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PubMed1979

Early increase of a new platelet coagulant activity in rats fed a thrombogenic diet.

A recently described platelet coagulant activity (factor X activating activity), whose pathophysiological significance is as yet unknown, was studied in rats fed a fat-rich (thrombogenic) diet for 1, 2 and 7 weeks and compared to rats fed normal laboratory chow. Whatever the duration of the special feeding period, a highly significant shortening of the clotting time, used for measuring this activity, was observed. When the platelet coagulant activity of individual "fat-fed"rats was quantitated by reference to that of individual control animals, we found a mean increase of 350% (n = 9) after one week and 267% (n = 3) after two weeks of dietary treatment. Partial thromboplastin time, thrombin time and soluble fibrin monomer complexes did not differ in control and treated animals. It seems that platelet coagulant activity, as measured in our test system, is one of the first laboratory parameters to be modified by fat-rich diets. These findings may be relevant to an understanding of the role of platelet coagulant activities other than platelet factor 3 in thrombotic phenomena.

Animals↗
PubMed1975

[Influence of cytostatic combination therapy with vincristine sulphate and iphosphamide on blood coagulation].

Disorders of blood coagulation were investigated before and during a cytostatic combination therapy with vincristine sulphate and iphosphamide (Asta Z 4942) in 12 patients with malignant tumours or haemoblastoses. Thromboplastin time, partial thromboplastin time, thrombin time, heat-dependent fibrin, clot retraction, and clotting factors II, V, VIII, IX, X, and the platelet count were determined. A change in the plasmatic coagulation system attributable to the combination therapy could not be demonstrated in any patient. The influence of the cytostatic combination on the platelet-dependent haemostasis was small; a decrease in platelet count could be observed in only one patient, in whom an additional causative damage to thrombopoiesis due to the underlying disease could be assumed. Regardless of the cytostatic therapy there were indications of a hypercoagulability in 10 patients. This explains the increased susceptibility of such patients for thromboses or consumption coagulopathy.

Adult↗
PubMed1978

The Passovoy defect: further characterization of a hereditary hemorrhagic diathesis.

We studied a coagulation abnormality present in 12 members of five kindreds who bruised easily and bled excessively after minor trauma. Their activated partial thromboplastin times were between 32 and 39 seconds (normal, 22.8 to 28.8 seconds). Prothrombin times, thrombin times, platelet-function tests and the levels of factors XII, XI, IX, VIII, prekallikrein and high-molecular-weight kininogen were normal. Within these kindreds inheritance of prolonged partial thromboplastin times followed an autosomal and probably dominant pattern. The prolonged thromboplastin times were corrected by normal plasma and by normal plasma adsorbed with celite, but there was no mutual correction between plasmas of the patients. These subjects shared a common defect in the intrinsic pathway of coagulation that we designate by the proband's surname, Passovoy.

Adolescent↗
PubMedDate not supplied

Gelfoam and autologous clot embolization: effect on coagulation.

An episode of disseminated intravascular coagulation following therapeutic gelfoam embolization to control bleeding from esophageal varices in a patient with liver disease is presented. We have since followed 13 patients prospectively (six control and seven gelfoam/autologous clot) to determine the effect of this procedure on clotting. We were unable to show significant differences between the two groups as measured by the prothrombin time, activated partial thromboplastin time, thrombin time, fibrinogen and platelet count. However, fibrin (ogen) degradation products were significantly elevated (p less than .01) in the gelfoam/autologous clot group. We suspect this occurred secondary to clot lysis at the site of embolization. No subsequent bleeding diathesis attributable to this abnormality occurred in any of the patients.

Disseminated Intravascular Coagulation↗
PubMed1977

Blood coagulations studies in pregnant patients with infective hepatitis.

Coagulation studies were made on 22 pregnant women with acute infective hepatitis and on 15 normal control pregnant women in third trimester. Fourteen hapatitis patients had clinical evidence of liver failure and all of them had a haemorrhagic diathesis; none of the patients without liver failure showed clinical evidence of haemostatic defects. Coagulopathy was present in most patients, its severity being greater in those with hepatic failure. Significant alterations were observed in bleeding time, whole blood clotting time, prothrombin time, thrombin time, plasma fibrinogen and serum levels of fibrinogen degradation products. The last three disturbances were most frequent in patients with liver failure. Increased fibrinolysis and disseminated intravascular coagulation also appeared to play a contributory role, particularly in patients with hepatic failure.

Adolescent↗
PubMed1975

Coagulation studies during experimental hemoglobinemia in humans.

Infusion of autologous hemolyzed blood in humans has served as a model for various experimental investigations for many years. Numerous studies have shown this model to be unattended by any adverse clinical reactions. In this study evidence of subclinical disseminated intravascular coagulation (DIC) was sought in normal humans infused with autologous hemolyzed blood. Hemoglobinemia was induced in 10 experiments by a single injection of frozen-thawed blood and in 4 experiments by such an injection of hemolysate followed by a 5-h maintenance infusion. Mean peak plasma hemoglobin following single dose injections was 540 mg/100 ml, while levels during continuous infusion averaged 240 mg/100 ml. The induction of hemoglobinemia was asymptomatic. Coagulation studies showed no significant alteration in prothrombin time, partial thromboplastin time, thrombin time, clottable fibrinogen, or WBC. Fibrin degradation products were not found. Platelet counts fell slightly in the 5-min postinfusion sample but returned to preinfusion levels within 30 min, suggesting a temporary sequestration of platelets rather than consumption. The induction of moderate brief experimental hemoglobinemia in normal subjects did not result in the development of demonstrable DIC.

Adult↗
PubMed1979

Congenital deficiency of alpha 2-plasmin inhibitor associated with severe hemorrhagic tendency.

alpha(2)-Plasmin inhibitor (alpha(2)PI) is a recently characterized, fast-reacting plasmin inhibitor in human plasma that appears to play an important role in regulation of in vivo fibrinolysis. We report here a case of complete deficiency of alpha(2)PI in man. The patient, a 25-yr-old Japanese man, had a life-long severe bleeding tendency (hemarthrosis and excessive bleeding after trauma). The following tests were within normal limits: platelet count, bleeding time, thrombin time, prothrombin time, partial thromboplastin time, titers of known clotting factors, platelet glass bead retention, Factor VIII-related antigen, platelet aggregation by ADP, collagen and ristocetin, and clot retraction. Routine liver function tests were also normal. The only abnormal finding was that whole blood clot lysis was extemely rapid and was complete in 4-8 h. The concentration of plasma protease inhibitors, including alpha(2)-macro-globulin, antithrombin III, alpha(1)-antitrypsin, and C1INH, were all normal. The concentration of alpha(2)-PI in the patient's plasma, assayed by immunological methods, was <0.1 mg/100 ml (normal concentration, 6.1+/-0.88 mg/100 ml [mean+/-SE]) and functional assays showed a complete deficiency of alpha(2)PI. Addition of purified alpha(2)PI to the patient's whole blood completely corrected the accelerated fibrinolysis. The patient's parents, four siblings, and four other members of this family were asymptomatic, but the titers of alpha(2)PI in their plasmas were congruent with50% of normal pooled plasma. There were three consanguineous marriages in this family, and the alpha(2)PI deficiency appears to have been inherited as an autosomal recessive trait. We speculate that alpha(2)PI deficiency in this patient has led to uninhibited in vivo fibrinolysis that probably causes the severe hemorrhagic tendency. Thus, this study indicates the important role of alpha(2)PI in hemostasis.

Adult↗
PubMed1979

Thrombus weight as a measure of hypercoagulability induced by drugs.

Thrombus weight was used as a measure of the thrombus enhancing effect of drugs in 135 rats. The weight of thrombus formed in one hour, on a 20 x 0.5 mm platinum wire, inserted in the vena cava was taken as a measure of thrombosis. The change in thrombus weight which followed the injection of ellagic acid to activate the coagulation system, adenosine diphosphate to activate the platelets, and epsilon-aminocaproic acid to inhibit the fibrinolytic system, was measured. Pilot studies showed that the drug doses used brought about the appropriate changes in the factors named. The mean thrombus weight in 45 control animals was 1.93 mg. Ellagic acid increased it about five-fold, and epsilon-aminocaproic acid almost two-fold, while adenosine diphosphate reduced it by almost a half. Concurrent controls were used in each case. Clotting tests (whole blood clotting time, kaolin-activated whole blood clotting time, thrombin time, and partial thromboplastin time), performed at the end of the hour, showed no significant correlation with thrombus weight.

Adenosine Diphosphate↗
PubMed1977

Soluble fibrin complexes in early fibrin digests.

Early fibrin digests were analyzed in the ultracentrifuge and were found to contain compounds with molecular weights up to 3 X 10(6); these compounds are considered to be soluble fibrin complexes. Their similarity with intermediate polymers in inhibited clotting systems has been stressed. Their viscosity at low shear rates is extremely high; therefore, a rapid method to establish their presence in plasma would be the measurement of plasma and serum viscosity at low shear rates, moreover, they shorten the clotting time (thrombin time) of fibrinogen considerably.

Animals↗
PubMed1978

Blood coagulation and fibrinolysis in haemorrhagic stroke.

Studies of 11 patients with haemorrhagic stroke revealed no significant change in kaolin cephalin clotting time, prothrombin time, thrombin time, PF 3 availability, platelet count and factor V and VIII during the first week. Plasma fibrinogen was significantly increased while factors VII + X were decreased (borderline significance). Prolongation of plasma recalcification time and decrease in heparin tolerance reached borderline significance. There was moderate, but significant, increase in serum antithrombin activity and plasma (euglobulin fraction) fibrinolytic activity.

Blood Coagulation↗
PubMed1977

The relationship of coagulation factors to clinical complications of acute pancreatitis.

Alterations in coagulation factors have been reported during acute pancreatitis. Therefore the relationship of coagulation measurements to complications of pancreatitis was evaluated prospectively in 35 patients in whom 130 serial coagulation profiles were performed, consisting of fibrinogen, platelet count (PC), fibrinogen-fibrin-related-antigen (FR-antigen), prothrombin time (PT), partial thromboplastin time, thrombin time, euglobulin clot lysis, and Factors II, V and VII-X levels. During attacks of acute pancreatitis, over-all mean initial fibrinogen and PC of 268 mg. per 100 ml. and 214,000 per cubic millimiter rose significantly (p less than 0.005) to peaks of 362 mg. per 100 ml. and 477,800 per cubic millimeter by day 6 to 10. Mean initial FR-antigen of 4.8 microgram per milliliter rose to peak 7.4 microgram per milliliter on day 5. In 21 patients with mild pancreatitis, mean highest fibrinogen, PC, FR-antigen, and PT were 329 mg. per 100 ml., 361,500 per cubic millimeter, 5.3 microng per milliliter and 14.1 seconds. These values were significantly higher (p less than 0.05 to 0.01) in patients with severe pancreatitis, being 422 mg. per 100 ml. 528,000 per cubic millimeter, 13.7 microng per milliliter, and 15.5 seconds, respectively. Evaluation of the relationship of coagulation measurements to early clinical features showd that mean initial fibrinogen levels were significantly higher (p less than 0.05 to 0.01) in patients with initial amylase greater than 1,000 Somogyi units percent, serum glutamic oxaloacetic transaminase (SGOT) greater than 250 S.F.U. percent, and initial 72 hour PAO2 less than 75 mm. Hg. Early hypoxemia also correlated (p less than 0.05) with elevated initial FR-antigen levels. Impaired early renal function correlated (p less than 0.01) with elevated initial PC only. Early hypocalcemia did not correlate with coagulation measurements. These findings demonstrate that marked changes in coagulation parameters occur during acute pancreatitis and are related to over-all morbidity. Correlation of early coagulation measurements with amylase levels and with respiratory, renal, and hepatic dysfunction suggests that enzyme-related intravascular coagulation may be implicated in the pathogenesis of these complications of pancreatitis.

Acute Disease↗
PubMed1977

[Factor XIII deficiency in burns].

In 34 patients with severe burn injuries platelets, fibrinogen, prothrombin time, partial thromboplastin time, thrombin time and factor XIII were measured daily. Half of the patients were administered 15 000 IE of heparin per 24 hours. In the first 4 days there was a rapid fall of factor XIII to a value of approximately 30%. Values remained very low during the whole observation period of up to 20 days. However, in patients treated with heparin, values tended to be 10--15% higher. After an initial decline on the tenth day, the platelets had risen to the lowest normal level. Platelets were identical in both groups. The causes for the changes in these haemostasis parameters, their significance, and possible consequences of therapy are discussed.

Blood Coagulation Tests↗
PubMedDate not supplied

Apgar score and blood coagulation factors.

Blood coagulation tests were performed in 93 newborn infants with different Apgar score at the 1st and 5th minutes of life. The laboratorial determinations were periodically performed at 0, 24 and 48 hours of life. The following tests were performed: bleeding time, whole blood clotting time, prothrombin time, kaolin-cephalin clotting time, thrombin time, dosage of factors I, V, VIII and X, clot retraction, platelet count, englobulin lysis time and the tourniquet test. Immediately after birth, the mean values of the blood coagulation factors were significantly different among the groups, with the exception of the whole blood clotting time and the platelet count. Those differences were due to the presence of the more depressed neonates. Although these results could indicate some degree of hepatic damage, it was apparent that an activation of the blood coagulation mechanisms took place, leading to a consumption coagulopathy. The infants who died (10) presented clinical and laboratorial data suggestive of disseminated intravascular coagulation (DIC). Necroscopic findings of microthrombosis in the liver and in the central nervous system were diagnosed in two infants.

Apgar Score↗
PubMed1976

Platelet aggregation as a sign of septicemia in thermal injury. A prospective study.

Serial measurements of coagulation activity, platelet counts, and platelet aggregation were done in patients with full-thickness burns involving 25% or more of body surface area to detect specific changes that might correlate with the onset of septicemia. Mean and maximal values for prothrombin time, partial thromboplastin time, thrombin time, activities of factor V and factor VIII, and concentrations of fibrinogen and fibrinogen-related antigens observed in the presence of bacterial septicemia did not differ significantly from those observed in the absence of septicemia. Mean platelet counts were significantly less with sepsis, but values in individual subjects were not indicative of the presence of septicemia. By contrast, platelet aggregation in response to adenosine diphosphate, epinephrine, and collagen always became severely abnormal with the onset of septicemia but not in the absence of sepsis.

Anti-Bacterial Agents↗
PubMed1976

Bleeding in uremic patients after carbenicillin.

Hemorrhagic diathesis was observed in patients with renal insufficiency after carbenicillin at serum levels greater than 300 mug/ml. Normal coagulation factors (F. I, II, V, VII, VIII, X), normal PTT, normal platelet counts, negative ethanol gelation test (fibrin monomers) were found as well as a prolongation of thromboplastin time (Quick), thrombin time, reptilase time and thrombin coagulase time. Platelet function was disturbed. In addition, the plasmatic system was involved: inhibition of fibrinogen-fibrin conversion (Belitser assay) and enhanced antithrombin III activity; in vivo the latter was ascribed to a heparin-like activity. In vitro, abnormal III was seen: however an enhanced antithrombin III activity in vitro was not found with carbenicillin and various penicillin derivatives. This study demonstrates that carbenicillin, in addition to its known effect on platelet function, also disturbs the plasmatic coagulation system. This additional effect of carbenicillin is clinically important since protamin chloride effectively blocks bleeding without interfering with antibacterial activity. Both penicillin and penicillin derivatives have been shown to interfere with hemostasis and to cause clinically manifest hemorrhagic diathesis (Fleming and Fish 1947, Lurie et al. 1970a, b, McClure et al. 1970, Yudis et al. 1972, Demos 1971, Waisbren et al. 1971). Carbenicillin interferes with ADP-, collagen- or thrombin-induced platelet aggregation and with the release reaction both in vivo (McClure et al. 1970, Cazenae et al. 1973) and in vitro (McClure et al. 1970, Cazenave et al. 1973). In addition Lurie and colleagues (1970b) concluded that an inhibition of the conversion of fibrinogen to fibrin is involved although no experimental details were given. Later Brown and colleagues (1974) concluded that carbenicillin at usual dose levels "only affects the platelet component of hemostasis and has little effect on fibrin formation or other phases of coagulation in patients with normal renal function".

Adult↗
PubMed1977

[Diagnostic therapeutic problems of defibrination syndrome in shock, sepsis, and neonatal hypoxia (author's transl)].

The diagnosis of defibrination syndrome in shock, sepsis and neonatal hypoxia is based, in addition to the clinical picture, upon a few parameters of the hemostatic system, which, in part as global tests, provide information about the course of coagulation. The parameters measured are partial thromboplastin time, thromboplastin time, plasma thrombin time, fibrinogen, thrombin-coagulase and reptilase times as well as platelet count. Normal values of these laboratory parameters were established for healthy newborns 1--5 days of age, and for healthy adults. It is suggested that especially partial thromboplastin time, the thrombin-coagulase and reptilase times, the latter influenced by fibrinolysis cleavage products, are representative for the tentative diagnosis of disseminated intravascular coagulation with fibrinolysis syndrome (DICFS). The platelet fall often lags 1--2 days behind the event. Moreover normal values for newborns, are markedly higher than those for older children or adults. In the presence of DICFS, a low-dose heparin therapy is immediately initiated. If completed defibrination is manifest, therapy is supplemented with urokinase and streptokinase, For DICFS with congenital sepsis, an exchange transfusion with heparinized fresh blood is the treatment of choice.

Asphyxia Neonatorum↗