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العنوان
Effect of statins as anti-inflammatory on atherosclerosis in chronic kidney disease patients guided by CD4+CD28nullT cells over duration of six months 1 /
المؤلف
Ibrahim, Mohamed Ashraf.
هيئة الاعداد
باحث / Mohamed Ashraf Ibrahim
مشرف / Ashraf Mahmoud Okba
مشرف / Hala Salah Abdelawi
مناقش / Malak Nabil Amin
تاريخ النشر
2019.
عدد الصفحات
188 P. :
اللغة
الإنجليزية
الدرجة
الدكتوراه
التخصص
الطب الباطني
تاريخ الإجازة
1/1/2019
مكان الإجازة
جامعة عين شمس - كلية الطب - قسم الامراض الباطنية
الفهرس
Only 14 pages are availabe for public view

from 188

from 188

Abstract

The CKD patients are at increased risk of atherosclerosis which is also associated with novel risk factors such as chronic inflammatory state. Upon that, CKD is being recognized as a chronic inflammatory condition, with alterations in both adaptive and innate immunity.
Now, it is already proven that atherosclerosis is essentially an inflammatory process, where T cells are essential for progression of the process. To be more specific, a population of CD4+ T cells lacking the CD28 molecule on their cell surface, known as CD4+CD28null T cells, has been implicated as a major contributor in the inflammatory process and destabilize the atherosclerotic plaques.
Beside the effects on the cholesterol, the statins present a lot of other actions, known as the pleiotropic effects. Statins exert their anti-inflammatory effects on the vascular wall through a variety of molecular pathways of the innate and adaptive immune systems, their impact on the circulating levels of pro-inflammatory cytokines.
Upon the above data, we conducted our study on ninety CKD patients divided into three groups according to the presence or absence of atherosclerosis and two of them (group A and B) were given statin therapy for six months, while the third group continue on only the conservative treatment for CKD patients. The anti-inflammatory effect of statin was assessed by CD4+CD28null T cells percentage and TNF-α serum level.
Our results revealed that mean CD4+CD28null T cells percentage was higher in the patients with atherosclerosis whether at the beginning of the study or after six months. The baseline TNF-α values showed no differences among the three groups. But, its values were much lesser in those patients who received statin at the end of the six months.
In both A and B groups, there was a decrease CD4+CD28null T cells percentage and TNF-α level after statin therapy. The percentage of CD4+CD28null T cells from baseline value in groups A and B decreased by -18.79 % and -18.64 % respectively. While, the percentage of reduction of TNF-α from baseline was by -16.43 % and -18.15 % in group A and B respectively.
In group A, we found a strong positive correlation between baseline and after 6 months’ of CD4+CD28null T cells percentage and baseline CIMT and with CIMT after 6 months respectively. Also, weak positive correlation was also observed with baseline proteinuria.
To conclude, the use of statin therapy for anti-inflammatory purpose in CKD patients specially with evidence of atherosclerosis lead to marked decrease in inflammatory markers such as CD4+CD28null T cells percentage and TNF-α serum levels which contribute to atherosclerosis.