Acquired activated protein C resistance in pregnancy.

Pregnancy induces several haemostatic perturbations. Some authors described possible acquired activated protein C resistance (APCR) during normal pregnancy. We wanted to test this possibility and to evaluate if this acquired APCR might contribute to the known increased tendency to thrombosis associated with pregnancy. To answer the first hypothesis, we tested APCR with standard and with modified (5) APTT assays; to explore the second one, we chose to test some hypercoagulability and hyperfibrinolysis markers, i.e. fibrinopeptide A (FPA), Fragment 1+2 (F1+2) and D-dimers, and to correlate them with APC-ratio.

Hemostasis in children undergoing liver transplantation.

We reviewed the records of 200 children who underwent 238 orthotopic liver transplantations in order to determine which preoperative factors could predict intraoperative blood loss. A coagulation abnormality score (CAS) was calculated by allowing one point for each abnormality in six preoperative coagulation tests. The mean CAS values were significantly greater in children suffering from fulminant hepatic failure (Fulm) or post-necrotic cirrhosis (PNC) and those having retransplantation (ReTx) than in those with disease of other etiologies. No correlation was found between the CAS and the mean blood requirements in the different etiology groups. According to the amount of blood transfused, children could be divided in two groups. Group 1 were those with biliary atresia and ReTx, who received more than 200 ml/kg. Group 2 included those with PNC, Fulm, metabolic diseases, and Alagille syndrome and Byler disease, who received less than 140 ml/kg. The mean CAS was significantly lower and the PT significantly better in Group 1. We conclude that preoperative coagulation tests were weak predictors of intraoperative bleeding. The etiology of the underlying liver disease and previous abdominal surgery play an important role in the occurrence of severe bleeding. Intraoperatively, children presented the same hemostatic changes as adults.

Fibrinolytic defect and chronic low-back pain.

Fifty five patients, with an history of chronic low-back pain, with or without leg pain, took part to the study. The fibrinolytic activity of these patients was studied after a 10 min occlusion test, aimed to enhance the fibrinolytic system. The presence of arachnoiditis was assessed by direct surgical observation or by unequivocal myelography plus CT scanner. The fibrinolytic defect entity appears not to be rare in our chronic low-back pain population and to be common in patients with arachnoiditis, the prevalence of fibrinolytic defect being respectively of 45% (25/55 patients) and of 75% (18/24 patients). The importance of a venous occlusion test to increase sensitivity (rejection of false positive) in the detection of a fibrinolytic defect and the relation between this defect and arachnoiditis, are discussed.

Pharmacokinetics, thrombolytic efficacy and hemorrhagic risk of different streptokinase regimens in heparin-treated acute myocardial infarction.

The systemic activator activity of 4 streptokinase (SK) regimens (250,000 IU intracoronary, group A; 500,000 IU, group B; 1.5 X 10(6) IU, group C; and 30 U anisoylated plasminogen streptokinase activator complex (APSAC) intravenously, group D) was tested with the fibrin plate technique. One hour after initiation of treatment, the activator activity was highest after APSAC (3.6 +/- 0.9 U), slightly but not significantly less after SK 1.5 X 10(6) IU (3.0 +/- 0.7), and significantly less after SK 500,000 IU (1.6 +/- 0.5) and 250,000 IU (0.6 +/- 0.5), p less than 0.001. After SK, activator activity half-lives were 184 minutes (group B) and 169 minutes (group C), and after APSAC 188 minutes (group D). These were all in agreement with greater than 12 hour duration of changes in other markers of systemic fibrinolysis (euglobulin lysis time) and substrates depletion (fibrinogen, plasminogen, alpha 2 antiplasmin). In extended pilot clinical groups given identical thrombolytic regimens during full anticoagulation with heparin, angiographic coronary patency was found in 83% (35 of 42) after intracoronary SK (group 1), in 73 and 75%, respectively, after 500,000 IU (31 of 43) and 1.5 X 10(6) IU (30 of 40) (group 2 and 3, difference not significant) and 80% (8 of 10) after the 30-U bolus of APSAC (group 4). The overall hemorrhagic risk was 24%, equally distributed among the 4 regimens and mostly (91%) related to catheters. The incidence of bleeding unrelated to vessel puncture was 4%; no deaths occurred. It is concluded that APSAC is the most fibrinolytic regimen but its potential thrombolytic superiority over SK remains to be demonstrated.(ABSTRACT TRUNCATED AT 250 WORDS)

[Treatment of the first episode of pulmonary embolism in the hospital. Anticoagulants, anti-platelet aggregation drugs and thrombolysis stimulants]. / Traitement du premier épisode d'embolie pulmonaire en milieu hospitalier. Anticoagulants, anti-agrégants plaquettaires et stimulants lytiques.

The treatment of the first pulmonary embolic accident in Hospital consist in the administration of anticoagulants. Heparin will be first used intravenously or subcutaneously during 10 to 12 days and will be followed by oral anticoagulants (VKA) during 3 to 12 months. These treatments must be controlled following national or international standardized technics and can be associated with antiplatelet drugs or thrombolytic activators. The most important and frequent complications observed are haemorrhages. They are consecutive to a non conformed administration of the drugs or overdosage bound to a non correct control or drugs interferences or to a misappreciated counterindication. They will be corrected in most of the cases by a simple anticoagulant dosage reduction and exceptionally by the interruption of the therapy with administration of antidotes and plasma substitutes. Other complications are extremely rare and bound to the nature of the drugs used.

Clinical and biological activity of the antiplatelet agent suloctidil in treatment of idiopathic recurrent vein thrombosis (I.R.V.T.).

A double blind cross over study with suloctidil (Sulocton, Continental Pharma) and placebo was carried out for 6 months in 31 patients with idiopathic recurrent vein thrombosis. They were previously unsuccessfully treated with vitamin K antagonists (VKA) (18 patients) or acetylsalicylic acid (ASA) (13 patients) combined or not the a fibrinolysis activator (theophylline nicotinate). Clinical features, ultrasonic venous flow and biological parameters were controlled monthly during the 6 month treatment. Relevant improvement of clinical, ultrasonic and biological parameters was only observed under suloctidil therapy: during placebo administration 12 patients developed new thrombotic events complicated in 2 by pulmonary embolism while none occurred under suloctidil therapy.

Effects of suloctidil on platelet survival time following cardiac valve replacement.

Platelet functions and blood clotting parameters were examined in 23 patients with a shortened platelet survival time after cardiac valve replacement. Treatment was given at random: for a first group antivitamin K with suloctidil and for the second group antivitamin K alone. Six weeks of treatment with antivitamin K alone did not induce any significant change in the platelet survival time, platelet retention or platelet factor 4 in plasma. In contrast, the shortened platelet survival time increased significantly after 6 weeks of treatment with suloctidil. Moreover the platelet retention and the amount of platelet factor 4 in plasma were significantly reduced, indicating that normalization of platelet survival is the result of decreased destruction, presumably at the level of the prosthetic surface. The clinical benefits expected from these results remain to be validated by a longer follow up period.