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Complement activation as a mediator of antiphospholipid antibody induced pregnancy loss and thrombosis.
| Content Provider | Semantic Scholar |
|---|---|
| Author | Girardi, Guillermina |
| Copyright Year | 2002 |
| Abstract | The antiphospholipid antibody syndrome (APS) is characterised by increased risk of vascular thrombosis involving venous, arterial, and placental circulations. The last of these is associated with poor obstetrical outcomes, including fetal death and growth retardation. Pregnancy loss is a defining criterion for APS and occurs with particularly high frequency in systemic lupus erythematosus (SLE) patients bearing this antibody. Patients meet the criteria for APS if they have three otherwise unexplained embryonic losses (before 10 weeks gestation) or one otherwise unexplained fetal loss after 10 weeks, with or without placental infarction or fetal growth restriction. Over the past two decades, APS has emerged as a leading cause of pregnancy loss and pregnancy related morbidity. It is now recognised that recurrent miscarriage occurs in 1% of couples, that up to 20% of women with recurrent miscarriage have antiphospholipid (aPL) antibodies, and that in about 15% of otherwise apparently normal women aPL is the sole explanation for recurrent fetal loss. 9 The primary treatment for these patients, anticoagulation throughout pregnancy, is inconvenient, sometimes painful, expensive, and fraught with potential complications, including haemorrhage and osteoporosis. Moreover, it is often ineffective. Thus, the identification of a novel mechanism for pregnancy loss in women with aPL antibodies holds the promise of new, safer, and better treatments. Awareness of the association of aPL antibodies with pregnancy complications has increased the frequency with which APS is diagnosed and generated substantial interest in elucidating its pathophysiology. At present, though the association of aPL antibodies with pregnancy loss and pregnancy morbidity is secure, its mechanism remains unknown. Defining this mechanism is crucial for several reasons. Firstly, there is considerable variability in the success rates of the various treatments, suggesting that different but still undefined treatments may be optimal in specific subsets of women with aPL. Secondly, current treatment regimens are imperfect and many treated pregnant patients suffer complications such as pre-eclampsia, uteroplacental insufficiency, intrauterine fetal growth restriction, and preterm birth. 12 Thirdly, understanding how aPL antibodies “cause” miscarriage will probably lead to important insights into the mechanisms of miscarriages in general, thereby benefiting women with non-aPL related miscarriages. |
| Starting Page | 6 |
| Ending Page | 21 |
| Page Count | 16 |
| File Format | PDF HTM / HTML |
| Alternate Webpage(s) | http://ard.bmj.com/content/annrheumdis/61/suppl_2/ii46.full.pdf |
| PubMed reference number | 12379621v1 |
| Volume Number | 61 |
| Journal | Annals of the rheumatic diseases |
| Language | English |
| Access Restriction | Open |
| Subject Keyword | Abortion, Habitual Addiction Potential Scale Adrenal cortical hypofunction Antiphospholipid Antibodies Antiphospholipid Syndrome Blood Circulation Cessation of life Discipline of obstetrics Eclampsia Fetal Death Fetal Diseases Growth retardation Hemorrhage Intrauterine Lupus Erythematosus, Systemic Mediator brand of benfluorex hydrochloride Morbidity - disease rate Osteoporosis Patients Placenta Placental infarction Pre-Eclampsia Pregnancy Complications Pregnancy in Diabetics Pregnancy loss Premature Obstetric Labor Spontaneous abortion Thrombosis of blood vessel benefit |
| Content Type | Text |
| Resource Type | Article |
