Enolase Levels In Patients Research Articles

Assessment of neuron-specific enolase, glycated haemoglobin and fasting plasma glucose levels in patients with diabetes peripheral neuropathy in Calabar Metropolis, Nigeria: A case control study

Background: Persistent hyperglycemia has been implicated in the development of neuronal complications in diabetes patients. Nerve damage and metabolic abnormalities may cause the release of neuron specific enolase into circulation. Aim: To investigate the relationship between serum neuron-specific enolase (NSE), fasting plasma glucose (FPG) and glycated haemoglobin (HbA1C) levels in diabetic patients with peripheral neuropathy. Methods: one hundred and five patients with peripheral neuropathy and 60 apparently healthy non-diabetic controls aged 45-69 years attending Clinics in General Hospital Calabar and the University of Calabar Teaching Hospital, Calabar, between July 2021 and January 2022, were recruited into the study. Fasting plasma glucose was estimated using glucose oxidase peroxidase method. Glycated haemoglobin and NSE were determined using Boronate Affinity High Performance Liquid Chromatography and ELISA methods respectively. Height and weight were measured and BMI computed, and data analyzed using Student’s t-test, ANOVA, post hoc analysis and Pearson’s correlation at P<0.05. Results: Body mass index, blood pressure, fasting plasma glucose, glycated haemoglobin and neuron specific enolase concentrations were significantly different (P=<0.05) between the diabetic patients and the controls. Neuron specific enolase vary significantly (P<0.05) among the diabetic patients with different forms of diabetes peripheral neuropathy. Fasting plasma glucose correlated positively with NSE (r=0.441, P=0.000) and HbA1C (r=0.328, P=0.001) respectively. Glycated haemoglobin correlated positively with BMI (r=0.412, P=0.000) and NSE (r=0.328, P=0.001) in that order. Conclusion: This study has shown that glycated haemoglobin and fasting plasma glucose are related with neuron specific enolase levels in patients with diabetes peripheral neuropathy. Thus, rising levels of glycated haemoglobin and fasting plasma glucose (poor glycemic control) may be associated with progressive nerve damage in patients with diabetes peripheral neuropathy.

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.

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.

Evaluation of serum neuron specific enolase levels among patients with primary and secondary burning mouth syndrome.

Burning mouth syndrome is a painful condition of the oral cavity with ambiguous pathogenesis and diagnosis. Neuron-specific enolase is increased in several conditions including peripheral neuropathy of diabetes, ophthalmopathies, spinal cord injuries and tumors. Evidence on association of burning mouth syndrome and neuron-specific enolase is limited. This study aims to evaluate neuron-specific enolase levels in primary and secondary burning mouth syndrome patients and compare the levels of neuron-specific enolase with associated conditions in secondary burning mouth syndrome. One hundred and twenty-eight patients of more than 18 years of age with no gender predilection and having clinical symptoms of burning mouth syndrome and 135 healthy subjects were included. All the patients fulfilled Scala's criteria for the diagnosis of burning mouth syndrome, including "primary" (idiopathic) and "secondary" (resulting from identified precipitating factors) burning mouth syndrome patients. Blood samples were obtained from burning mouth syndrome patients. Serum neuron-specific enolase was evaluated using enzyme-linked immunosorbent assay. To compare means and standard deviations, among primary and secondary burning mouth syndrome, data was analysed with analysis of variance and multiple comparisons test. The mean age of the study participants for burning mouth syndrome and healthy subjects was 53.30 and 51.6 years, respectively. Amongst the secondary burning mouth syndrome group, 32 (25%) of the patients had menopause, 15 (11.7%) had diabetes, eight (6.2%) of the patients had nutritional deficiency, seven (5.4%) had combined diabetes, menopause, and depression, six (4.6%) had combined diabetes and depression, four (3.1%) were diagnosed with Sjögren's syndrome. A minor percentage of 2.3% (three) had gastroesophageal reflux disease, while the remaining three (2.3%) patients in the secondary burning mouth syndrome group were on anti-depressants. There was a statistically significant increase in the levels of neuron-specific enolase in primary burning mouth syndrome as compared to the secondary burning mouth syndrome and healthy groups. Among the subgroups of secondary burning mouth syndrome, diabetic individuals showed a significant increase in neuron-specific enolase level when compared with other conditions in the secondary burning mouth syndrome patients.Discussion and conclusion: The raised serum neuron-specific enolase levels in patients suffering from primary burning mouth syndrome highlight a possible neuropathic mechanism. It was also increased in the sub-group of secondary burning mouth syndrome patients having diabetes. Although it cannot be ascertained whether the deranged values in the diabetic group were due to burning mouth syndrome or due to diabetes, the raised quantity of neuron-specific enolase in the primary burning mouth syndrome group is a reliable diagnostic indicator. Future studies on the assessment of neuron-specific enolase levels as a diagnostic tool for onset and management of primary and secondary burning mouth syndrome are recommended.

Diagnostic Value of Serum Neuron-Specific Enolase Level in Patients With Acute Ischemic Stroke; A Systematic Review and Meta-Analysis

Background: We aim to assess the predictive value of serum neuron-specific enolase (NSE) level in patients with acute ischemic stroke referring to the emergency department. Methods: This systematic review and meta-analysis performed, considering the PRISMA and MOOSE statement guidelines. A computerized literature search of the known medical database conducted by using the relevant keywords. We included studies published before November 2016 in which stroke patients compared with non-stroke controls and also studies evaluating the serum levels of NSE in the study groups. Statistical analysis was pooled in a random effect model analysis using the Comprehensive Meta-Analysis software. Results: We included 12 articles in the qualitative and quantitative analysis, that their quality acceptable based on the Newcastle Ottawa Scale (NOS scale). The pooled effect estimates showed that NSE is significantly higher in ischemic stroke patients in comparison with their controls with a high effect estimate [OR 9.68, 95% CI (3.06 to 30.6)]. The effect estimate remained statistically significant under the fixed and random effects model. Conclusion: Our results show higher levels of NSE in patients with stroke than in the control group, indicating that NSE plays a role in the diagnosis of stroke. In terms of prognosis, there is evidence regarding the direct and indirect relationship; and it founded that serum levels of NSE is higher in larger stroke volume, which needs further research.

Neuron- specific enolase level in patients with metabolic syndrome and its value forecasting acute stroke

Neuron- specific enolase level in patients with metabolic syndrome and its value forecasting acute stroke

073_16742-H5 Evaluation of Acute Brain Injury With Serum Neuron-Specific Enolase Levels in Patients Undergoing Catheter Ablation for Atrial Fibrillation

Catheter ablation of atrial fibrillation (AF) is related with tromboembolic complications. We aimed to measure periprocedural serum neuron-specific enolase (NSE) levels, which is known as biomarker of neuronal injury. Forty three patients with paroxysmal AF underwent pulmonary vein isolation

High-Dose Propofol Reduces S-100β Protein and Neuron-Specific Enolase Levels in Patients Undergoing Cardiac Surgery

In a variety of experimental models, propofol has been shown to protect the brain. It was hypothesized that a clinically achievable high dose of propofol would induce cerebral protective effects in patients undergoing cardiac surgery with cardiopulmonary bypass (CPB). The authors investigated the effects of different target plasma concentrations of propofol on cerebral injury by measuring serum S-100β protein and neuron-specific enolase (NSE) levels in patients undergoing single-valve replacement with CPB. A prospective, randomized study. A university hospital. Forty-two patients undergoing single-valve replacement with CPB. Patients were randomly divided into 3 groups (n = 14 each). Each group received a target-controlled infusion of propofol with plasma concentrations of 1.8 μg/mL (low dose, Group-L), 2.4 μg/mL (medium dose, Group-M), or 3.2 μg/mL (high dose, Group-H). The propofol target concentrations were unchanged throughout the surgery. In all 3 groups of patients, at all time points after CPB, the plasma S-100β protein and NSE levels, which served as biochemical markers of brain damage, were significantly higher than the preoperative levels (p<0.05). Group-H showed significant decreases in S-100β protein and NSE compared with Group-L (p< 0.05). In the range of commonly used clinical concentrations, administration of a high dose of propofol during CPB attenuated the biochemical markers of brain damage as compared with low-dose propofol anesthesia.

Neuron specific enolase levels in patients undergoing aortic surgery under hypothermic circulatory arrest

Neuron specific enolase levels in patients undergoing aortic surgery under hypothermic circulatory arrest

Elevated S100B and neuron specific enolase levels in patients with migraine-without aura: evidence for neurodegeneration?

Although migraine has mainly been considered as a benign disease, there is cumulative evidence of silent changes in the brain, brainstem, or cerebellum and subtle subclinical cerebellar dysfunction. In this study, in order to investigate a possible neuronal and/or glial damage at the cellular level in migraine, we measured and compared serum levels of S100B which is a protein marker of glial damage or activation, and neuron specific enolase (NSE) which is a marker of neuronal damage, in migraine patients and control subjects. Serum levels of S100B and NSE were measured in blood samples from 41 patients with migraine-without aura taken during a migraine attack (ictal) and in the attack-free period between migraine attacks (interictal) and 35 age- and sex-matched controls. Patients with migraine-without aura had significantly higher ictal serum levels of S100B and NSE (P < 0.05, for both) than control subjects; whereas in the interictal phase, there was a significant increment only in S100B levels (P < 0.05) compared to controls. On the other hand, serum levels of S100B and NSE in ictal and interictal blood samples did not differ significantly. The findings of increased ictal serum S100B and NSE levels together with increased interictal levels of S100B suggested that migraine might be associated with glial and/or neuronal damage in the brain and a prolonged disruption of blood-brain barrier. Increased interictal serum levels of S100B might point out to an insidious and slow damaging process in migraine patients.

Influence of Methylprednisolone on Levels of Neuron-Specific Enolase in Cardiac Surgery: A Corticosteroid Derivative to Decrease Possible Neuronal Damage

Cerebral injury is a well-known complication after cardiac surgery with cardiopulmonary bypass (CPB), especially in adult patients. Specific biochemical markers like neuron-specific enolase (NSE) and S-100beta protein were developed previously for early detecting neuronal damage after CPB. Corticosteroids are shown to reduce multisystemic deleterious effects of cardiopulmonary bypass due to their anti-inflammatory characteristics. The aim of this study is to demonstrate the decrease of serum neuron-specific enolase levels in patients who received corticosteroids before CPB. Thirty patients scheduled for elective coronary bypass surgery were included in the study. Patients were divided randomly into two groups as the control group (n = 15) who underwent a standard coronary bypass surgery without any additional medication and the study group (n = 15) who received 1 gm of methylprednisolone before CPB. Blood samples for analysis of serum NSE, interleukin-6 (IL-6), and IL-10 were drawn before CPB, 4 and 24 hours after the end of extracorporeal circulation. Serum cytokine and NSE levels were significantly increased after CPB above their normal range in both groups. In the study group, IL-6 and NSE levels were significantly reduced while IL-10 levels were much higher after CPB. High NSE levels significantly correlated with IL-6 levels in the control group. The lower levels of NSE in patients who received methylprednisolone may suggest that corticosteroids might be useful in decreasing possible neuronal damage during heart surgery. However, we were not able to demonstrate an adverse neurological outcome.

Serum neurone-specific enolase levels in patients with neuroendocrine and carcinoid tumours

We have examined concentrations of neurone-specific enolase (NSE) in sera from 18 patients with various neuroendocrine tumours, 26 patients with carcinoid tumours, 21 patients with non-neuroendocrine tumours and 37 control individuals. No statistically significant difference between the concentrations in patients with neuroendocrine tumours and patients with carcinoid tumours was found. However the NSE concentrations in patients with carcinoid and neuroendocrine tumours, when these two groups were combined, were significantly different from the patients with non-neuroendocrine tumours or the control individuals ( P ≤ 0.01). 38.5% of the patients with carcinoid tumours had raised NSE concentrations in serum; 55.5% of those with non carcinoid neuroendocrine tumours had raised concentrations. There appeared to be no correlation between the NSE concentrations and the extent of metastases.

Serum neurone specific enolase levels in patients with cerebral infarction

A radioimmunoassay has been developed and used to measure serum neurone specific enolase (NSE) concentrations in 24 patients, following cerebral infarction. A significant correlation between cerebral infarct volume and maximum serum NSE concentration was observed (P= 0·047). Serum NSE was also assayed at times 24, 48, 72 and 96 h post ictus. At 72 h a significant correlation existed between serum NSE levels and infarct volume (P= 0·012), and levels appeared to be approaching statistical significance at 48 h (P=0·067). No correlation existed at 24 and 96 h. In addition serum concentrations of NSE were compared to clinical outcome as determined by the Glasgow Outcome Score. Using the Mann-Whitney U test, there was no significant difference in maximum NSE level between patients graded 1–3 on the Glasgow Outcome Score and those graded 4 and 5. However, further studies are required on a larger population to more completely assess this. NSE may prove to be a useful marker of neuronal damage in the study of stroke, with particular application in the assessment of treatment.