Tranexamic Acid in Control of Haemorrhage after Dental Extraction in Haemophilia and Christmas Disease

Forbes, C.D.; Barr, RD; Reid, Gregor; Thomson, C.; Prentice, C. R. M.; Nicol, Graeme; Douglas, A. S.

doi:10.1136/bmj.2.5809.311

Cited by 107 publications

(66 citation statements)

References 16 publications

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“…In patients with impaired thrombin generation related to deficiency of coagulation factors and/or platelet defects, prolonged bleedings are seen especially at sites rich in local fibrinolytic activity such as the oral cavity and the gastrointestinal tract [12], supporting the hypothesis that full thrombin generation is necessary for the formation of tight fibrin hemostatic plugs resistant against lysis. Antifibrinolytic therapy is being used with some success in these situations [13,14]. On the other hand, thrombi formed in the presence of antithrombotic agents [15–17] have been shown to have a looser structure and an increased solubility in plasmin.…”

Section: Discussionmentioning

confidence: 99%

The effect of platelets on fibrin gel structure formed in the presence of recombinant factor VIIa in hemophilia plasma and in plasma from a patient with Glanzmann thrombasthenia

He¹,

Ekman

Hedner

2005

Journal of Thrombosis and Haemostasis

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To cite this article: He S, Jacobsson Ekman G, Hedner U. The effect of platelets on fibrin gel structure formed in the presence of recombinant factor VIIa in hemophilia plasma and in plasma from a patient with Glanzmann thrombasthenia. J Thromb Haemost 2005; 3: 272-9.Summary. Fibrin gel structure has been shown to be dependent on the thrombin concentration as well as the rate of thrombin generation. Accordingly, factor VIII (FVIII)-and FIX-deficient plasma (hemophilia A and B) form loose fibrin clots with high permeability constants. By adding rFVIIa in vitro to FVIII-deficient plasma containing platelets (frozen and thawed), the fibrin gel permeability constant normalized, indicating that extra rFVIIa (1.2 lg mL )1 or higher) induced a tight fibrin structure. Thrombin generation is highly dependent on the number of platelets, and in this study it was demonstrated that the addition of rFVIIa (5 lg mL )1) normalizes the fibrin gel permeability in samples containing platelets (frozen-thawed) in numbers of at least down to 20 · 10 6 mL )1. The effect of rFVIIa was not observed when unfrozen platelets instead of frozen-thawed platelets were added. Neither was any effect on the fibrin permeability seen, in the presence of annexin V, known to block the effect of phospholipids on the platelet surface. This indicates an important role of platelet phospholipids for the effect of rFVIIa. A similar effect on the fibrin permeability of rFVIIa was observed when added to platelet-rich plasma from a patient with Glanzmann thrombasthenia. Recombinant FVIIa has been found to induce hemostasis in patients with hemophilia and inhibitors against FVIII/FIX as well as in patients with Glanzmann thrombasthenia, indicating the importance of the formation of a tight fibrin gel structure, more resistant against premature proteolysis, for maintaining hemostasis. In conclusion, the addition of rFVIIa (5 lg mL ). A similar pattern was obtained in plasma from a Glanzmann patient. No effect was found in the presence of unfrozen instead of frozen-thawed platelets. Annexin V blocked any effect of rFVIIa. A normalization of the overall fibrinolysis potential (OFP) during the same condition supports the effect of rFVIIa on the fibrin permeability in the presence of a limited number of platelets.

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Section: Discussionmentioning

confidence: 99%

The effect of platelets on fibrin gel structure formed in the presence of recombinant factor VIIa in hemophilia plasma and in plasma from a patient with Glanzmann thrombasthenia

He¹,

Ekman

Hedner

2005

Journal of Thrombosis and Haemostasis

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“…Randomized controlled trials have shown that both TXA and EACA significantly reduce bleeding after dental surgery in patients with hemophilia [15,16]. World Federation of Hemophilia guidelines recommend starting oral antifibrinolytic therapy the day before dental surgery (EACA 50 mg/kg four times daily or TXA 1 g three times daily) and continuing treatment for total of 7 days [17].…”

Section: Tonsillectomy/adenoidectomymentioning

confidence: 99%

General Surgical Management of Patients with Hemophilia

Leissinger

Kruse‐Jarres

2014

Textbook of Hemophilia

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“…In these circumstances any clot formed is friable and can be disrupted by plasmin produced by normal fibrinolytic activity. There is now good evidence that blood loss from dental extraction and the amount of factor VIII transfused in haemophilia may be reduced by routine use of antifibrinolytic agents before and after the operation.38 39 However, there is insufficient evidence to justify the routine use of antifibrinolytic drugs in haemophilia.40 The hazards of ureteric obstruction by clot after haematuria in haemophilia have been reviewed.4'…”

Section: Hereditary Coagulation Disordersmentioning

confidence: 99%

Basis of antifibrinolytic therapy

Prentice¹

1980

Journal of Clinical Pathology

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Tranexamic Acid in Control of Haemorrhage after Dental Extraction in Haemophilia and Christmas Disease

Cited by 107 publications

References 16 publications

The effect of platelets on fibrin gel structure formed in the presence of recombinant factor VIIa in hemophilia plasma and in plasma from a patient with Glanzmann thrombasthenia

The effect of platelets on fibrin gel structure formed in the presence of recombinant factor VIIa in hemophilia plasma and in plasma from a patient with Glanzmann thrombasthenia

General Surgical Management of Patients with Hemophilia

Basis of antifibrinolytic therapy

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