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العنوان
The Impact of Tissue Plasminogen Activator On Neuronal Degeneration In Acute Ischemic stroke patients /
المؤلف
Sayed, Somia Ahmed.
هيئة الاعداد
باحث / سمية احمد سيد
ahmed.comander@gmail.com
مشرف / حاتم انور المصرى
مشرف / محمد مبروك مسعود
مشرف / شيماء على عبد الكريم
الموضوع
Thrombolytic therapy. Cerebral ischemia. Tissue plasminogen activator Therapeutic use. Plasminogen Activator, Tissue-Type Therapeutic use.
تاريخ النشر
2020.
عدد الصفحات
122 p. :
اللغة
الإنجليزية
الدرجة
ماجستير
التخصص
الطب الباطني
الناشر
تاريخ الإجازة
16/3/2020
مكان الإجازة
جامعة بني سويف - كلية الطب - الامراض العصبية
الفهرس
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Abstract

Stroke was the third leading cause of mortality worldwide and more than 5 million people die as a consequence of stroke. Intravenous thrombolytic therapy with recombinant tissue type plasminogen activator (rtPA) improves clinical outcome after acute ischemic stroke. Recently, studies pointed to the crucial role of TPA in neuroplasticity participating in the recovery of ischemic stroke patients and decrease Neuronal degeneration.
The aim of the present study to assess the impact of treating stroke patients with rTPA on serum levels of NSE; the marker of neuronal degeneration.
The current study is a prospective observational study conducted on 53 patients having acute ischemic stroke; 28 patients diagnosed as having acute ischemic stroke in the therapeutic window for treatment with rTPA (first 4.5 hours) and had no contraindication for (rTPA), and 25 patients diagnosed as having acute ischemic stroke in the first 4.5 hours of onset but have contraindication for (rTPA) or (from 4.5-24 hours from the onset of stroke). The mean age for patients was 59.14 ±13.8years and for controls 60.48 ±13.6 years. There was no statistically significant difference between patients and controls regarding age or sex.
Eligible Patients for rTPA received intravenous (i.v.) rTPA (0.9 mg/kg, Actilyse, Boehringer Ingelheim).
All included patients were subjected to the following:
• History taking regarding: stroke risk factors (DM, HTN, AF, smoking, drug abuse, family history or past history of stroke).
• Clinical assessment including: BMI and neurological assessment using the NIHSS at the onset of stroke, after 24hours and at day 7 from the onset.
• Laboratory investigations including: lipid profile (cholesterol, TG, LDL and HDL) and uric acid.
• Serum NSE measurement after 24 hours of stroke onset using commercial sandwich-ELISA kits (Human NSE ELISA Kit, Epitope Diagnostics, Inc).
• Radiological assessment including: C.T. or MRI brain at the onset of stroke. Infarction site and size were assessed using the pure ellipsoid model of ABC/2.
• Cardiovascular assessment using echocardiography to assess the presence of valvular disease, ejection fraction, left atrium dilatation and pulmonary hypertension.
• Carotid and vertebrobasilar duplex to detect atherosclerosis or stenosis of the carotid and vertebrobasilar arteries.
The results of our study were summarized in the following:
• rtPA treated patients were found to have significantly lower NSE serum level than controls.
• There was a statistically significant positive correlation between NSE serum level and infarction size, stroke severity assessed by NIHSS and MRS at 3 months.
• Patients with favorable outcome had significantly lower NSE serum level than patients with unfavorable outcome.
• Patients with past history of stroke were found to have significantly higher NSE level than those without past history of stroke.
• There was a statistically significant positive correlation between NSE serum level and HDL.
• Patients with mild pulmonary hypertension had significantly lower NSE level than patients without pulmonary hypertension.
• There was no statistically significant difference between NSE serum level regarding age or sex.
• There was no statistically significant difference in NSE serum level between subjects with and without DM or HTN.
• There was no statistically significant difference between abusers and non-abusers, smokers and non-smokers in NSE serum level.
• There was no statistically significant difference in NSE serum level between subjects with and without valvular heart diseases, cardiomyopathy or AF.
• There was no statistically significant difference in NSE serum level between subjects with and without carotid atherosclerotic changes.
• There was no statistically significant correlation between serum level of NSE and uric acid, cholesterol, TG or LDL.