrence and metastasis group (n=28) and a non-recurrence and metastasis group (n=54) according to their prognosis. Another54healthy volunteers examined in the present study's hospital during the same period were selected as the control group. To compare the changes of NSE and SCC levels in serum in patients with lung cancer at admission and after radiotherapy, and to explore their clinical significance. After intervention, NSE and SCC levels in the serum of the two groups of patients were significantly lower than those before intervention, and the levels of CD4+ and CD4+/CD8+ were significantly higher than those before intervention (p<0.05); the level of CD8+ was not significantly different from that before intervention (p > 0.05). And NSE and SCC levels in the intervention group were significantly lower than those in the routine group, the levels of CD4+, CD4+/CD8+ were significantly higher than those in the routine group (p<0.05). NSE and SCC in serum can preliminarily evaluate the effect of radiotherapy in patients with lung cancer and have a certain predictive effect on prognosis.

Serum brain damage biomarkers as a diagnostic and prognostic tool in ischemic stroke

To study serum quantities of neuron specific enolase (NSE), glial fibrillary acidic protein (GFAP) and NR2-antibodies (NR2-ab) in various cerebrovascular pathology and assess their value as a panel used as a diagnostic and predictive tool for stroke. NSE, GFAP and NR2-ab serum levels were measured twice for 84 patients with ischemic stroke (IS) and 8 patients with hemorrhagic stroke (HI), once for 8 patients with transient ischemic attack (TIA), 26 patients with chronic brain ischemia (CBI), 27 healthy volunteers (HV). NSE and GFAP levels were significantly higher in IS than in CBI and HV patients, and NR2-ab levels in IS were higher than in TIA and lower than in HV. In patients with more pronounced neurological deficiency and less favorable functional outcome by day 10-14 of IS, the levels of NSE, GFAP and NR2-ab were higher. Sensitivity and specificity of biomarker panel was higher than with their separate application. The NSE, GFAP and NR2-ab biomarkers have a diagnostic and predictive value for IS.

Effects of auriculotherapy on anxiety and biomarkers in Primary Health Care: a clinical trial.

to assess the effects of auriculotherapy on anxiety and brain-derived neurotrophic factor (BDNF), neuron-specific enolase (NSE) and S100 calcium-binding protein B (S100B) serum levels in adults assisted in Primary Health Care. a pre-experimental pilot clinical trial. Information was obtained from 19 patients using the State-Trait Anxiety Inventory (STAI) and analysis of BDNF, NSE and S100B serum levels. the pre-intervention anxiety score in the IDATE-Trait was 52.11±6.691 (CV 12.84%) and the assessment after auriculotherapy was significantly lower (43.72±8.141; CV 18.62%; P=0.0007). S100B levels were significantly reduced after auriculotherapy (from 64.03±72.18 to 54.03±68.53 pg/mL; CV 126.8%; P=0.0023). auriculotherapy effectively reduced anxiety levels. It proved to be safe and easy to apply, allowing nurses to perform this technique autonomously. A reduction of S100B was also evidenced, demonstrating possible prevention of neuronal damage.

CSF neuron-specific enolase as a biomarker of neurovascular conflict severity in drug-resistant trigeminal neuralgia: a prospective study in patients submitted to microvascular decompression.

Although neurovascular conflict (NVC) is the most widely accepted cause of trigeminal neuralgia (TN), few articles have analyzed molecular and biochemical mechanisms underlying TN. In the present study, we dosed neuron-specific enolase (NSE) on serum and CSF samples of 20 patients submitted to microvascular decompression (MVD) and correlated these findings with the type of NVC. Blood samples were obtained preoperatively and 48 h after MVD. CSF from trigeminal cistern was intraoperatively obtained. NSE levels were measured using the Diasorin kit (LIAISON®NSE). NVC was classified as "contact" or "trigeminal nerve distortion/indentation" or "trigeminal root atrophy" based on MRI and intraoperative findings. Clinical outcome was measured by acute pain relief (APR) and Barrow Neurological Institute (BNI) scale at last available follow-up (FU; 6.40 ± 5.38 months). APR was obtained in all patients. A statistically significant BNI reduction was obtained at latest FU (p < 0.0001). Serum NSE levels significantly decreased following MVD (from 12.15 ± 3.02 ng/mL to 8.95 ± 2.83 ng/mL, p = 0.001). The mean CSF NSE value was 48.94 ng/mL, and the mean CSF/serum NSE rate was 4.18 with a strong correlation between these two variables (p = 0.0008). CSF NSE level in "trigeminal root atrophy" group was significantly higher compared to "contact" (p = 0.0045) and "distortion/indentation" (p = 0.010) groups. NSE levels seem to be related to the etiopathology and severity of NVC. A significant reduction of serum NSE levels could be related to the resolution of the NVC and clinical TN improvement.

Advantages and clinical significance of enhanced CT combined with BRAF V600E gene detection in the diagnosis of papillary thyroid carcinoma

The diagnosis of papillary thyroid carcinoma (PTC) remains the focus of clinical research. Studies have shown that the BRAFV600E gene mutation is closely related to the development of PTC. In this study, we used the advantages and clinical significance of enhanced CT combined with BRAFV600E gene testing in the diagnosis of PTC. A total of 170 PTC patients who received treatment in our hospital between January 2020 and December 2020 were collected and divided into group A (enhanced CT combined with BRAFV600E gene detection) and group B (fine needle aspiration cytology, FNAC) according to different diagnostic methods. We recorded the general information of the patients and measured the levels of serum tumor markers including carcinoembryonic antigen (CEA), cytokeratin fragment 19 (CYFRA21-1), neuron-specific enolase (NSE) and carbohydrate antigen 125 (CA125). After pathological diagnosis, the specificity, sensitivity, accuracy, positive predictive value, and negative predictive value of the two diagnostic methods were contrasted. The accuracy of the two methods and the pathological test in identifying benign lesions, malignant tumors, was also compared. All patients' serum tumor markers CEA, CYFRA21-1, NSE and CA125 levels were above normal. The detection rate of specificity, sensitivity, accuracy, positive predictive value and negative predictive value of enhanced CT combined with BRAF V600E gene detection were superior to those of FNAC. And the accuracy of enhanced CT combined with BRAF V600E gene detection, which was confirmed by corresponding pathological detection results, was significantly increased (P<0.05). Enhanced CT combined with BRAF V600E gene detection can improve the diagnostic accuracy of PTC, and its clinical indicators and safety are superior to FNAC.

The role of neuron-specific enolase (NSE) and S100B protein in the incidence of acute postoperative cognitive dysfunction (POCD) in geriatric patients receiving general anesthesia

Introduction: Postoperative cognitive dysfunction (POCD) following general anesthesia is frequent among geriatric patients worldwide. Neuroinflammation and neuronal injury have been associated with the incidence of POCD. Some biomarkers of brain damage including neuron-specific enolase (NSE) and S100B protein have been widely studied; however, their association with the incidence of POCD is still controversial. This study aimed to assess the correlation of serum NSE and S100B levels with the incidence of POCD among geriatric patients receiving general anesthesia. Methods: A prospective cohort study was conducted among geriatric patients receiving general anesthesia at Dr. Soetomo Hospital, Surabaya from July to October 2022. The Montreal Cognitive Assessment (MoCA) INA instrument was used to assess POCD, and enzyme-linked immunosorbent assay (ELISA) was used to quantify the levels of serum NSE and S100B. Spearman’s rank correlation was implemented to identify the correlation of MoCA INA scores with the levels of NSE and S100B. Mann-Whitney analysis was used to determine the association between NSE and S100B levels with the incidence of POCD. A p-value of ≤0.05 was considered statistically significant. Results: A total of 48 patients were enrolled in the study and 16.7% of them had POCD. Spearman’s correlation test suggested no significant correlation between MoCA INA score with serum NSE level (rs:-0.095; p=0.522) and S100B level (rs:-0.213; p=0.146). Mann-Whitney analysis indicated no significant difference in the NSE and S100B levels of patients with and without POCD (p=0.3470 and p=0.097, respectively). Conclusion: There was no significant association between NSE and S100B levels with the incidence of POCD among geriatric patients receiving general anesthesia during elective surgeries at Dr. Soetomo Hospital, Surabaya.

Are Interictal Discharges Associated with Neuronal Cell Loss in Electrical Status Epilepticus in Sleep?

Neuron-specific enolase is an established biomarker of neuronal damage. This study aimed to reveal the relationship between serum neuron-specific enolase level and continuous interictal discharges in a group of encephalopathy with electrical status epilepticus in sleep patients for the first time and determine whether there is a neuronal cell loss or damage. We analyzed serum neuron-specific enolase levels in patients with an electrical status epilepticus in sleep pattern on their electroencephalographs with age- and sex-matched control subjects. Patients with a spike-wave index of at least 50% and acquired neuropsychological regression were included in the study. Magnetic resonance imaging of all electrical status epilepticus in sleep patients and control subjects included in the study was within normal limits. Neuron-specific enolase is measured by the enzyme-linked immunosorbent assay kit based on the sandwich technique. In this study, 14 patients diagnosed with electrical status epilepticus in sleep and 21 healthy controls were included. The median age of electrical status epilepticus in sleep patients was 7.1 years (min-max: 4.5-10.7 years) and 7.7 years (min-max: 3.2-14 years) in the control subjects. According to the results of serum neuron-specific enolase measurements, the mean ± standard deviation level of neuron-specific enolase was 7.61 ± 3.19 ng/dL for the electrical status epilepticus in sleep group and 6.93 ± 2.55 ng/dL for the control group. Serum neuron-specific enolase levels between electrical status epilepticus in sleep patients and the control group were not statistically significant (P = .749). No significant difference was observed in serum neuron-specific enolase levels between electrical status epilepticus in sleep patients and control subjects. Our results may indicate that frequent interictal discharges do not result in neuronal cell loss or damage in electrical status epilepticus in sleep patients.

Prevention of Dexmedetomidine on Postoperative Delirium and Early Postoperative Cognitive Dysfunction in Elderly Patients Undergoing Thoracoscopic Lobectomy.

Objective To investigate the effect of dexmedetomidine on postoperative cognitive function and delirium in elderly patients undergoing thoracoscopic lobectomy. Methods 109 elderly patients (age is more than 65 years) who underwent thoracoscopic lobectomy in our hospital from June 2020 to Feb 2022 were randomly divided into the dexmedetomidine (DEX) group (n = 54) and the control group (n = 55). The patients in the experimental group were given dexmedetomidine by intravenous pump, intravenous pump 0.5 μg/kg within 10 minutes, and maintained the speed of 0.5 μg/(kg. h) to 30 min before the operation was ended. The control group was given the same amount of normal saline. Delirium assessment-severity (CAM-S) assessment and Mini-Cog were used to assess the severity levels of POD and POCD 24 h before, 6 hours after, one day after the operation, three days after the operation, and 1 week after the operation. Serum TNF-αα and NSE levels were assessed by using enzyme-linked immunosorbent assay. NRS pain marks were assessed in the DEX group at postanesthesia care unit (PACU) and 24 postoperation. Surgical pierhysmographic index (SPI) evaluation was performed at five time points. Results The Mini-Cog scores in the DEX group were markedly enhanced compared with those in the saline group 6 and 24 hours after the operation. The SPI values in the DEX group were markedly reduced within 2 min after intubation and at surgical sutures. Moreover, the CAM scores in the DEX group were markedly reduced 24 hours after the operation. Tumor necrosis factor-α (TNF-α) and neuron-specific enolase (NSE) levels were significantly decreased in the DEX group at T1∼T3. Conclusion The use of dexmedetomidine in the thoracoscopic lobectomy in elderly patients could reduce the occurrence and severity of postoperative cognitive dysfunction and delirium.

The monoacylglycerol lipase inhibitor, JZL184, has comparable effects to therapeutic hypothermia, attenuating global cerebral injury in a rat model of cardiac arrest

Post-resuscitation cerebral ischemia-reperfusion injury (IRI) is a vital contributor to poor neurological prognosis. Exploring novel therapeutics that attenuate cerebral IRI is of great significance. Inflammation plays a role in the development of cerebral IRI after successful cardiopulmonary resuscitation (CPR). Monoacylglycerol lipase (MAGL) is an enzyme that is predominantly responsible for the metabolism of endocannabinoid 2-arachidonoylglycerol (2-AG) to arachidonic acid (AA) metabolites, which are associated with inflammation. Therefore, we investigated the efficacy of the MAGL inhibitor, JZL184, on cerebral IRI and further compared the effects to therapeutic hypothermia (TH). Thirty-six rats were randomized into three groups: 1) JZL184; 2) Control; 3) TH (N = 12 for each group). Animals underwent 6 min of ventricular fibrillation (VF) followed with 8 min of CPR. After return of spontaneous circulation (ROSC), rats received an intraperitoneal injection of JZL184 (16 mg/kg) or DMSO (20 mg/ml) or body cooling was initiated. Cerebral microcirculation, brain edema, blood brain barrier (BBB) permeability, serum neuron-specific enolase (NSE), S-100β, interleukin-6 (IL-6) and interleukin-10 (IL-10) were quantified at 6 h post ROSC. Compared to control, treatment with JZL184 or TH was associated with significantly ameliorated cerebral microcirculation, mitigated brain edema, attenuated BBB permeability, decreased serum levels of NSE, S-100β and IL-6, and increased serum IL-10 levels (p < 0.05). There was no significant difference in the above measurements between JZL184 and TH. JZL184 has comparable neuroprotective effects to therapeutic hypothermia on global cerebral IRI in a rat model of cardiac arrest (CA).

A retrospective study of the correlation between herpes zoster neuralgia and the serum neuron-specific enolase level in the largest dermatological hospital in Zhejiang province, China.

We studied the changes and clinical significance of the serum neuron-specific enolase (NSE) level in peripheral blood of patients with post-herpetic neuralgia (PHN).Material and methodsPatients with PHN were divided into a mild PHN group and a severe PHN group according to their scores on a 100-point Likert scale representing the degree of neuralgia. NSE levels in neuralgia patients and healthy volunteers were then compared by t-test. Receiver operating characteristic curve analysis was performed to evaluate the diagnostic efficiency of NSE for PHN. The correlation between NSE level and Likert scale score after treatment was analyzed.ResultsNSE levels in PHN patients were higher than those in the healthy volunteers. Patients in the severe PHN group had higher NSE levels than those in the mild PHN group. NSE level at admission was associated with the Likert scale score recorded on the 14th day of treatment (136.1 ± 32.81 vs. 87.53 ± 16.23 pg/mL) (P < 0.05). The ROC curve of NSE levels for PHN is shown that the area was 0.8713 (95% confidence interval, 0.7861–0.9564; p < 0.0001).ConclusionsThere was a correlation between NSE and PHN, in that the NSE level positively correlated with the short-term prognosis of patients with PHN.

Hiponatremili hastalarda serum nöron spesifik enolaz düzeyleri ile beyin hasarı arasındaki ilişki

Purpose: In this study, we aimed to investigate the effects of serum neuron specific enolase on the prediction of central nervous system injury and the clinical course in patients to have hyponatremia.&#x0D; Materials and Methods: 75 adult patients with serum sodium levels less than 135 mEq/L were evaluated. The patients were grouped according to serum neuron specific enolase levels (group 1 ≤ 17.0 ng/mL and group 2 &gt; 17.0 ng/mL). The groups were compared according to demographic and laboratory data. &#x0D; Results: The incidence of hypertension, heart failure, and loss of consciousness was significantly higher in group 2 patient. High neuron specific enolase levels were related to lower serum sodium levels. The mean sodium levels were 129.5 ± 4.3 mEq/L and 126 ± 4.5 mEq/L in groups 1 and 2, respectively. Of the patients in group 2 (n = 45), 8 patients with loss of consciousness (low Glasgow Coma Scale scores) (i.e.

Are Interictal Discharges Associated with Neuronal Cell Loss in Electrical Status Epilepticus in Sleep?

Neuron-specific enolase is an established biomarker of neuronal damage. This study aimed to reveal the relationship between serum neuron-specific enolase level and continuous interictal discharges in a group of encephalopathy with electrical status epilepticus in sleep patients for the first time and determine whether there is a neuronal cell loss or damage. We analyzed serum neuron-specific enolase levels in patients with an electrical status epilepticus in sleep pattern on their electroencephalographs with age- and sex-matched control subjects. Patients with a spike-wave index of at least 50% and acquired neuropsychological regression were included in the study. Magnetic resonance imaging of all electrical status epilepticus in sleep patients and control subjects included in the study was within normal limits. Neuron-specific enolase is measured by the enzyme-linked immunosorbent assay kit based on the sandwich technique. In this study, 14 patients diagnosed with electrical status epilepticus in sleep and 21 healthy controls were included. The median age of electrical status epilepticus in sleep patients was 7.1 years (min-max: 4.5-10.7 years) and 7.7 years (min-max: 3.2-14 years) in the control subjects. According to the results of serum neuron-specific enolase measurements, the mean ± standard deviation level of neuron-specific enolase was 7.61 ± 3.19 ng/dL for the electrical status epilepticus in sleep group and 6.93 ± 2.55 ng/dL for the control group. Serum neuron-specific enolase levels between electrical status epilepticus in sleep patients and the control group were not statistically significant (P = .749). No significant difference was observed in serum neuron-specific enolase levels between electrical status epilepticus in sleep patients and control subjects. Our results may indicate that frequent interictal discharges do not result in neuronal cell loss or damage in electrical status epilepticus in sleep patients.

OS01.5.A Neuron-specific enolase (NSE) and S100 serum levels in patients with active brain metastases from HER2-positive breast cancer treated with trastuzumab-deruxtecan (T-DXd): A biomarker analysis from the TUXEDO-1 trial

Abstract Background T-DXd is a novel antibody-drug conjugate with high activity in HER2-positive metastatic breast cancer. The prospective, single-arm, single-centre phase II TUXEDO-1 trial showed clinically relevant activity of T-DXd in HER2-positive BC pts with active BM with an intracranial response rate of 73.3%. This biomarker sub-study of TUXEDO-1 aimed to investigate changes in the extent of metastases-induced brain damage in patients with and without response to therapy by measuring the serum levels of two proteins constitutively expressed in the human brain and measurable upon brain damage in the blood serum: NSE and S100. Material and Methods We assessed serum NSE (sNSE) and serum S100 (sS100) levels in a total of 37 blood samples drawn at cycles 1, 4 and end of treatment (EOT) in all patients of the intent-to-treat population of the TUXEDO-1 trial using commercially available ELISA assays. Intracranial radiological response was centrally assessed by a board-certified neuro-radiologist using RANO criteria. sNSE and sS100 levels were compared between responders and non-responders using the Mann Whitney U test and a significance level of 0.05. Results At baseline, we detected no significant difference of sNSE or sS100 levels between T-DXd responders and non-responders, respectively. Baseline median sNSE level was 10.6 ng/ml (interquartile range (IQR) 8.6-12.2) in T-DXd responders as compared with median 12.5 ng/ml (IQR 12.2-12.9) in the non-responder group (n.s.). At cycle 4, corresponding numbers were 8.1 ng/ml in responding patients (IQR 7-11.2) and 12.7 ng/ml (IQR 12.2-12.9) in non-responders, respectively (p=0.009). No differences in sS100 levels were observed between the groups at any time point. Conclusion In patients showing intracranial objective response to T-Dxd, sNSE levels were significantly lower at cycle 4 as compared with non-responders, suggesting a reduction in metastases-induced brain damage as a direct treatment effect. sNSE may be a clinically useful biomarker for longitudinal assessment of brain metastasis burden.

Is serum NSE a useful biomarker in multiple system atrophy?

Objective: Multiple system atrophy (MSA) is a rapidly progressive and devastating neurodegenerative disease with limited lifespan. Biomarkers in diagnosing and evaluating the prognosis of MSA is a rapidly developing field. Neuron-specific enolase (NSE) is a biomarker of neuronal damage applicable in many neurological disorders. This study aimed to determine the usefulness of serum NSE as biomarker of MSA. Methods: In this case-control study involving 50 patients with MSA, electrochemiluminescence assay was used to investigate whether serum NSE levels. The disease severity of patients was assessed by Unified System Atrophy Rating Scale (UMSARS part II). The correlation between NSE levels and clinical features in MSA patients was analyzed. Results: The NSE levels were higher in MSA patients (11.59±2.52 ng/mL) than the control group (11.30±2.73 ng/mL); however, the difference was not statistically significant (P=0.581). In addition, no statistically significant difference was detected in the NSE levels between the parkinsonian (MSA-P) and cerebellar subtypes (MSA-C). No distinct difference was also detected between males and females of MSA patients. Furthermore, no correlations were established between NSE levels and age, disease duration, and UMSARS II score. Conclusions: This study suggest that serum NSE is not a useful biomarker of MSA. Future studies should examine whether there is a role for CSF NSE in reflecting neuronal damage in MSA patients.

The ratio of serum neuron-specific enolase level to admission glasgow coma scale score is associated with diffuse axonal injury in patients with moderate to severe traumatic brain injury.

BackgroundModerate to severe traumatic brain injury (TBI) is frequently accompanied by diffuse axonal injury (DAI). Considering the low sensitivity of computed tomography (CT) examination for microbleeds and axonal damage, identification of DAI is difficult using conventional diagnostic methods in the acute phase. Neuron-specific enolase (NSE) has been demonstrated to be increased in serum following various types of TBI and is already clinically/commercially available. We conjecture that serum NSE level to admission GCS score ratio (NGR) may be a useful indicator for the early diagnosis of DAI.MethodsThis study included 115 patients with moderate-to-severe TBI who underwent NSE measurements within 6 h after injury and brain magnetic resonance imaging (MRI) within 30 days. The positive and negative DAI groups were divided according to MRI findings.ResultsAmong the 115 patients, 49 (42.6%) were classified into the DAI group and 66 (57.4%) patients into the non-DAI group by clinical MRI. The NGR of patients without DAI was found to be significantly lower than those of patients with DAI (p < 0.0001). NGR presented the largest Pearson r value (r = 0.755, 95% CI 0.664–0.824, p < 0.0001) and high diagnostic accuracy for DAI [area under the curve (AUC) = 0.9493; sensitivity, 90.91%; and specificity, 85.71%]. Patients with TBI presenting with higher NGR were more likely to suffer an unfavorable neurological outcome [6-month extended Glasgow Outcome Scale (GOSE) 1–4].ConclusionsThe NGR on admission could serve as an independent predictor of DAI with moderate-to-severe TBI.