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At least 19 recordsLinked to original sources
PubMed1975

Effect of pneumococci on blood clotting, platelets, and polymorphonuclear leukocytes.

Infections due to Streptococcus pneumoniae and products from the organism have been associated with alterations in blood clotting and function of platelets. Pneumococci and pneumococcal polysaccharide shortened the clotting times of whole blood, platelet-rich plasma (PRP), and platelet-poor plasma (PPP) in vitro. Clotting times of PPP and PRP from C6-deficient animals were likewise decreased. The bacteria had no effect on the one-stage prothrombin time or the partial thromboplastin time when the organisms were used as activating agents. Platelets aggregated in the presence of pneumococci, but aggregation was prevented by the addition of cyclic adenosine 3', 5'-monophosphate (cAMP). Furthermore, cAMP corrected the shortened clotting time of PRP in the presence of pneumococci. The clumping and release of polymorphonuclear coagulant that was induced by pneumococci was not prevented by cAMP. Thus, pneumococci exert several dose-dependent thromboplastic effects: (i) release of platelet thromboplastic substances; (ii) a direct thromboplastic effect; and (iii) release of polymorphonuclear coagulant.

Animals↗
PubMed1976

The effect of hemorrhagic shock on disseminated intravascular coagulation.

Experiments tend to confirm the hypothesis that a thromboplastic substance in the blood stream causes little DIC if blood flow is normal. However, if the same quantity of thromboplastic material is present in a slow capillary flow, it will produce DIC and possible death, with a marked clotting defect.

Animals↗
PubMed1976

Pathophysiology of disseminated intravascular coagulation in saline-induced abortion.

Our previous studies suggested that disseminated intravascular coagulation (DIC) may be a sequel to saline-induced abortion. A hypothetical mechanism for the DIC is that hypertonic saline produces cellular disruption in the products of conception with the release of thromboplastic substances into the amniotic fluid. These substances, in turn, diffuse through the damaged membranes into the maternal circulation. To examine this hypothesis we obtained samples of amniotic fluid (AF) from 5 patients just prior to and at 1 hour, 6 hours, and 24 hours after intraamniotic instillation of hypertonic saline. The procoagulant and thromboplastic properties of the various AF specimens were quantitated using the prothrombin time (PT), partial thromboplastin time (PTT), and activated clotting time (ACT) as in vitro test systems. The results indicate that a change in the procoagulant and/or thromboplastic activity of AF following saline instillation is not afactor in the pathophysiology of DIC associated with saline abortion.

Abortion, Induced↗
PubMed1975

Intrauterine death and circulating anticoagulant ("antithromboplastin").

A report is presented of a young, otherwise apparently healthy, woman who had three pregnancies which for some unknown reason terminated in intrauterine death (macerated foetuses). During the third pregnancy a coagulation defect was diagnosed, which was characterized by prolonged coagulation times and prolonged one-stage prothrombin time. This defect disappeared after the end of the pregnancy, but returned during the fourth pregnancy. This time a circulating anticoagulant was found, which inhibited the action of thromboplastin. The values found for the various coagulation factors were normal. The anticoagulant titre rose during the pregnancy from 1/2 to 1/10. Leucocyte agglutinating as well as lymphocytotoxic antibodies directed against the husband's cells were demonstrated in the patient during the pregnancy. In this case, by passage of cell fragments and thromboplastic substances to the mother, the foetus had probably induced the development of antibodies against the foetal tissues. The foetus may be regarded as an incompatible transplant. The fourth pregnancy was terminated by caesarean section in the 34th week. The child weighed 1440 g and, after three exchanges of blood, did very well. The placenta was severely infarcted. It is postulated that the development of antithromboplastin during pregnancy may be a contributory cause of intrauterine death.

Adult↗
PubMed1975

Plasminogen activators in ovarian tumours.

Ovarian tumours obtained at laparotomy were histochemically examined for their local fibrinolytic activity, and simultaneous fibrin/fibrinogen degradation products (FDP) were determined in the serum. The fibrinolytic activity was confined mainly to vessels of both malignant and benign tumours. A very close correlation was demonstrated between the fibrinolytic activity and the vascularity of the sections. FDP were found in the serum in 13 of 14 patients with malignant tumours, but in none with benign tumours. The difference in occurrence of FDP in patients with malignant and benign tumours might be due to the invasive growth of the former with the entrance of thromboplastic substances, fibrinolytic activators or locally formed FDP into the bloodstream.

Biopsy↗
PubMed1973

Fibrinogen-fibrin degradation product levels in different types of intravascular haemolysis.

To examine the possibility that intravascular haemolysis may lead to intravascular coagulation we have compared the degree of fibrin deposition, as measured by levels of serum fibrinogen-fibrin degradation products (F.D.P.), in two different types of intravascular haemolysis associated with red cell fragmentation. F.D.P. levels in 56 patients with intravascular haemolysis secondary to prosthetic heart valves were compared with those in 18 patients who had microangiopathic haemolytic anaemia (M.H.A.) associated with malignant hypertension or renal disease. F.D.P. levels were raised in almost all the patients with M.H.A., and this group had significantly higher levels than any of the valve replacement groups. In contrast, in the prosthetic valve patients F.D.P. levels were usually normal and bore no relation to the degree of haemolysis. It is suggested that in the absence of other precipitating factors intravascular haemolysis will not initiate intravascular coagulation. In M.H.A., while the intravascular haemolysis appears to be a consequence of an underlying intravascular coagulation, it is likely that persistence of the coagulation disturbance is related more to factors such as small vessel damage than to the release of any thromboplastic substances from fragmented red cells.

Adult↗
PubMedDate not supplied

[Observation of D-dimer levels in serum of patients with acute leukemia].

The blood coagulation and fibrinolysis disorders are common complications observed in patients with acute leukemias, particularly in acute myelogenous leukemia. These abnormalities are mediated by thromboplastic substances released from the blast cells and the alteration of hemostatic properties of vascular endothelium. The plasma concentration of D-dimer (cross-linked fibrin degradation products), measured by enzyme immunoassay, using monoclonal antibodies, serves as a specific marker of the coagulation activation and fibrinolysis system. In our study, the plasma concentration of D-dimer was investigated in 142 patients with acute leukemia during clinical course--at the time of initial diagnosis, complete remission, relapse or in cases resistant to chemotherapy. It has been revealed that, at the time of initial diagnosis, the plasma level of D-dimer was elevated in most patients, irrespective of the type of acute leukemia. However, the initially elevated plasma concentration of D-dimer was significantly lower when complete remission had been achieved. Furthermore, in the majority of cases of relapse or resistance to chemotherapy, a further increase of plasma concentration of D-dimer is commonly observed.

Adolescent↗
PubMedDate not supplied

[Composition and various properties of acetylcholinesterase from human erythrocytes].

Composition and some properties of human erythrocyte acetylcholinesterase prepared for use in medical practice were studied. After electrophoresis 5 protein bands, two of which exhibited the enzymatic activity, were detected in the preparation. Three isoenzyme forms of acetylcholinesterase, dissimilar in their electrophoretic mobility, were detected in the preparation by ion exchange chromatography on DEAE Sephadex A-50. The preparation did not contain hemoglobin, thromboplastic substances and group isoagglutinogens A and B.

ABO Blood-Group System↗
PubMed1979

[Disseminated intravascular coagulation in the practice of the pathologist].

Disseminated intravascular coagulation (DIC) of blood develops as a result of a sharp increase in the release of thromboplastic substances. The mechanism of disseminated thrombosis is switched in at the level of the microcirculatory bed with defibrination of the peripheral blood and subsequent hemorrhages and bleedings. The causes of DIC development may include complications of pregnancy and delivery, different kinds of shock including endotoxin shock, hemorrhage, hemolysis. Histomorphological findings in DIC are as follows: hemorrhagic syndrome, fibrin thrombi in capillaries, arterioles and venules of the skin, kidneys, adrenals, hypophysis, gastrointestinal tract, lungs and other organs followed by necroses and hemorrhages in these organs. Clinically, DIC is manifested by symptoms of insufficiency of the affected organs (acute renal insufficiency, Waterhouse-Fridericksen syndrome, etc).

Disseminated Intravascular Coagulation↗
PubMed1981

[Association of disseminated intravascular coagulation and cutaneous crystal cholesterol emboli (author's transl)].

The case of a 72-year-old man with cutaneous cholesterol emboli in association with disseminated intravascular coagulation (D.I.C.) is described. Favouring the crystal cholesterol emboli hypothesis are the livedo reticularis and purpura in the lower extremities, palpable pulses, arterioles containing cholesterol clefts. Favouring the hypothesis of D.I.C. are the purpuric lesions on the ears and nose, acral cyanosis and haemorrhagic bullae on the hands, intravascular fibrinous thrombi, hemostatic abnormalities and the efficacy of heparin. Two pathogenic hypotheses are discussed: 1) "spontaneous" crystal cholesterol emboli have started a D.I.C. following the release of thromboplastic substances; 2) a D.I.C. with its secondary fibrinolysis has provoked a dissolution of the thrombosis which covered the atheromatous plaques and started cholesterol crystal emboli.

Aged↗