1952
DOI: 10.1097/00006254-195208000-00010
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PLASMA Ac-GLOBULIN CHANGES IN PLACENTA ABRUPTIO

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Cited by 3 publications
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“…Jackson , Hartmann, and Busby (1955) observed slightly reduced prothrombin values in plasma in 7 patients with P.S.P.. Sharp, Howie, Biggs, and Methuen (1958) found prolonged one stage prothrombin time in 3 patients with P.S.P. Johnson, Seegers, and Braden (1952) observed a prothrombin level reduced to about 40 per cent. Schneider (1951a) recorded prothrombin values reduced to about 50 per cent of normal in two patients with P.S.P.…”
Section: Previous Investigationsmentioning
confidence: 96%
“…Jackson , Hartmann, and Busby (1955) observed slightly reduced prothrombin values in plasma in 7 patients with P.S.P.. Sharp, Howie, Biggs, and Methuen (1958) found prolonged one stage prothrombin time in 3 patients with P.S.P. Johnson, Seegers, and Braden (1952) observed a prothrombin level reduced to about 40 per cent. Schneider (1951a) recorded prothrombin values reduced to about 50 per cent of normal in two patients with P.S.P.…”
Section: Previous Investigationsmentioning
confidence: 96%
“…11 In this report was de scribed and incorporated the role of the accelerated conversion of prothrombin to thrombin, thus leading to subsequent defibrinogenation and hemorrhagic complications of pregnancy. 11 In 1953, this original work was extended to the clinical field and published by Seegers and coworkers, 12 who developed guide lines for early cesarean section to abort the hemor rhagic syndrome, which they called "defibrination." Major clinical extensions of this initial observation were shortly thereafter reported by Ratnoff and co workers.…”
Section: Historical Perspectivesmentioning
confidence: 99%
“…182 Fetal DIC has also been reported in association with chorioangioma 183 and the retained fetus syndrome with death of a cotwin resulting in DIC with serious organ damage, in cluding bilateral renal cortical necrosis, 184 multicystic encephalomalacia, 185 hydrops fetalis, 178 and other structural defects. [186][187][188] As initially proposed by Seegers and others, [1][2][3] the mechanisms of activation of the coagulation system in obstetric complications appear to be the result of release into the maternal circulation of: (1) amniotic fluid (with activity sim ilar to thromboplastin, platelet factor III or phospholipoprotein); [189][190][191] (2) placental enzymes or tis sues (with thromboplastin-like activity); 21,26173,175 and (3) necrotic fetal tissue or enzymes (with activation of the maternal procoagulant system). 192,193…”
Section: Obstetrical Complicationsmentioning
confidence: 99%