bluuebunny/crossref_metadata_2025_split huggingface dataset:
INCIDENCE OF DEFECTIVE T-PA RELEASE IN 158 UNRELATED YOUNG PATIENTS WITH VENOUS THROMBOSIS IN COMPARISON TO PC-, PS-, AT III-, FIBRINOGEN- AND PLASMINOGENDEFICIENCY
Authors: Scharrer I , Hach-Wunderle V , Heyland H , Kuhn C 
Published: August 2018

The incidence of defective T-PA release in 158 young unrelated patients (<45 years old) with deep vein thrombosis was studied and compared to that of PC-, PS-, AT III-, fibrinogen- and plasminogen deficiency. Thrombotic episodes were documented using venography with contrast medium. Venous occlusion test (VO) over 20 min. was performed in all patients, 8-12 weeks after thrombosis. T-PA antigen (Biopool kit) , T-PA activity (on fibimplates) and PAI (T-PA-inhibitor, Biopool kit) were measured before and after VO in the fasting morning samples. Furthermore we investigated the functional and immunologic levels of PC,PS,AT III, fibrinogen and plasminogen. We detected 28 patients (15 females, 13 males)= 17.7% with abnormal T-PA release. In these patients the VO test was repeated three times in an interval of 6-8 weeks. Release of T-PA activity and T-PA-Ag was diminished in all these patients. PAI levels were enhanced in 12 of these 28 patients. The rate of recurrency of thrombosis was 52%. A family history of thrombosis was reported only in 20%The incidence of PC def. was 9.4%, of PS def. 6.3%, of AT III def 5%, of dysfibrinogenemia 0.6% and of plasminogen def. 1.2%. No combined defect of abnormal T-PA release with other known hereditary coagulation or fibrinolysis disorders could be detected.In 11 healthy volunteers we investigated 4 different time periods of VO, 5, 10, 15 and 20 min. in an interval of 10 days in order to find the suitable time for VO. It was striking that T-PA activity (on fibrin plates) did not decrease to the same extent as T-PA-Ag. The different behaviour is demonstrated on table 1. Decrease in % is compared to the values of 20 min. VO.
URINARY FIBRINOPEPTIDE A IN A HEALTHY POPULATION AND IN PATIENTS WITH PERIPHERAL VASCULAR DISEASE
Authors: Dawes J , Drummond D , Goodfield N 
Published: August 2018

Urinary fibrinopeptide A (FpA) concentrations may be a useful clinical marker of the activation of coagulation. They are not susceptible to false positives resulting from ex vivo activation, and sampling is noninvasive.Individual urine voidings were collected from cohorts of 30 healthy subjects in each age decade from birth to 70 years, and a further 24 between 70 and 100 years. Below the age of 70 the urinary FpA concentration was 1.72 ± 0.76 ng/ml, and there was no effect of age or sex. Within this population, 4% of samples contained FpA concentrations above the upper limit of normal (mean + 2.5 SD); intensive investigation of one case failed to reveal any renal or coagulative disorder, though the urinary FpA levels remained high (8.4 − 14.2 ng/ml). Above 70 years old, 29% of urinary FpA concentrations exceeded the upper limit of normal established on a younger population. Thus, urinary FpA does increase with advanced age, but this may well result from occult diseaseSampling of every urine voiding over 48h in 3 healthy individuals established that there is no diurnal pattern either in urinary FpA concentration or in rate of FpA excretion. Urinary FpA was unaffected by the phase of the menstrual cycle. Urine samples from patients with peripheral vascular disease were assayed, and 24% contained elevated concentrations of FpA. Urinary FpA is probably a valuable marker of low grade activation of coagulation, particularly in chronic conditions where the assay of plasma samples is frequently uninformative
BIOLOGICAL PRETHROMBOTIC MARKERS AND COAGULATION INHIBITORS IN NEPHROTIC SYNDROME
Authors: Picard P , Borg J Y , Vasse M , Boudhabhay D , Soria J , Fillastre J P , Soria C , Hannedouche T , Godin M , Monconduit M 
Published: August 2018

Nephrotic syndrome (NS) has long been recognized as a clinical prethrombotic state, because of severe thrombo-embolic complications. But underlying mechanisms are still poorly defined. In 56 untreated nephrotic adult patients (most of them without renal failure), we investigate in vivo coagulation activation by measuring 0 plasmatic specific fibrin degradation products (FbDP) (immuno-enzymological assay using a monoclonal anti D-neo antibody) and (2) the ratio of factor VII coagulant activity (V11c) to factor VII:Anti gen (VII;Ag) tested by an ELISA method. We examined coagulation inhibitors in plasmas and urines (antithrombin III—AT III, heparin cofactor II-HC II by amidolytic and laurell methods; protein C-PC by an ELISA assay ;free and bound protein S—PS:Ag by laurell assays). In few patients we also determinecjfribronectin and t-PA inhibitor.Results in plasma are submitted and expressed as mean ± DS and compared (t test) with controls (C) without nephropathySignificantly elevated activated factor VII and FbDP levels show an “in vivo activation” of coagulation in NS. Plasmatic fibronectin, HC II, PC:frg, and tPA-I levels are alsp significantly elevated and roughly paralleled fibrinogen (6,25 ± 2,9 g/1) and other acute-phase proteins measurements. Significant amounts of AT 111:Ag were present in about half tested urines, but in a degraded form with low or absent heparin cofactor activity. Mean plasmatic AT III concentration was in normal range, but three of the 4 patients with a thrombotic disease had the lowest values of AT III and the highest fibrinogen levels.We could demonstrate a biological prethrombotic state in NS and suggest the way of identifying patients with high risk of thrombosis.
COAGULATION AND FIBRINOLYSIS IN SICKLE CELL DISEASE
Authors: Dautzenberg M D , Monge F , Fischer A M , Girot R , Cornu P 
Published: August 2018

Sickled erythocytes appear to be primarily responsible for occlusion of microvasculature in patients with homozygous sickle cell disease (SCD), but it is unknown whether the activation of the coagulation pathway is also contributory to these vaso-occlusive crisis and other complications as leg ulcers, aseptic necrosis of bone, strokes. Thus, we studied coagulation and fibrinolysis parameters in 12 patients (ages 2 to 26 years with SCD, in steady-state, far from thrombotic events which occurred in 3 of them) to determine if it would be possible to detect a high-risk group for thrombosis. We were surprised to observe that all the vitamin K dependent factors levels (II, VII+X, IX, protein C) were found next to the lowest values of the normal range.But in 3 out of 12 patients, protein C was significantly lower and 2 of them have had thrombotic events (stroke, leg ulcers). Factor V level was in the normal range except for 3 patients with low levels. As other authors, we observed normal fibrinogen, plasminogen and a 2 antiplasmin values and always very high factor VIII levels. Antithrombin III activity was normal or even high contrasting with the lower levels of the other factors synthesized in the liver. However all these abnormalities seem to balance since the thrombin generation test performed in the patients plasmas are in the normal range. As a marker of high-risk group for thrombosis, fibrin-D-Dimer levels (using a latex bead agglutination assay) were measured and found to be positive in 4 patients, 3 of them having suffered from thrombosis associated in two cases with a protein C deficiency. Thus, if the hemostatic modifications observed are involved in the mechanism of thrombosis, fibrin-D-Dimer and protein C seem to be the most significant parameters in this study.
ALTERATIONS OF THE HAEMOSTATIC SYSTEM IN SEVEN PATIENTS WITH HOMOCYSTINURIA
Authors: Stenzier W , Ostermann H , Ullrich K , van de loo J 
Published: August 2018

Homocystinuria is an inborn error of methionine metabolism accompanied by an increased risk of thromboembolism. Seven patients (5 female and 2 male) aged 16 to 25 years were investigated. Some showed highly pathological homocystine serum levels during the last year despite treatment. One patient’s history revealed a thrombotic event. All patients were studied for changes in coagulation and the platelet and fibrinolytic systems (the latter before and after venous occlusion). Among the data obtained the following were pathological:After venous occlusion normal values were obtained. These findings show a weak activation of both coagulation and the fibrinolytic system suggesting a prethrombotic state with consumption of protein C. It remains unclear whether the activation of the fibrinolytic system reflects endothelial cell damage associated with homocystinuria or a reaction to the activation of the coagulation system.
STUDY OF THE PROCOAGULANT ACTIVITY OF ASCITIC FLUID
Authors: Rodzynek J J , Van Rissenghem C , Leautaud P , Delcourt A 
Published: August 2018

The aims of the study were to determine the nature of the procoagulant activity present in the ascitic fluid and the means to inhibit the thrombotic complications appearing after peritoneovenous shunting. In a prospective study, 10 ascitic fluids (5 exsudates, 5 transsudates) were studied. The procoagulant activity was defined as the capacity of ascitic fluid to shorten the recalcification time of a control plasma.Our results showed :1. All the ascitic fluids exhibited a procoagulant activity.2. The procoagulant activity of the cellular fraction was related to the presence of platelet factor 3 (PF3) and polymorphonuclear elastase and may be inhibited by the combination of inhibitors of PF3 (phospholipase A inhibitor calbio-chem) and elastase antibody.3. The procoagulant activity of the free cellular fraction was related to the presence of thrombin, factor Xa, PF3 and tissular thromboplastin, and may be inhibited by a combination of Antithrombin III, phospholipase A and Diisopropyl-fluorophosphate.Conclusion :1. The important procoagulant activity of ascitic fluid is present in both cellular and acellular fractions and is related to the presence of different coagulation activators (PF3, elastase, Xa, thrombin, tissular thromboplastin).2. The administration of a combination of AT III and phospholipase A in the ascitic fluid before the contact with the whole blood allows to inhibit the procoagulant activity of ascitic fluid and could prevent the thrombotic complications appearing after peritoneovenous shunt.
FIBRINOLYSIS AND HAEMOSTASIS DURING ASCITES RECIRCULATION
Authors: Cooper P C , Triger D R , Kennedy H , Malia R G , Preston F E 
Published: August 2018

The use of ascites recirculation in liver disease removes litres of incapacitating fluid and the patient is reinfused with the concentrated ascites, a rich source of albumin. Ascites is thought to contain plasminogen activator (PA) which may further affect deranged haemostasis in these patients. We have examined the effect that ascites recirculation has on levels of tPA, fibrinogen, FDP and platelet count on samples taken pre and approximately 4 hours into ascites recirculation. Using plasminogen rich fibrin plates we were able to demonstrate PA in unfractioned ascitic fluid (N=10, mean diameter lysis=10.2mm); this activity was quenched by addition of antibody to tPA (mean diameter lysis=0.2mm). Despite demonstrating tPA in unfractioned ascitic fluid, we were unable to demonstrate an increase in plasma tPA, mid recirculation, using a sensitive chromogenic assay (pre, geometric mean tPA = 0.061Iu/ml; mid, geometric mean tPA = 0.024Iu/ml). In addition we have also measured the effect that an intra-abdominal injection of the glucocorticoid, dexamethosone (dex), 24 hours prior to recirculation, has on PA content of the ascites, as well as the effect on coagulation screening tests. Fibrin plate lysis showed only a small, though significant reduction in mean lysis diameter in 9 of 10 patients receiving dex, (mean 11.6 to 10.2mm). Results of the coagulation tests showed marked changes during recirculation which were similar in both groups.In conclusion, we have demonstrated free tPA in unfractionated ascites fluid of patients with liver disease, and shown a small reduction in tPA level 24 hours post injection of dex in ascites. Dexamethosone did not influence the changes in coagulation profile post recirculation. We suggest that the changes in coagulation are not due to primary fibrinolysis, but may be due to either dilution effect or DIG.
EVIDENCE AGAINST DIC IN LIVER CIRRHOSIS
Authors: Fiori G , Mombelli G , Haeberli A , Straub P W 
Published: August 2018

To evaluate the hypothesis of disseminated intravascular coagulation (DIC) in liver cirrhosis (LC), we measured the plasma levels of fibrincpeptide A (FPA) and of fibrinogen-fibrin degradation fragment E (FgE) in 58 patients with LC, and compared the results with those measured in 32 healthy subjects as well as in 42 patients with ongoing fibrin formation and lysis related to acute thromboembolism (TE, n = 33) and overt DIC (n = 9).Results: Mean plasma FPA in LC was 2.4 ng/ml compared to 1.8 ng/ ml in normals (p < 0.05) and 12.2 ng/ml in patients with TE or DIC (p < 0.0001). Mean plasma FgE in LC was 108 ng/ml compared to 31.2 ng/ml in normals (p < 0.0001) and to 616 ng/ml in patients with TE or DIC (p < 0.0001). 15 patients with LC (26%) had hypo-fibrinogenemia (fibrinogen< 1.7 g/L). Among these patients, plasma FPA and FgE were 2.3 and 134 ng/ml, as compared to 22.1 and 1310 ng/ml in patients with hypofibrinogenemia related to DIC (p < 0.0001). Intravenous heparin (60 IU/kg) resulted in a prompt decrease of plasma FPA in 14 patients with TE or DIC from 11.8 to 4.3 ng/ml (p < 0.005), but did not significantly change the FPA level in 15 patients with LC as well as in the healthy subjects. Discussion: The present data indicate that thrombin mediated proteolysis of fibrinogen is only marginally increased in LC regardless of whether hypofibrinogenemia is present or not. The data are strongly against the hypothesis of DIC as a frequent and quantitatively important complication of LC and substantiate the conclusion that a “oonsunption coagulopathy” is not a major determinant of impaired hemostasis in liver cirrhosis.
USEFULNESS OF FOLLOW UP OF ANTIGENIC AND FUNCTIONAL LEVELS OF PROTEIN C AND FACTOR VII FOR EARLY DIAGNOSIS OF LIVER TOXICITY
Authors: Scrobohaci M L , Drouet L , Bertin L 
Published: August 2018

Protein C (PC) and Factor VII (F VII) are both vitamino-K dependent factors with similar short half-life. Differential behaviour of both factors in their two expressions was assessed on :- 16 resolutive liver toxicity due to reinforced chemotherapy,- 7 specific liver toxicity of Asparaginase or Bisanthrene- 6 veno-occlusive disease complicating an allogenic bone marrow transplantation- 5 cirrhotic liver insufficiencies- 10 patients submitted to stabilised treatment by oral anticoagulant- 3 families of congenital deficiencies in F VII.In case of congenital deficiency in F VII, both expressions of this factor were parallely decreased and PC was normal. During anti-vitamin K therapy, functional levels of PC and F VII were parallely decreased, more profondly than antigenic dosages. In case of severe liver insufficiencies both expressions of both factors were parallely decreased. Evoluated V0D behaved as severe liver insufficiency. Onset of therapy by asparaginase and bisanthrene, resolutive toxicity due to reinforced chemotherapy and early phase of the V0D were characterized by a decrease of the functional activities of these factors before molecular decrease and despite a systematic preventive treatment by injection of vitamin K. Often one of these factors was more affected than the other (in these cases : PC more often than F VII). The ratio activity/antigenicity of these factors proved to be an early and sensitive marker of liver involvement. Changes occured earlier than modifications in prealbumin or in liver enzymes. Considerations of these tests to follow liver functions and specially to assess early diagnosis of VOD must be considered.
PESTICIDE INDUCED CHANGES IN COAGULATION AND FIBRINOLYSIS IN EXPERIMENTAL ANIMALS
Authors: Grover Anjana , Pandey K C , Satija N K , Rai R M 
Published: August 2018

A relationship between the quality of environment and incidence of human health has been recognized in recent years. While the diseases such as carcinogenesis, respiratory diseases, skin disorders are often correlated with exposure to environmental toxins, the possibility of a link between blood coagulation and chemical contaminants in food, water and air has rarely been suspected. Wide usage of DDT in public health and plant protection programmes have led to a considerably higher levels of the pesticide in the blood and body fat of Indian population. Therefore, in order to explore the possibilities of an alteration in blood coagulation and fibrinolysis in response to pesticide insult, a study was undertaken in experimental animals.Adult male albino rats were administered technical grade DDT, 100 mg per kg body weight i.p. for 3 consecutive days for acute exposure study and fed food containing the pesticide at a concentration of 100 mg per kg diet for a duration of 90 days for chronic exposure. Coagulation and fibrinolytic status was assessed at the end of exposure period. Acute exposure to DDT significantly increased platelet count but decreased wall adherence of blood while chronic exposure to DDT elevated platelet counts by 21% and increased wall adherence of blood by 28%. Plasma clotting times were found to be shortened considerably both in acute and chronically exposed animals. DDT seemed to activate both extrinsic and intrinsic pathway of coagulation as evident by marked acceleration in prothrombin time and partial thromboplastin time. Plasma fibrinogen concentrations were found to be higher by 31.6% in rats given acute treatment but 40% lower in chronically exposed animals. A marked increase in fibrinolytic activity was observed in both acutely and chronically exposed animals. Thus, administration of chlorinated pesticides like DDT seemed to have a prothrombotic effect in experimental animals.
COAGULATION ABNORMALITIES IN LEAD EXPOSED RATS
Authors: Satija Narendra Kumar , Singh Har Bhajan , Grover Anjana , Rai Ram Mohan 
Published: August 2018

The accelerated rate of development of modern technology has greatly expanded the range of health hazards. Lead, a widely used industrial material, is a significant environmental pollutant that contaminates food, water, soil and air. Although much progress has been made in elucidating its adverse effects on various systems of the body like hepatic, CNS, renal etc., its effect on coagulation remains to be established. In view of this an experimental study was carried out in animals to understand how lead influences hemostasis.Male albino rats were exposed to lead either acutely by administering 20 mg lead acetate per kg body weight daily i.p. for 3 days or chronically by administering lead through drinking water containing 5 ppm lead for 150 days. Acute exposure to lead caused severe coagulopathy characterized by significant prolongation of plasma recalcification time, decrease in platelet count and decreased wall adherence of blood, decreased fibrinogen and euglobulin lysis time and significant increase in prothrombin time, thrombin time, and partial thromboplastin time. Similar observations were found in chronically exposed animals. It is concluded that exposure to heavy metals like lead may lead to a state of hypocoagulability.
LOW MOLECULAR WEIGHT HEPARIN, STANDARD HEPARIN AND ANCR0D AS ANTICOAGULANT FOR EXTRAC0RP0REAL MEMBRANE LUNG CO2 REMOVAL IN DOGS
Authors: Reber G , de Moerloose Ph , Sinclair M , Schweizer A , Gardaz J P , Bouvier C A 
Published: August 2018

A low molecular weight heparin (LMWH, Sandoz), a standard heparin (SH, LiqueminR) and ancrod (Arvin^)have been compared in an extracorporeal veno-venous bypass for CO2 removal using a membrane lung in dogs. Four animals received 150 anti-FXa U/kg in bolus followed 90 min later by 40 anti-FXa U/kg/h of LMWH and four other 300 IU/kg followed by 100 IU/kg/h of SH. Six dogs received 1 U/Kg of ancrod intravenously during 2 h before bypass started.Mean FXa inhibition was 49% in LMWH group and 29% in SH group, mean FI la inhibition 31% and 49% respectively. No statistically significant differences were found between LMWH and SH groups for any of the parameters measured (fibrinogen, FV, antithrombin III, plasminogen, α 2-anti piasmin, platelet counts). At the end of bypass 5000 U protamine abolished both anti-FXa and anti-FIIa activities in SH group, but failed to neutralize more than half of anti-FXa in LMWH group. In ancrod group no clottable fibrinogen was detectable. A dramatic fall of α2-antiplasmin was observed after ancrod infusion and, during bypass, sharp decreases in FV and platelet counts without significant antithrombin III and plasminogen consumption were noted.No bleeding occurred in any group throughout the seven hours of bypass. The main finding was fibrin deposition in the tubing in three out of four dogs receiving LMWH, whereas no fibrin deposition occurred either in SH or in ancrod group.These results suggest that in this model which involves blood contact with artificial surfaces (1) SH and ancrod are efficient to prevent clotting, but not the LMWH used at the dosage reported (2) high anti-FIIa activities are required to prevent fibrin formation (3) ancrod defibrination does not protect against severe haemostatic disturbances and (4) the use of LMWH may raise problems when emergency neutralisation procedures are required.
THE THROMBOGENICITY OF PTFE ARTERIAL GRAFTS INCREASES IN THE WEEKS FOLLOWING IMPLANTATION
Authors: Chidlow A , Meek A C , Lane I F , Pate P , McCollum C N 
Published: August 2018

Despite few failures in the initial weeks, polytetrafluoro-ethylene (PTFE) femoro-popliteal grafts, which have a non-thrombogenic flow surface, frequently occlude between 2 and 6 months following implantation [1]. Radiolabelled platelet uptake was studied during this risk period.In 20 greyhounds, 6cm lengths of 6mm PTFE were implanted in the femoral artery and autologous 111In-platelet accumulation measured 1 and 8 weeks later. Radioactivity over the graft was compared to the contralateral thigh and the daily rise in this ratio expressed as the Thrombogenicity Index (TI). At 8 weeks the graft was excised, 111In-platelet content counted in a well crystal and pseudointimal hyperplasia measured by grid microscopy.Mean (± sem) TI of 0.054±0.02 at 1 week almost doubled in the grafts that remained patent at 8 weeks to 0.10±0.02 (p<0.05). Radioactivity on the excised grafts was 0.012±0.0027 percent of injected activity and this correlated closely with TI at 8 weeks (r=0.83, p<0.001). Even in grafts remaining patent, this late accumulation of radiolabelled platelets correlated closely (r=0.63, p<0.02) with pseudointimal hyperplasia which narrowed the graft by a mean of 18±4.7 percent of luminal area.PTFE grafts had a low initial thrombogenicity which increased by the second month. This rising thrombogenicity, which presumably follows luminal deposition of fibrin and platelets, is associated with pseudointimal hyperplasia which may explain why these grafts frequently occlude in the months following discharge from hospital.1. Veith FJ, Gupta S, Daly V. Management of early and late thrombosis of expanded PTFE femoro-popliteal bypass grafts. Surgery 1980; 87: 531-587.