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PubMed1987

[Homozygous infant in a family with hereditary protein C deficiency].

We report on a female infant homozygous for protein C deficiency in a Jordanian family with frequent intermarriage. A protein C antigen of 0.6% was determined. The parents first noticed painful nodular indurations in subcutanous tissue as well as blue-red skin coloration at the age of 6 months. The girl repeatedly suffered from microthrombotic events in parts of the body with large areas of subcutaneous fat. In contrast, the numerous heterozygous carriers with partial protein C deficiency did not show an increased tendency to thrombosis. From the history an autosomal-recessive inheritance may be inferred. Other authors reporting on homozygous cases also postulate the presence of a recessive gene. It is of interest that the infant described here differs from those in other case reports in the age at manifestation of the disease. The homozygous infant showed the first symptoms as late as the age of 6 months, whereas other case reports describe severe symptoms immediately after birth. All symptoms of disease were treated successfully with prothrombin complex concentrate without additional heparin protection. Microthrombotic events subsided quickly, and a large ulcer in the left flank healed almost completely within 6 days.

Adult↗

PubMed2003

Treatment of patients with haemophilia and inhibitory antibodies.

The development of inhibitory antibodies is a complication which arise in approximately 10% of patients with haemophilia A. The underlying genetic mutation is the single most important predisposing cause, although other risk factors have been identified. Periodic screening for inhibitors is a vital aspect of haemophilia care. The consequences of inhibitor development are very significant in terms of morbidity and cost. Several agents are now available for control of bleeding, but these are often very expensive. The most useful agents include recombinant activated factor VII, prothrombin complex concentrates and porcine factor VIII. It is possible to suppress antibody production with immune tolerance, which is successful in approximately 85% of cases and relapse is rare.

Blood Coagulation Factor Inhibitors↗

PubMed2006

Perioperative management of patients receiving vitamin K antagonists.

PURPOSE: As the number of patients taking vitamin K antagonists (VKA) is growing, the clinician is increasingly faced with having to make decisions regarding anticoagulation therapy before, during and immediately after surgery. In this article we review the indications for VKA and assess their use in the perioperative period based on available pharmacological and clinical data. SOURCE: An on-line computerized search of Medline was conducted limited to English and French language articles. The bibliographies of relevant articles and additional material from other published sources were retrieved and reviewed. PRINCIPAL FINDINGS: Assessment of patients taking VKA who need surgery must include three factors: 1) the indication for anticoagulation, which determines the thromboembolic risk; 2) the pharmacokinetics of VKA, which determine the moment at which treatment should be discontinued; and 3) the type of surgery, which determines the hemorrhagic risk. Some patients will need to stop VKA treatment and start a substitution or "bridging" anticoagulant therapy, such as unfractionated heparin or low molecular weight heparin, prior to and after surgery. In patients requiring emergency surgery, prothrombin complex concentrate can be used to improve coagulation and is preferable to, although more expensive than fresh frozen plasma. CONCLUSIONS: For the perioperative setting, further studies are required to determine the optimal substitution ("bridging") regimen and the clinical circumstances that necessitate substitution therapy.

Anticoagulants↗

PubMed2000

[Acquired inhibitory body hemophilia].

Although autoantibodies against factor VIII or factor IX are a rare phenomenon, they are associated with a high risk of bleeding and high mortality. The condition, termed acquired haemophilia, occurs equally in both sexes and is most frequent in higher age groups. Patients typically present with severe bleedings in muscles and skin. In contrast to patients with congenital haemophilia and inhibitors, joint bleedings are very rare. In approximately half of all cases an associated disease state can be identified as the cause of autoantibody formation. An immediate and comprehensive diagnosis is essential for a rapid initiation of therapy. Equally important are a careful diagnostic differentiation between congenital and acquired factor deficiencies and the exclusion of non-specific inhibitors, which increase the occurrence of thrombolic events. The inhibitor titre, quantified using the Bethesda assay, is an important criterion for selecting the appropriate therapy. A wide range of treatment options is now available for the management of bleedings in patients with acquired haemophilia, namely porcine factor VIII, recombinant factor VIIa, prothrombin complex concentrates, and immunoadsorptions. In addition, immunosuppressive therapies are used to achieve permanent reduction or elimination of inhibitors.

Autoantibodies↗

PubMed2005

[Avoiding emergency situations under anticoagulant therapy with vitamin K antagonists].

Despite 50 years of clinical experience with vitamin K antagonists such as phenprocoumon or warfarin, many clinicians are uncertain how to start treatment, deal with overdose or bleeding complications, and how to bridge anticoagulation when treatment with vitamin K antagonists is interrupted. Patients with overdose of vitamin K antagonists or bleeding complications are treated with vitamin K, prothrombin complex concentrates (PCC), or recombinant factor VIIa. Rapid reversal of anticoagulation is only achieved by using PCC or recombinant factor VIIa. Both should be combined with vitamin K for a sustained effect. For elective surgery, treatment with vitamin K antagonists is paused and vitamin K given either orally or intravenously. Unfractionated or low molecular weight heparin is given when INR levels are below therapeutic range. Patients with contraindications to heparin may be treated with alternative anticoagulants such as danaparoid, lepirudin or fondaparinux.

Anticoagulants↗

PubMed1999

Emergency correction of coagulation for mitral valve replacement in an orally anticoagulated 17-year-old patient with pronounced hepatic dysfunction.

A 17-year-old patient with Shone's disease had to be readmitted to the hospital 3 months after implantation of an artificial aortic valve because of extreme mitral insufficiency with consecutive pulmonary edema and hepatic dysfunction. He had been orally anticoagulated and presented with a high international normalized ratio of 6.7. Emergency replacement of the mitral valve was possible only after administration of prothrombin-complex concentrate, as vitamin K(1) and fresh frozen plasma did not correct the hemostatic defect sufficiently.

Adolescent↗

PubMed2005

Myocardial infarction, other arterial thrombosis and invasive coronary procedures, in hemaophilia B: a critical evaluation of reported cases.

Myocardial infarction and other arterial thrombosis are commonly maintained to be rare in hemophilia patients. This, in general, seems true but the occurrence of a thrombotic event in hemophilia B is not exceptional. A thorough search of the literature has yielded 13 patients with myocardial infarction and 1 patient with a cerebrovascular accident. There were three fatalities. In five cases MI occurred after infusion of Prothrombin Complex Concentrates. In three additional patients the event occurred after infusion of plasma, Feiba or cryoprecipitate supernatant. Four patients had an antero-lateral infarction. Two had a non-Q infarction and one each showed a multiple or a posterior-inferior form. Several therapeutic coronary procedures (GABG and PTCA) were carried out in hemophilia B patients without undue complication providing adequate level of FIX were maintained. Heparin prophilaxis was used in all patients but one. The analysis of the literature indicates that (1) MI may occur in hemophilia B patients and (2) that invasive coronary artery therapeutic procedures may be carried out without complications.

Coronary Thrombosis↗

PubMed2003

Need for Continued Use of Anticoagulants After Intracerebral Hemorrhage.

One of the unsolved dilemmas in cerebrovascular disease is the ideal timing to restart anticoagulant therapy (ACT) safely in patients who have suffered an intracranial hemorrhage and have an indication to continue ACT. No randomized studies with evidence-based data are available to settle this issue. Only a few reports have been published; their shortcomings include small numbers of patients evaluated retrospectively, a broad spectrum of indications for ACT, different types of hemorrhage, and variable methods of reversing and restarting ACT. Despite this variability, most reports agree that 1) ACT has to be immediately reversed to decrease the risk of hemorrhage progression; 2) a period between 1 and 2 weeks appears sufficient to allow for management and monitoring of the hemorrhage off ACT; and 3) ACT can be safely restarted after the period off of treatment. A physician confronting a patient with intracranial hemorrhage and the need for ACT faces a situation of individually focused clinical decision making. The problem rests in balancing the risks of a worsening or recurring hemorrhage on one side, and the risk of thromboembolism on the other. From available information and personal experience, an unvalidated risk stratification can be proposed to categorize patients in low- and high-risk groups for hemorrhagic complications and embolic phenomena, assigning them to 5 or 15 days off ACT, respectively. Intermediate-risk patients can have ACT restarted in 5 to 15 days from the onset of the intracranial hemorrhage. Anticoagulation should be immediately reversed. Fresh frozen plasma is the standard treatment in most institutions. Prothrombin complex concentrate is an alternative, but issues of availability make its use impractical. The use of recombinant factor VIIa is an attractive new option.

Journal Article↗

PubMed2000

Coagulopathy of Liver Disease.

Coagulopathy in patients with liver disease results from impairments in the clotting and fibrinolytic systems, as well as from reduced number and function of platelets. Parenteral vitamin K replacement corrects coagulopathy related to biliary obstruction, bacterial overgrowth, or malnutrition. Vitamin K is less effective for coagulopathy caused by severe parenchymal liver injury. Transfusion of fresh frozen plasma is the hallmark of treatment of significant coagulopathy in patients with liver disease and active bleeding. Transfusion of fresh frozen plasma also reverses moderate to severe coagulopathy of cirrhosis prior to invasive procedures. Cryoprecipitate is useful for severe coagulopathy with hypofibrinogenemia, especially when avoidance of volume overload is desired. Exchange plasmapheresis is useful in selected patients with coagulopathy due to liver disease, in whom fresh frozen plasma fails to correct coagulopathy or in patients who have coexistent severe fluid overload. Platelet transfusions, pooled or single donor, are useful in thrombocytopenic patients prior to performing invasive procedures or in the presence of significant bleeding, especially when the platelet count is below 50,000/mL. The use of recombinant factor VIIa and thrombopoietin therapy for correction of coagulopathy and thrombocytopenia, respectively, in patients with cirrhosis, is currently under investigation. Therapy with prothrombin complex concentrates, 1-deamino-8-d-arginine vasopressin and antithrombin III concentrates for the management of coagulopathy caused by liver disease can be hazardous and the use of these products is considered investigational at the present time.

Journal Article↗

PubMed1988

Arthropathy and surgery in congenital factor VII deficiency.

A 35-year-old woman with severe (less than 1 percent) factor VII deficiency had recurrent hemarthroses involving the left knee, leading to deformity, pain, and virtually complete loss of function. It was elected to perform a total knee replacement. In preparation for surgery, the patient received heat-treated prothrombin complex concentrate containing 870 units of factor VII per vial. A dose of 50 U/kg raised the factor VII level to 115 percent. At surgery, dense adhesions were found within the joint, the articular cartilage was overgrown with pannus extending out to the lateral patella, and there was extensive deformity of the femoral condyle and tibial plateau. The joint was excised and replaced by a cemented Microloc prosthesis. Postoperatively, factor VII levels were maintained above 10 percent by six-hourly infusions of concentrate. Beginning on Day 4, single daily infusions of 25 U/kg were given prior to physical therapy. No bleeding occurred, and the patient was ambulating at the time of discharge 20 days postoperatively. This experience indicates that despite its short half-life (less than four hours), factor VII levels sufficient to prevent bleeding can be maintained in factor VII-deficient patients undergoing major operative procedures.

Adult↗

PubMed1983

Dental management of the classic hemophiliac with inhibitors.

Approximately 15 percent of patients with hemophilia A will develop inhibitors (antibodies) to Factor VIII after replacement infusion. Since Factor VIII replacement therapy is the mainstay of treatment in the hemophiliac, destruction of infused Factor VIII by inhibitors presents significant problems in the treatment of these patients. Different methods of treatment are discussed, including infusion of high doses of Factor VIII and infusion of prothrombin-complex concentrate. Two inhibitor patients who presented for dental treatment are examined. One patient had very low inhibitor titers, and the other had very high inhibitor titers. These patients show that dental treatment must be individualized according to severity of the disease process.

Adult↗

PubMed1986

PROPLEX vs. PROPLEX SX: a controlled double blind study of the effectiveness in treating acute hemarthroses in hemophilia A patients with inhibitors to factor VIII.

A blinded randomized multicenter trial of two non-activated prothrombin complex concentrates was carried out to determine the clinical effectivity in the treatment of acute hemarthrosis in hemophiliac patients with inhibitors. The one product was prepared via DEAE Sephadex chromatography, while the second was fractionated via various precipitation procedures including polyethylene glycol. Equivalence of the two products was established with less than 15% difference in efficacy rates.

Blood Coagulation Factors↗

PubMed1990

Inhibition of activated protein C by aprotinin and the use of the insolubilized inhibitor for its purification.

The study of the interaction between activated protein C (APC) and non-plasmatic inhibitors allowed us to demonstrate that aprotinin is a potent competitive inhibitor of APC with a Ki of 1.35 mumol/L. It was possible to adsorb immunopurified protein C (PC) activated by venom activator to insolubilized aprotinin and to recover the active enzyme after elution by HCl 0.1 N or by a chaotropic ion, for example KSCN 3 mol/L. The interaction involved the active-site of the enzyme since PC and DIP-APC did not bind to the matrix. Thus, APC could be purified, after activation, in a one-stage procedure out of a mixture of protein such as a prothrombin complex concentrate.

Amides↗

PubMed1994

Comparative studies on the inhibitory spectrum of recombinant hirudin, DuP 714 and heparin on thrombin and factor Xa generation in biochemically defined systems.

The effect of antithrombotic drugs on the generation of serine proteases was studied in a biochemically defined system in which the prothrombin complex concentrate Konyne provided the necessary coagulation factors in the absence of plasma. The amount of thrombin and factor Xa generation was measured with a chromogenic substrate on a microcentrifugal analyzer. Furthermore, the assay was modified by supplementation with either purified antithrombin III or factor V. The synthetic peptide Ac-(D)Phe-Pro-boroArg-OH (DuP 714) was shown to be the most effective inhibitor of thrombin and also had strong inhibitor actions against factor Xa generation. Recombinant hirudin (rH) was nearly as active as DuP 714 on thrombin generation, however, it was less effective on factor Xa generation. With rH no concentration-dependent inhibition of factor Xa generation was found, i.e. over a wide range of concentration it only produced a steady inhibition of about 40-50% without further increase. The addition of AT-III to the system did not influence the action of DuP 714 or rH, but it strongly increased the inhibitory effects of unfractionated heparin (PMH) as well as of a low molecular weight heparin (LMWH) on both thrombin and factor Xa generation. The addition of factor V to the assay system did not cause any changes in the activity of all agents on protease generation.

Amino Acid Sequence↗

PubMed1994

Inhibitory effects of TFPI on thrombin and factor Xa generation in vitro--modulatory action of glycosaminoglycans.

The effect of tissue factor pathway inhibitor (TFPI) on thrombin and factor Xa generation was studied in an in vitro system using a prothrombin complex concentrate. It was found that TFPI, via the direct inhibition of factor Xa and the tissue factor/factor VIIa complex, inhibited both the further generation of factor Xa and the generation of thrombin in a concentration-dependent manner. The generation of thrombin (IC50 255 ng/ml) was more pronounced than that of factor Xa (IC50 684 ng/ml). The inhibitory activity of TFPI was significantly enhanced when unfractionated heparin was present in the assay system at a concentration of 10 micrograms/ml which did not show any inhibitory effects on protease generation in the same system. Furthermore, the influence of TFPI at subthreshold concentrations (100 ng/ml and 200 ng/ml, resp.) on the inhibitory action of unfractionated heparin (UFH), a low molecular weight heparin (LMWH), heparan sulfate (HS) and the synthetic heparin pentasaccharide (PS) was investigated. Whereas in the concentration range used (0.3-40 micrograms/ml) these glycosaminoglycans did not inhibit thrombin and factor Xa generation, after supplementation of the system with TFPI a concentration-dependent inhibition of the generation of the proteases up to 40-50% was seen for UFH, LMWH and HS. TFPI did not increase the activity of PS.

Animals↗

PubMed1990

Superficial thrombophlebitis. II. Secondary hypercoagulable states.

Secondary hypercoagulable states are complex clinical conditions associated with an increased risk of thrombosis in which the exact pathophysiology is poorly understood. Secondary causes of superficial thrombophlebitis include malignancy, pregnancy, use of oral contraceptives, infusion of prothrombin complex concentrates, Behçet's disease, Buerger's disease, Mondor's disease, infectious agents, conditions that promote venous stasis, intravenous catheters and intravenous drug use. Conditions that may stimulate superficial thrombophlebitis include dermatophyte cellulitis at saphenous phlebectomy sites, sarcoidal granulomas, cutaneous polyarteritis nodosa, and hyperalgesic pseudothrombophlebitis in patients who test positive for human immunodeficiency virus. The distinguishing features, clinical evaluation, treatment, and histologic characteristics of the various disorders are reviewed.

Adult↗

PubMed1994

Quality of plasma for fractionation--does it matter?

Many plasmapheresis techniques cause greater activation of platelets, complement and coagulation than does simple whole blood collection. Activation of the coagulation cascade has been particularly evident in tests for potential thrombogenicity in prothrombin complex concentrates made from apheresed plasma. Attempts to improve the factor VIII content and fractionation yield of source plasma have centred on rapid freezing, increased concentration of anticoagulants and the exploitation of anticoagulants optimal for the preservation of coagulant, rather than cellular, activities. The cumulative advantage is of the order of 10% over recovered plasma. There are potential pitfalls in applying low-citrate anticoagulation strategies to plasmapheresis. Recalcification of citrated plasma, under cover of an optimal concentration of heparin, might be explored more vigorously.

Chemical Fractionation↗

PubMed2006

Plasma and plasma products in the treatment of massive haemorrhage.

Massive haemorrhage requires the use of plasma products when it is accompanied by a coagulopathy or when the more than one blood volume has been lost and intractable bleeding continues. The coagulopathy results from haemorrhagic shock, hypothermia, and activation, consumption and dilution of coagulation factors. Plasma products have a critical role in maintaining sufficient levels of coagulation proteins to ensure haemostasis can occur. Fresh frozen plasma is a source of all coagulation proteins and is required when the prothrombin time and activated partial thromboplastin time exceed 1.5 times the normal control. Cryoprecipitate is the plasma product of choice if fibrinogen, the most critical coagulation protein, is required rapidly and to maintain levels at >1g/L. Prothrombin complex concentrates, monocomponent factor therapy and fibrin sealants each have a role in specific clinical settings. Recombinant factor VIIa has now been shown to have a role in massive haemorrhage. Randomised controlled trials are currently underway to determine the optimal dose and timing of its administration. The physiology and management of the coagulation disturbance using plasma products in the massive haemorrhage of specific clinical situations are described.

Blood Coagulation Factors↗