Fitzgerald factor (high molecular weight kininogen) clotting activity in human plasma in health and disease in various animal plasmas.
Fitzgerald factor (high molecular weight kininogen) is an agent in normal human plasma that corrects the impaired in vitro surface-mediated plasma reactions of blood coagulation, fibrinolysis, and kinin generation observed in Fitzgerald trait plasma. To assess the possible pathophysiologic role of Fitzgerald factor, its titer was measured by a functional clot-promoting assay. Mean +/- SD in 42 normal adults was 0.99+/-0.25 units/ml, one unit being the activity in 1 ml of normal pooled plasma. No difference in titer was noted between normal men and women, during pregnancy, or after physical exercise. Fitzgerald factor activity was significantly reduced in the plasmas of eight patients with advanced hepatic cirrhosis (0.40+/-0.09 units/ml) and of ten patients with disseminated intravascular coagulation (0.60+/-0.30 units/ml), but was normal in plasmas of patients with other congenital clotting factor deficiencies, nephrotic syndrome, rheumatoid arthritis, systemic lupus erythematosus, or sarcoidosis, or under treatment with warfarin. The plasmas of 21 mammalian species tested appeared to contain Fitzgerald factor activity, but those of two avian, two repitilian, and one amphibian species did not correct the coagulant defect in Fitzgerald trait plasmas. (+info)
Coagulation and fibrinolysis in intact hydatidiform molar pregnancy.
Tests of coagulation, fibrinolysis, and platelet function were performed in 17 patients with intact molar pregnancies. Women with intact molar pregnancies had higher fibrinogen factor VIII, and fibrinogen degradation products, concentrations and lower prothrombin, factor X, plasminogen, and plasminogen activator concentrations than controls with normal pregnancies. They also had reduced platelet counts and thromboelastographic values, which indicated hypocoagulability. These results suggest that intravascular coagulation occurs in intact hydatidiform molar pregnancies. (+info)
Values of three coagulation screening tests of precolostral calves.
Prothrombin times, partial thromboplastin times and platelet counts were performed to determine normal values and to screen for coagulation defects of precolostral calves. The precolostral calves were in two groups: one group of a few calves was tested two years before the second larger group. The results for both groups were similar. The tests were performed on postcolostral calves and on mature cows to compare their values with those of precolostral calves. The mean values of prothrombin times and partial thromboplastin times of precolostral calves in the first group were 18.8 seconds and 54.8 seconds respectively. The mean values of prothrombin times and partial thromboplastin times of precolostral calves in the second group were 18.8 seconds and 50.8 seconds respectively. The mean platelet count was 422,400/cmm for the first group and 482,800/cmm for the second group. (+info)
Aetiologies and prognosis of Chinese patients with deep vein thrombosis of the lower extremities.
Deep vein thrombosis (DVT) of the lower extremities is not frequently encountered in Oriental patients. We investigated its aetiology and prognosis in 143 patients (65 males, 78 females), presenting to the National Taiwan University Hospital over 4.3 years, diagnosed by colour Doppler ultrasonography. Swelling and pain of the lower extremities were the most frequent presenting symptoms. The left femoropopliteal veins were more frequently involved than other parts of the lower extremities. In these patients, malignancy with or without intravenous catheterization was the most frequent cause (39 patients, 27%). Other common aetiologies included coagulopathy (29 patients, 20%), immobilization (24 patients, 17%) and catheter-related (13 patients, 9%). No definite aetiology could be determined in 37 patients (26%). During follow-up, 27 patients (19%) died, mostly with malignancy. Pulmonary embolism was noted in 16 patients and was not significantly directly related to death. Compared to similar studies in Caucasian patients, there were significant differences in the aetiology of DVT, with malignancy and coagulopathy more common in these Chinese patients. (+info)
Inflammation, sepsis, and coagulation.
The molecular links between inflammation and coagulation are unquestioned. Inflammation promotes coagulation by leading to intravascular tissue factor expression, eliciting the expression of leukocyte adhesion molecules on the intravascular cell surfaces, and down regulating the fibrinolytic and protein C anticoagulant pathways. Thrombin, in turn, can promote inflammatory responses. This creates a cycle that logically progresses to vascular injury as occurs in septic shock. Most complex systems are regulated by product inhibition. This inflammation-coagulation cycle seems to follow this same principle with the protein C pathway serving as the regulatory mechanism. The molecular basis by which the protein C pathway functions as an anticoagulant is relatively well established compared to the mechanisms involved in regulating inflammation. As one approach to identifying the mechanisms involved in regulating inflammation, we set out to identify novel receptors that could modulate the specificity of APC in a manner analogous to the mechanisms by which thrombomodulin modulates thrombin specificity. This approach led to the identification of an endothelial cell protein C receptor (EPCR). To understand the mechanism, we obtained a crystal structure of APC (lacking the Gla domain). The crystal structure reveals a deep groove in a location analogous to anion binding exosite 1 of thrombin, the location of interaction for thrombomodulin, platelet thrombin receptor and fibrinogen. Thrombomodulin blocks the activation of platelets and fibrinogen without blocking reactivity with chromogenic substrates or inhibitors. Similarly, in solution, EPCR blocks factor Va inactivation without modulating reactivity with protease inhibitors. Thus, these endothelial cell receptors for the protein C system share many properties in common including the ability to be modulated by inflammatory cytokines. Current studies seek to identify the substrate for the APC-EPCR complex as the next step in elucidating the mechanisms by which the protein C pathway modulates the response to injury and inflammation. (+info)
Systemic lupus erythematosus-associated catastrophic antiphospholipid syndrome occurring after typhoid fever: a possible role of Salmonella lipopolysaccharide in the occurrence of diffuse vasculopathy-coagulopathy.
We report a case of well-documented typhoid fever in a 30-year-old woman with inactive systemic lupus erythematosus with asymptomatic lupus anticoagulant and high-titer anticardiolipin antibody (aCL). Despite prompt eradication of the Salmonella typhi obtained with appropriate antibiotic therapy, multiple organ system dysfunction occurred. The central nervous system was involved, with ischemic infarcts in the occipital lobes. High-dose corticosteroid therapy failed to improve the neurologic manifestations, which responded to repeated plasmapheresis. A sharp fall in aCL and anti-beta2-glycoprotein I antibody titers was recorded before the start of plasmapheresis. At the same time, IgM and IgG antibodies to Salmonella group O:9 lipopolysaccharide became detectable; the IgM antibodies disappeared within 4 months, whereas the IgG antibodies remained detectable during the next 13 months. Despite treatment with high-dose corticosteroids and cyclophosphamide, rapidly progressive glomerulonephritis developed, leading to chronic renal failure. There is convincing evidence of a link between the S. typhi infection and the ensuing catastrophic syndrome in this patient, probably precipitated by bacterial antigens. (+info)
Incidence and possible reasons for discordant results between positive FDP and negative D-dimer latex assays in clinical specimens.
In general, FDP and D-dimer values have a correlation in clinical conditions associated with disseminated intravascular coagulation(DIC) or coagulation activation. However, there are some patients with discordant results who demonstrate elevated FDP and negative D-dimer results by latex agglutination assays. The incidence and possible reasons for the discordance between FDP and D-dimer results were investigated through simultaneous measurements (n = 763) from clinical patients with suspected DIC or coagulation activation. 24.8% (189/763) of samples with elevated FDP were negative for D-dimer assays by the latex agglutination method. Further detailed analysis on randomly-selected discordant samples (n = 41) revealed that the most common reason for the discordance was the lower sensitivity of the semiquantitative latex agglutination method for D-dimer, compared with quantitative enzyme or other latex immunoassay. The other contributing factors to the discordance were accelerated fibrinogenolysis without secondary fibrinolysis, elevated soluble fibrin monomer and rheumatoid factor. (+info)
Review: infectious diseases and coagulation disorders.
Infection, both bacterial and nonbacterial, may be associated with coagulation disorders, resulting in disseminated intravascular coagulation and multiorgan failure. In the last few decades a series of in vivo and in vitro studies has provided more insight into the pathogenetic mechanisms and the role of cytokines in these processes. Because of the growing interest in this field, the complexity of the subject, and the fact that many physicians must deal with a variety of infections, current data are reviewed on the association between infectious diseases and the coagulation system. Novel therapeutic intervention strategies that will probably become available in the near future are mentioned, along with those of special interest for infectious disorders for which only supportive care can be given. (+info)