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العنوان
The value of a1-antitrypsin in chronic liver diseases /
المؤلف
El-Madbouh, Ibrahim Shehata Aly.
هيئة الاعداد
باحث / Ibrahim Shehata aly El-madbouh
مشرف / Ahmed Abbas M.Raouf
مشرف / Hossam El-din Bdel-Latif Taha
مشرف / Hossam El-din Bdel-Latif Taha
الموضوع
Biochemistry. chronic liver- diseases.
تاريخ النشر
1994.
عدد الصفحات
142 p. :
اللغة
الإنجليزية
الدرجة
ماجستير
التخصص
الكيمياء الحيوية (الطبية)
تاريخ الإجازة
4/12/2013
مكان الإجازة
جامعة المنوفية - كلية الطب - Clinical Biochemistry
الفهرس
Only 14 pages are availabe for public view

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Abstract

al-AT is a 52-55 KDa glycoprotin produced mainly in the hepatocyte and released into circulation at a rate of 34mg/kg/day. It serves as the major inhibitor of neutrophil elastase, a powerful proteolytic enzyme stored in neutrophile leukocytes. It consists of a folded polypeptide chain of 394 amino-acids and three carbohydrate side chains. It probably function as a major control protein against the tissue damaging effects of both endognous and exogenous enzyme. a I -AT is coded by a signie gene of spans 12.2 kb. located on long arm of chromosome 14 atq 31-32,3.
al-AT gene is composed and 7 exons and 6 introns. al-AT is a highly polymorphic protein more than 75 al-AT variants have been described, It is inherited as autosomal codominant pattern.
Many factors cause variation in concentration of a I -AT in common population such as sex, age, pregnancy, contraceptive pills containing oestrogen, smoking, air pollution and alcohol.
Pathological increased levels of al-AT occur in cases of tissue destruction, surgery, trauma, acute and chronic inflammatory disorders, after typhoid vaccine administration, myocardial infarction, cancer, and haematologic abnormalities.
Decreased levels of al-AT are associated with a number of diseases including arthritis psoriasis, panniculitis and pancreatitis. However two strongest association are with lung and liver diseases. Rarely al-AT level may be severely depressed in acute hepatic necrosis, end stage liver cell failure. Low levels of al-AT are often secondary to urinary protein loss as in nephrotic syndrome or intestinal protein loss as in protein