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العنوان
CLINICAL SIGNIFICANCE OF PLASMA THRDMBDMDDULIN LEVEL IN DIABETES MELLITUS
المؤلف
Nasr, Salah Eldin Ahmed
هيئة الاعداد
باحث / صلاح الدين احمد نصر رزق
مشرف / ايناس احمد عصفور
مشرف / نورا محمد الخولى
مشرف / حنان حامد
تاريخ النشر
1997
عدد الصفحات
150 ص.
اللغة
الإنجليزية
الدرجة
ماجستير
التخصص
الطب الباطني
تاريخ الإجازة
1/1/1997
مكان الإجازة
جامعة عين شمس - كلية الطب - باطنى عام
الفهرس
Only 14 pages are availabe for public view

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Abstract

Thrombomodulin (TM) IS a surface glycoprotein which
neutralizes thrombin clotting and platelet aggregatory activity and acts
as a cofactor for thrombin catalyzed activation of anticoagulant protein
c.
Circulating thrombomodulin is not constantly secreted by
endothelial cells but results from cellular damage. Unlike von
Willebrand factor and tissue plasminogen activator, circulating TM is
not a maker of endothelial cell stimulation, and the endothelial
membrane TM is hardly leaked in absence of endothelial inJurY The
liver is considered the major site of clearance of circulating TM, and
patients with liver disease especially fulminant hepatitis were reported
to have elevated plasma TM levels (Takahashi et al., 1992) In
addition the change in urinary excretion of TM may modifi,· its plasma
(Ishii and Majerus, 1985).
Plasma TM has been frequently reported to be elevated in a
variety of diseases including DIC, pulmonary thromboembolism, acute
respiratory distress. chronic renal failure. collagen diseases,
hematological malitmancies as well as in thrombotic diseases These findings suggest that the endothelial damage may occur more frequently
than hitherto supposed (Ta Kahashi et a!., 1992 ).
Subclinical elevation of urinarY albumin, microalbwninurea. is
well described as being a predictor for cardiovascular disease in both
diabetic and nondiabetic subjects It reflects the presence of
generalized vascular damage and represents a crucial event in the
natural histories of diabetes melhtus and essential hypertension
(Yudkin et al., 1988). An increased risk of cardiovascular mortalitv in
both insuhn - dependent ODD) and noninsulin-dependent (NIDD 1
diabetics has been recorded in association with microalbwninurea and
the risk becomes 10 - to 40 fold higher with development of clinical
proteinuria, macroalbuminurea in IDD (Borch et a!., 1985).