Plasma Fibrinogen and Fibrin Degradation Product (FDP) in Preeclampsia

Abstract

2) late onset preeclampsia (after 34 wks gestation) 5 .Preeclampsia creates a functional derangement of multiple organ system. Complications of preeclampsia include eclampsia, placental abruption, ascities, hepatic infarction and rupture, intra-abdominal bleeding, pulmonary edema and acute renal failure. Twenty percent (20%) of women with severe preeclampsia develops HELLP syndrome (hemolysis, elevated liver enzymes, low platelets) and the same percentage (20%) among HELLP syndrome develops disseminated intravascular coagulation (DIC). Complications affecting the developing fetus include intrauterine growth retardation, prematurity, oligohydramnios, bronchopulmonary dysplasia and increased risk of perinatal death 2 . During normal pregnancy profound changes occur in the coagulation and fibrinolytic system of the mother causing a hypercoagulable state. In preeclampsia there is a distinct possibility of accentuation of this hypercoagulable state of pregnancy 4 .Numerous studies observed coagulation abnormalities in preeclampsia. The level of anticoagulants such as antithrombin III, protein C and protein S are decreased in these groups. The clotting factors such as factor VIII and von Willebrand factors are elevated in preeclampsia. There is also increase in plasminogen activator inhibitor type 1(PAI-1) in preeclampsia. So preeclampsia is a highly thrombotic and procoagulant state 1 .Fibrinogen is the primary blood clotting factor. Fibrin clot is formed from fibrinogen. Fibrinogen plays a vital role in the process of inflammation, atherogenesis and thrombogenesis. Fibrinogen is a cofactor in platelet activation and may directly contribute to platelet plaque