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1.
J Med Assoc Thai ; 99 Suppl 4: S48-53, 2016 Jul.
Artículo en Inglés | MEDLINE | ID: mdl-29916681

RESUMEN

Background: Soluble LOX-1 (sLOX-1) and nitric oxide (NO) are potential biomarkers for vascular oxidative stress that affect to atherosclerotic plaque. Atherosclerotic narrowing of the internal carotid artery is a well-known cause of acute ischemic stroke (AIS). Objective: To measure serums LOX-1and NO levels in acute ischemic stroke patients with or without ICA stenosis after 24-hour stroke symptom onset. Material and Method: 118 patients with AIS within 24 hours-stroke symptom onset. Peripheral venous blood of all patients was collected for measuring blood sugar, cholesterol, triglyceride, HDL-c and LDL-c concentrations by standard laboratory techniques. Serum sLOX-1 and NO concentrations were measured by ELIZA kits. The patients were divided into two groups i.e. non-internal carotid artery stenosis (NICAS, n = 65) and internal carotidartery stenosis (ICAS, n = 53) by measuring internal carotid artery stenosis by ultrasound carotid duplex. Results: Baseline characteristics were not significantly different between NICAS and ICAS except LDL-c levels. Serum NO level had significantly lower in ICAS (50.09±7.36 µmol/l) when compared with NICAS (54.85±11.81 µmol/l). sLOX-1 had significantly higher in ICAS (1.82±0.34 ng/ml) compared with NICAS (1.13±0.40 ng/ml). Conclusion: There are higher sLOX-1 and lower NO levels in AIS patients with ICAS when comparing those with NICAS. These parameters may become the novel potential biomarkers for predicting risk to acute ischemic stroke.


Asunto(s)
Estenosis Carotídea/sangre , Óxido Nítrico/sangre , Receptores Depuradores de Clase E/sangre , Accidente Cerebrovascular/sangre , Adulto , Anciano , Biomarcadores/sangre , Arteria Carótida Interna , Estenosis Carotídea/complicaciones , Estenosis Carotídea/fisiopatología , Femenino , Humanos , Masculino , Persona de Mediana Edad , Factores de Riesgo , Accidente Cerebrovascular/etiología , Accidente Cerebrovascular/fisiopatología
2.
Neurol Res Int ; 2018: 7268924, 2018.
Artículo en Inglés | MEDLINE | ID: mdl-29850244

RESUMEN

BACKGROUNDS: Stroke is the leading cause of death and long-term disability. Oxidative stress is elevated during occurrence of acute ischemic stroke (AIS). Soluble LOX-1 (sLOX-1) and NO are used as biomarkers for vascular oxidative stress that can reflect stabilization of atherosclerotic plaque. Previous study showed that simvastatin can reduce oxidative stress and LOX-1 expression. OBJECTIVES: To evaluate neurological outcomes and serum sLOX-1 and NO levels in patients with AIS treatment with low dose 10 mg/day and high dose 40 mg/day of simvastatin. METHODS: 65 patients with AIS within 24 hours after onset were randomized to treatment with simvastatin 10 mg/day or 40 mg/day for 90 days. Personal data and past history of all patients were recorded at baseline. The blood chemistries were measured by standard laboratory techniques. Serum sLOX-1 and NO levels and neurological outcomes including NIHSS, mRS, and Barthel index were tested at baseline and Day 90 after simvastatin therapy. RESULTS: Baseline characteristics were not significantly different in both groups except history of hypertension. Serum sLOX-1 and NO levels significantly reduce in both groups (sLOX-1 = 1.19 ± 0.47 and 0.98 ± 0.37 ng/ml; NO = 49.28 ± 7.21 and 46.59 ± 9.36 µmol/l) in 10 mg/day and 40 mg/day simvastatin groups, respectively. Neurological outcomes including NIHSS, mRS, and Barthel index significantly improve in both groups. However, no difference in NO level and neurological outcomes was found at 90 days after treatment as compared between low dose 10 mg/day and high dose 40 mg/day of simvastatin. CONCLUSION: High-dose simvastatin might be helpful to reduce serum sLOX-1. But no difference in clinical outcomes was found between high- and low-dose simvastatin. Further more intensive clinical trial is needed to confirm the appropriate dosage of simvastatin in patients with acute ischemic stroke. This trial is registered with ClinicalTrials.gov ID: NCT03402204.

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