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#26614707   2016/03/10 Save this To Up

The lectin complement pathway serine proteases (MASPs) represent a possible crossroad between the coagulation and complement systems in thromboinflammation.

ESSENTIALS: The lectin pathway's MASP-1/2 activates coagulation factors but the trigger of the activation is unknown. MASP-1/2 activation was assessed by quantifying complexes between MASPs and antithrombin/C1-inhibitor. Activated platelets and fibrin were demonstrated to activate MASP-1 and MASP-2 both in vitro and in vivo. These findings may represent a crossroad between the complement and the coagulation systems.

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#25467084   2014/12/20 Save this To Up

Consequences for the APTT due to direct action of factor XIa on factor X, resulting in bypassing factors VIII-IX.

It has recently been reported that factor XIa can activate factor X directly and can bypass factors VIII-IX. We evaluated the consequences for factor analysis with the one-stage APTT.

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#18677590   2008/08/04 Save this To Up

The neonatal coagulation system and the vitamin K deficiency bleeding - a mini review.

Coagulation factors do not cross the placental barrier but are synthesized independently by the conceptus. At birth, activities of the vitamin K dependent factors II, VII, IX, and X and the concentrations of the contact factors XI and XII are reduced to about 50% of normal adult values. The levels of the factors V, VIII, XIII, and fibrinogen are similar to adult values. Plasma concentrations of the naturally occurring anticoagulant proteins (antithrombin, protein C, and protein S) are significantly lower at birth than during the adult years. Plasminogen is reduced by approximately 50%. Platelet counts are within the normal range, regarding function, however, neonatal platelets seem to be hyporeactive. The von Willebrand factor contains large multimers and its concentration is increased. Properties and functions of vitamin K as well as requirement and plasma concentrations in newborns are reviewed. Regarding vitamin K deficiency bleeding (VKDB), the classical nomenclature is used: "early" (presenting within the first 24 h of life), "classical" (day 1-7 after birth), and "late" (8 days to 6 months). After the presentation of the history of vitamin K prophylaxis, vitamin K levels are described as can be expected after the administration of prophylactic doses at various routes. Subsequently, the actual schedule of vitamin K prophylaxis as recommended by the "Osterreichische Gesellschaft für Kinder- und Jugendheilkunde" is given as follows: i) the oral treatment of healthy full-term babies and orally fed preterm babies, ii) the parenteral treatment of small preterm and sick full-term babies, and iii) the treatment of mothers under medication with enzyme-inducing drugs with vitamin K during the last 15-30 days of pregnancy. The regimes of prophylactic vitamin K treatment of different countries are also given. Finally, the therapeutic use of vitamin K is addressed; the potential use of fresh-frozen plasma, prothrombin complex preparations, and recombinant factor VIIa is discussed.

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#12574817   2003/02/07 Save this To Up

Blood coagulation and fibrinolytic factors in 105 patients with hemorrhagic syndrome caused by accidental contact with Lonomia obliqua caterpillar in Santa Catarina, southern Brazil.

Haemostatic disorders caused by Lonomia obliqua caterpillars has reached epidemic proportions in southern Brazil. Here we evaluated coagulation and fibrinolysis in 105 patients after accidental contact with Lonomia obliqua caterpillars. Global coagulation tests were prolonged in most cases and patients were divided into 3 groups according to fibrinogen (Fg) level: 1.5 g/l (group C). There was a significant reduction of factors V, XIII, VIII and prekallikrein in group A, with no change in factors X, II and von Willebrand factor. Thrombin-antithrombin and prothrombin F1+2 were elevated in most patients. Antithrombin and protein S were not changed whereas protein C levels were reduced in group A. Plasminogen and alfa2-antiplasmin levels were significantly reduced in group A and D-Dimer levels were extremely high in all groups, showing that fibrinolysis had been activated, possibly secondary to fibrin production. Levels of t-PA were normal and PAI-1 was mildly elevated in group A. The platelet count remained above 150 x 109 platelets/ml in 97% of cases. In summary, our results suggest that Lonomia obliqua envenoming is characterized by a consumption coagulopathy and secondary fibrinolysis.

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#12070020   2002/06/18 Save this To Up

Thrombin functions during tissue factor-induced blood coagulation.

Tissue factor-induced blood coagulation was studied in 20 individuals, for varying periods of time during 54 months, in contact pathway-inhibited whole blood at 37 degrees C and evaluated in terms of the activation of various substrates. After quenching over time with inhibitors, the soluble phases were analyzed for thrombin-antithrombin III (TAT) complex formation, prothrombin fragments, platelet activation (osteonectin release), factor Va generation, fibrinopeptide (FP) A and FPB release, and factor XIII activation. TAT complex formation, for 35 experiments, showed an initiation phase (up to 4.6 +/- 0.6 minutes) in which thrombin was generated at an average rate of 0.93 +/- 0.3 nM/min catalyzed by about 1.3 pM prothrombinase yielding approximately 26 nM thrombin. During a subsequent propagation phase, thrombin was generated at a rate of 83.9 +/- 3.8 nM/min by about 120 pM prothrombinase, reaching ultimate levels of 851 +/- 53 nM. Clot time, determined subjectively, occurred at 4.7 +/- 0.2 minutes and correlated with the inception of the propagation phase. The thrombin concentrations associated with the transitions to rapid product formation are 510 +/- 180 pM for platelet activation (1.9 +/- 0.2 minutes), 840 +/- 280 pM for factor XIII activation and factor Va generation (2.2 +/- 0.6 minutes), 1.3 +/- 0.4 nM for FPA release (2.5 +/- 0.7 minutes), 1.7 +/- 0.5 nM for FPB release and prethrombin 2 (2.8 +/- 0.8 minutes), 7.0 +/- 2.2 nM for thrombin B chain (3.6 +/- 0.2 minutes), and 26 +/- 6.2 nM for the propagation phase of TAT formation (4.6 +/- 0.6 minutes). These results illustrate that the initial activation of thrombin substrates occurs during the initiation phase at less than 2 nM thrombin (0.2%). Most thrombin (96%) is formed well after clotting occurs.

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#11098974   2000/12/11 Save this To Up

Contact activation in shock caused by invasive group A Streptococcus pyogenes.

The aim of this study was to characterize abnormalities of coagulation in mice with experimental, invasive group A, streptococcal shock, in an attempt to explain the prolongation of the activated partial thromboplastin time identified in patients with streptococcal toxic shock syndrome.

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#11086223   2000/12/13 Save this To Up

Lonomia genus caterpillar toxins: biochemical aspects.

In 1967 we reported for the first time five cases of an acquired bleeding disorder in humans which developed after contact with saturnidae caterpillars. Since that time, other cases have been reported in Brazil, French Guyana, Peru, Paraguay and Argentina. The caterpillars have been identified as Lonomia achelous (LA) in Venezuela and northern Brazil and as Lonomia obliqua (LO) in southern Brazil. All patients present pain and a burning sensation at the site of contact. Within a few hours hematomas and hematuria are seen in combination with intracerebral and intraperitoneal hemorrhage (in some cases also renal failure). Hematological tests show: mild anemia with leucocytosis; prolonged PT, PTT and ThT; decreased fibrinogen, factor V, factor XIII, plasminogen and alpha2-antiplasmin levels; increased factor VIII:c, von Willebrand factor, and FDPs/D-dimers levels with normal ATIII and platelets. Factor VII, factor II and PC levels varied. Several activities similar to or directed against blood clotting factors have been identified in LA: fibrinolytic enzymes, which degrade fibrinogen producing abnormal FDPs; prothrombin activators: one direct and one factor Xa-like; a thermostable factor V activator; a thermolabile factor V inhibitor; a factor XIII proteolytic/urokinase-like activity; and a kallikrein-like activitiy. In LO three activities have been described: a prothrombin activator called 'Lonomia obliqua prothrombin activator protease' (LOPAP); a factor X activator; and a phospholipase A(2)-like activity called Lonomiatoxin. No fibrinolytic activity has been described in LO. Subcutaneous injection of crude hemolymph and some chromatographic fractions of LA induce a decrease in fibrinogen, plasminogen and factor XIII. Intravenous injection of factor XIII proteolytic/urokinase-like activity induce a dose-dependent thrombolysis with a decrease in plasmatic factor XIII without hemorrhagic manifestations. Intradermal injection of LO bristle extracts in rats and rabbits produce incoagulability whereas intravenous injection of LOPAP induced DIC in mice.

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#1378651   1992/08/20 Save this To Up

Six new cases of a caterpillar-induced bleeding syndrome.

We describe six new cases of a hemorrhagic diathesis induced by contact with Lonomia achelous caterpillars. Onset of clinical bleeding varied between a few hours and 10 days post-exposure. Laboratory coagulation tests showed prolonged PT, PTT and ThT; normal platelets and a marked decrease of fibrinogen, factor V, plasminogen and factor XIII (including its subunits A and S). Factors VII, II and alfa 2 anti-plasmin were variably affected. In addition, activation of the fibrinolytic system and the generation of a procoagulant effect could also be demonstrated. Two cases developed severe hemorrhagic diathesis and one of them died of a cerebral hemorrhage. Different aspects of this rare syndrome are discussed in relation to its complex physiopathology and the variability observed in all clinical and laboratory manifestations. Therapeutic recommendations and some possible hazards following replacement transfusions are also considered.

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#1912663   1991/11/20 Save this To Up

Inherited bleeding disorders.

Congenital bleeding disorders comprise a heterogeneous group of diseases that reflect abnormalities of blood vessels, coagulation proteins and platelets. Studies of these diseases, many of which are rare and several of which result in a mild bleeding diathesis only, have significantly increased our understanding of normal haemostasis. Two lessons have been learned. First, quantitative abnormalities of coagulation proteins and platelets are an important, but not the only, cause of significant haemorrhage; some cases of inherited bleeding disorders reflect synthesis of a dysfunctional coagulation protein or production of abnormal platelets. Diagnostic tests that reflect qualitative abnormalities are therefore important in the evaluation of selected patients with inherited bleeding disorders. Second, in occasional patients the inherited disorder is complex and reflects combined abnormalities of coagulation proteins alone or in association with platelet disorders. In clinical practice it is useful to distinguish disorders that cause significant clinical bleeding from those that cause few or no symptoms. Examples of the former include severe deficiencies of factors VIII and IX, and the homozygous forms of factor II, V, VII, X, XI, XIII, fibrinogen and von Willebrand factor. Comparable platelet disorders include the inherited thrombocytopenias with platelet counts less than 20 x 10(9) litre-1 and the homozygous forms of Bernard-Soulier syndrome and Glanzmann's thrombasthenia. The most frequently encountered mild haemostatic abnormalities include type I von Willebrand's disease, the platelet storage pool deficiency syndromes and the mild and moderate forms of haemophilia A and B; occasionally heterozygous or homozygous forms of the rarer coagulation disorders, e.g. factor XI deficiency, may present with a mild bleeding diathesis. Finally, some disorders are entirely asymptomatic, e.g. factor XII deficiency and deficiencies of other contact coagulation factors. Management of patients with inherited bleeding disorders should reflect knowledge of the specific disorder to be treated plus careful consideration of the clinical circumstance for which therapy is proposed. In all cases, once a decision to treat has been made, the safest efficacious therapy should be given (for example DDAVP in the treatment of patients with mild haemophilia A or type I von Willebrand's disease). Although blood products are now much safer and the risk of blood transmitted viral infections is low, there still remains a risk that transfusion of any blood product may be associated with serious side-effects. As a result, therapy should be given only after careful consideration of the risk: benefit ratio and not merely to treat an abnormal laboratory result.(ABSTRACT TRUNCATED AT 400 WORDS)

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#2287954   1991/03/28 Save this To Up

Congenital coagulation protein deficiencies in the perinatal period.

Less common than acquired bleeding disorders in the perinatal period, congenital deficiencies of the clotting proteins, particularly the hemophilias A and B, can be just as devastating. Detection of these disorders may be delayed because a suspect family history is lacking in up to one third of the cases of hemophilia, and parents are usually asymptomatic in the other congenital factor deficiencies. Physiologically low levels of the liver-dependent and contact factors can make the interpretation of the common hemostasis screens difficult. Hence, the use of age-adjusted tables such as those presented here is essential. Congenital deficiencies of clotting proteins should be suspected when serious CNS bleeding occurs in an otherwise healthy baby generally after a day or two. Factor XIII or other less common factor deficiencies should be sought when there is prolonged bleeding from the umbilical stump. Bleeding after circumcision is a rare early indicator nowadays with better techniques. The availability of bedside ultrasound to detect CNS hemorrhage early and of fresh frozen plasma for treatment preceding the results of specific factor assays should prevent serious sequelae. Elective cesarean section is currently recommended when an unborn infant is known to have hemophilia.

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