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العنوان
Plasma Adamts 13 In Patients With Chronic Hepatitis C/
المؤلف
Sherif, Reem Mahmoud.
هيئة الاعداد
باحث / Reem Mahmoud Sherif
r-sherif@live.com
مناقش / Ali Mahmoud El Kady
مناقش / Fatma Mohamed Abdel-Aziz
مشرف / Magdi Mamdouh El Bordini
الموضوع
Tropical Medicine. Hygiene.
تاريخ النشر
2013.
عدد الصفحات
74 p.:
اللغة
الإنجليزية
الدرجة
ماجستير
التخصص
الطب (متفرقات)
تاريخ الإجازة
31/1/2013
مكان الإجازة
جامعة الاسكندريه - كلية الطب - Tropical Medicine & Hygiene
الفهرس
Only 14 pages are availabe for public view

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from 114

Abstract

The liver plays a major role in hemostasis by synthesizing all clotting factors (except vWF), coagulation inhibitors and several fibrinolytic proteins. The progressive loss of hepatic parenchymal cells results in decreased synthesis of clotting factors and hence their deficiencies.
The risk of bleeding associated with the coagulopathy of ESLD depends on the number and severity of clotting factor deficiencies.
The balance between the levels of procoagulant and anticoagulant proteins determines the overall effect on hemostasis and resulting risk of hemorrhage and thrombosis. Although bleeding occurs more frequently, the hemostatic imbalance in ESLD occasionally favors hypercoagulability, predisposing to thrombosis.
ADAMTS13 is a metalloproteinase that specifically cleaves multimeric vWF between Tyr1605and Met1606 residues in the A2 domain. In the absence of ADAMTS13 activity ULVWFM are released from vascular endothelial cells.
Studies have shown that ADAMTS13 is significantly decreased in patients with hepatic veno-occlusive disease (VOD), alcoholic hepatitis, liver cirrhosis, and those undergoing living donor related liver transplantation and partial hepatectomy.
The aim of the present work was to study plasma level of ADAMTS13 and correlate the results with plasma levels of fibrinogen and CRP in patients with chronic hepatitis C with and without liver cirrhosis.
This study was conducted on 100 subjects classified into three groups:
Group I: Included 40 patients with chronic viral hepatitis C without liver cirrhosis.
Group II: Consisted of 40 patients with chronic viral hepatitis C with liver cirrhosis, who were further divided according to the Child-Pugh Classification.
Group III: 20 healthy subjects with comparable age and sex were enrolled as control group for laboratory assessment.
All patients and controls were interviewed and subjected to the following:
1. Clinical evaluation.
2. Routine laboratory investigations including.
 Complete blood picture.
 Liver functions tests (serum ALT, AST, GGT, Alkaline phosphatase, serum bilirubin, serum albumin, prothrombin time and activity).
 Renal functions tests (serum urea and creatinine).
 Blood chemistry (serum calcium and phosphorus, fasting blood sugar and 2-hr postprandial blood sugar).
3. Viral markers for hepatitis B (HBs Ag) and hepatitis C (Anti HCV) by ELISA.
4. Abdominal imaging.
5. Liver Biopsy (whenever possible).
6. Estimation of plasma ADAMTS13 levels.
7. Estimation of plasma fibrinogen and CRP levels.