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العنوان
Assessment Of The Role Of Serum And Follicular Fluid Antiphospholipid Antibodies In Patients Undergoing Assissted Reproductive /
المؤلف
Mahmoud, Reham Mohammed Atef.
هيئة الاعداد
مشرف / ريهام محمد عاطف محمود
مشرف / محمد مصيلحى فراج
مشرف / أميمة محفوظ محمد محمود
مشرف / منى موريس
الموضوع
Human Anatomy & Embryology.
تاريخ النشر
2015.
عدد الصفحات
141 p. ;
اللغة
الإنجليزية
الدرجة
ماجستير
التخصص
علم الوراثة (السريرية)
تاريخ الإجازة
1/1/2015
مكان الإجازة
جامعة قناة السويس - كلية الطب - Human Anatomy & Embryology
الفهرس
Only 14 pages are availabe for public view

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from 167

Abstract

Antiphospholipid antibodies (aPLs) are a group of autoantibodies associated with poor obstetric outcomes such as recurrent pregnancy loss, stillbirth, fetal growth restriction and pre-eclampsia, as well as thrombosis, thrombocytopenia and other autoimmune disorders (Chamley, 2002).
More recently, attention has focused on their possible association with infertility and IVF implantation failure. (Birdsall et al., 1996; Kutteh et al., 1997; Stern et al., 1998). The mechanism by which aPLs induce fetal demise or thrombosis is currently unknown, but most aPLs are now known to bind to a complex antigen consisting of a negatively charged phospholipid. (Kutteh et al., 1997; Chamley, 2002).
Older studies suggested that aPLs may induce thrombosis of the uterine spiral arteries leading to fetal demise, but more recent studies suggest that other mechanisms, such as the direct disruption of placental trophoblast functions, are more likely to explain how aPLs adversely affect pregnancies (Di Simone et al., 2005; Chamley et al., 1998). It is difficult however, to envisage how aPLs in the maternal blood could prevent the implantation of an apparently healthy embryo conceived in vitro. A small study has suggested a mechanism whereby aPLs may be selectively concentrated in follicular fluid (el-Roeiy et al., 1987) from where the antibodies could potentially bind to the oocyte. Other studies have shown that aPLs may bind to oocytes and embryos and arrest
embryo development, usually at the ≥16 cell stage (Sthoeger
et al., 1993; Kaider et al., 1999). As many IVF programmes
return human embryos to the uterus at the 4- to 8-cell stage,
developmental arrest at a later stage would present clinically as
an IVF implantation failure. This may therefore be a mechanism by which aPLs cause IVF implantation failure.
Therefore, the aim of the present work was to detect if there is any relation between the levels of (APLs) in follicular fluid and serum, and (IVF) failure.