Platelet aggregation in portal cirrhosis.

Primary and secondary platelet aggregation in response to adenosine diphosphate was studied in 24 patients with portal (Laënnec) cirrhosis and compared with platelet aggregation in 14 normal subjects. In 12 patients with cirrhosis, platelet aggregation was diminished when compared to controls. Of the 12 patients with impaired aggregation, 6 had elevated levels of fibrinogen-fibrin degradation products (FDPs), 11 had thrombocytopenia, 10 had shortened euglobulin lysis times, 11 had prolonged bleeding times, 4 had hypofibrinogenemia, and all had prolonged thrombin clotting times. The data suggest that elevated levels of serum FDPs do not explain fully the impairment of platelet aggregation or the prolongation of the thrombin clotting time that was noted in patients with advanced liver disease. A possible explanation for the prolongation of the thrombin clotting time is the presence of "altered" plasma fibrinogen.

High-dose, brief-duration intravenous infusion of streptokinase in acute myocardial infarction: description of effects in the circulation.

The effects in the circulating blood of a 1-hour intravenous infusion of 1.5 X 10(6) units of streptokinase (SK) were measured during the subsequent 24-hour period in 7 patients with acute myocardial infarction. At the end of the infusion, the activator activity, expressed in SK units, averaged 65 U/ml, all of the plasminogen had disappeared, only a small amount of free plasmin was still present and functionally active alpha 2 antiplasmin had been reduced to 21% of the preinfusion level. All of the native fibrinogen had been degraded and the thrombin-coagulable protein was composed entirely of fragment X species, but the circulating plasma also contained significant amounts of the more extensively degraded fragments Y, D and E. The biologic half-life of the SK-induced activator activity was 23 minutes and that of the fibrinogen degradation products was 6.3 hours. The lytic effects persisted for 4 hours before any signs of recovery from the hemostatic defect were evident; considerable recovery was present at 25 hours.

Detection of fibrin degradation products. A simplified technic.

An agglutination inhibition technic using CrCl3-treated erythrocytes for the quantification of circulating fibrin degradation products in patients with thromboembolic and fibrinolytic states is described.

Serum fibrin/fibrinogen degradation products as a prognostic index in acute myocardial infarction.

A study of the prognostic value of serum fibrin/fibrinogen degradation products (FDP) in 137 consecutive patients with acute myocardial infarction showed a positive correlation between high FDP levels and poor prognosis. Both the frequency of complications and the mortality were related to increased levels of FDP, the highest of which were found between the fourth and eighth days after infarction.

Fibrin-fibrinogen degradation products in cerebrospinal fluid.

An increase in low molecular weight fibrin-fibrinogen degradation products (FDP) was demonstrated in cerebrospinal fluid (CSF) from 17 of 18 patients with bacterial or viral meningitis compared with 29 patients without meningitis. The CSF also showed an increase in coagulation proteins of molecular weight less than 90000 (factors VII, IX, and plasminogen) but did not contain fibrinogen (MW 340000) or plasminogen activator. It is concluded that low molecular weight FDP in the CSF in infective meningitis result from leakage through a damaged blood-CSF barrier rather than from local digestion of fibrin deposited on the meninges.

Relationship between elevated plasma levels of crosslinked fibrin degradation products (XL-FDP) and the clinical presentation of patients with myocardial infarction.

To assess whether the intense thrombotic state known to occur early after the onset of acute myocardial infarction is further exacerbated by impaired intrinsic fibrinolysis, we compared the intensity of fibrinolysis as measured by the level of crosslinked fibrin degradation products (XL-FDP) in plasma with the intensity of thrombosis as assessed by fibrinopeptide A (FPA) in 98 patients with transmural and 14 patients with non-Q wave infarction. Patients without complications of infarction such as shock, mural thrombi, or malignant arrhythmias requiring countershock generally had normal plasma levels of XL-FDP, less than or equal to 300 ng/ml (81% of those presenting less than 8 hours after onset and 66% of those presenting greater than 8 hours after onset) on admission despite elevated FPA indicative of ongoing thrombosis. In contrast, patients with complications generally had elevated levels of XL-FDP greater than 300 ng/ml (80% of those presenting early and 62.5% of those presenting late) and 50% of these patients had marked elevations to greater than 1000 ng/ml. FPA was markedly elevated in patients with complications whether they presented early or late after onset of infarction. Our direct measurements at the time of infarction support previous data indicating that intrinsic fibrinolysis is impaired in patients with acute infarction, despite marked thrombin activity, when complications are not present. However, when complications are present initially, a more exuberant fibrinolytic response is observed perhaps due to thrombosis associated with the complications themselves.

Monitoring of antifibrinolytic therapy following subarachnoid hemorrhage. The importance of CSF fibrin/fibrinogen degradation products.

Ten cases of subarachnoid hemorrhage (SAH) from ruptured cerebral aneurysm are reported. Fibrin/fibrinogen degradation product (FDP) levels were determined simultaneously in blood and cerebrospinal fluid (CSF) at an average frequency of 1.7 days, extended over periods of 8 to 63 days. Successful antifibrinolytic therapy (AFT) correlated with FDP levels in CSF of less than 16 micrograms/ml. Five patients failed to respond to AFT. Levels of FDP in the CSF fluctuated widely in these five patients, and remained at or above 16 micrograms/ml for most of the monitoring period. Blood FDP levels were normal or minimally elevated, and could not be used in predicting or preventing rebleeding episodes. A hypothesis is presented to explain the significance of the presence of FDP's in CSF. In spite of the many techniques employed in monitoring AFT and reviewed in this paper, little information has been gained to improve the results and therapeutic strategies. Among the different methods available, FDP measurements in the CSF have correlated best with rebleeding, and thus may be used in modifying and individualizing therapy. Suggestions are given for future studies.

Effects of protease inhibitors on coagulation abnormalities in acute canine pancreatitis.

Coagulation abnormalities associated with severe pancreatitis were studied in 24 dogs. Group I consists of six control subjects who had duodenotomy alone. Group II consists of six dogs with pancreatitis induced by bile injection ( lcm3 /kg) into the pancreatic duct. The six dogs in Group III and the six in Group IV were given aprotinin (trasylol) 1.0 mg/kg and S-2441 (10mg/kg), a new synthetic protease inhibitor, respectively. These were given over 10 minutes by intravenous infusion, 20 minutes after bile induced pancreatitis. Blood was drawn for amylase, prothrombin time (PT), partial thromboplastin time (PTT), fibrinogen, and platelets, in addition to markers for hypercoagulation, fibrinopeptide A, antithrombin III, and markers for fibrinolysis, B beta 15-42 immunoreactive peptides and alpha 2 antiplasmin at baseline, 30 minutes, 1 hour, 3 hours, 6 hours, and daily for 3 days after injection of bile or duodenotomy. There was no significant difference in PT, platelets, antithrombin III, and fibrinopeptide A among the four groups. Fibrinogen levels and PTT were minimally elevated in animals with bile induced pancreatitis, but these changes reached significance only at 24 hours and 48 hours, respectively (P less than 0.05). Immunoreactive B beta 15-42 became elevated at 30 minutes indicating fibrinolysis in animals with pancreatitis, and these changes were significant compared with Group I control subjects (P less than 0.05) throughout the study. Levels of alpha 2 antiplasmin were decreased in Group II animals with pancreatitis, which also suggests fibrinolysis. Amylase was elevated in Group II animals with pancreatitis (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

High molecular fibrin derivatives in pre-eclamptic and eclamptic patients.

Soluble fibrin monomer complexes were assayed by agarose gel filtration and by ultracentrifugation. Increased values of SFMC were found in the normal third-trimester pregnancies. They were considerably higher in plasma of patients with pre-eclampsia. Concentrations were higher using ultracentrifugation as compared to gel chromatography. Using ultracentrifugation 4 components were identified, indicating that SFMC in this disease are not a homogeneous group.

Screening test for decompression sickness.

The fibrin-fibrinogen degradation products (FDP) tests were studied in 18 patients having a history of illness associated with diving. FDP tests were performed prior to hyperbaric oxygen therapy (OHP). Eight patients were serious neurologic signs had positive FDP tests and required repetitive therapy. Six patients had negative FDP tests with local musculoskeletal complaints and all were asymptomatic following the first OHP treatment. Three patients were found to be suffering from other diseases. These three patients had normal levels of FDP. One patient treated at another facility 3 months earlier and having paraplegia had a positive FDP test. Serious decompression sickness with neurologic complaints appear to have some degree of disseminated intravascular coagulation (DIC) as reflected by the FDP tests. The FDP test appears to be a useful screening test that may be able to delineate therapy.

[Intravascular disseminated coagulation syndrome in patients with acute leukemias]. / Zespól rozsianego krzepniecia sródnaczyniowego u chorych na ostre bialaczki

The author discusses the occurrence of disseminated intravascular clotting syndrome in patients with acute leukaemias in the light of personal material comprising 9 cases. The syndrome may appear as a complication of the main disease or of chemotherapy applied in it. It is most frequent in acute promyelocytic leukaemia and this fact may suggest that promyelocytes play a role in initiation of blood clotting. The problem of diagnosis and treatment of this syndrome in patients with acute leukaemia is discussed.