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• W2010809596 abstract "The pathophysiology of venous thrombosis is incompletely understood, but one of the characteristic features is a disturbed hemostatic balance, contributing to increased generation of thrombin and fibrin. This balance may be tipped in a procoagulant direction by specific congenital defects, such as the factor (F)V Leiden mutation. In the presence of stimuli such as stasis, or damage of the vessel wall, venous thrombosis may occur. Blood cells contribute to this process, primarily by catalyzing coagulation reactions. In this regard, platelets are thought to be more prominent in arterial thrombosis, than in venous thrombosis. This hypothesis is supported by histological observations that score arterial clots (white) as platelet rich and venous thrombi as platelet poor (red). Furthermore, in clinical studies, platelet inhibition with aspirin either was ineffective [1, 2], or moderately effective in the prevention of venous thromboembolism [3]. Recent publicity around the possible association of venous thrombosis and highly prevalent conditions associated with immobilization such as long-distance flying raises the question whether agents such as aspirin taken before flying would confer adequate prophylaxis against venous thrombosis. The present case report reinforces the assumption that platelets are of limited significance in the pathogenesis of venous thrombosis due to immobilization. The patient was a 48-year-old Caucasian male with Glanzmann's type 1 disease. He was first diagnosed with a spontaneous proximal deep venous thrombosis (DVT) in 1998, for which he was treated with low molecular weight heparin (LMWH). The family history did not reveal any thromboembolic disease. He smoked 35 pack years, used a moderate amount of alcohol and did not use any medication. In 1999, he suffered from life-threatening upper gastrointestinal bleeding due to a reflux oesophagitis. He was treated with a protonpomp inhibitor and remained stable. However, he next suffered from a recurrent DVT in the same leg for which he was again treated with LMWH during 3 months. Because of the unusual combination of recurrent DVT and Glanzmann's disease the patient was scrutinized for underlying morbidity. CT scanning of the abdomen did not show any signs of neoplasia or flow impairing processes. Tumor markers in blood were negative. Screening for risk factors revealed a heterozygous FV Leiden mutation but no other abnormalities including normal levels of antithrombin, proteins C and S, no prothrombin 20120 mutation. APTT, PT and fibrinogen levels were all normal and tests for lupus anticoagulant and anticardiolipin antibodies were negative. After the second episode of DVT he was treated with LMWH for a prolonged period during which he suffered from a traumatic hip fracture, complicated by a large hematoma in the leg. Six months later he suffered from a third episode of DVT in the same leg, after which he has been on maintenance therapy with LMWH and during the past 4 years he has been free from malignancy or other apparent disorders. This case report illustrates that venous thrombosis may occur in spite of a severe functional platelet defect. The initiating factors in this patient are unclear. At least in one instance prolonged immobilization might have occurred, while the absolute risk was enhanced by the FV Leiden mutation. Two comparable cases of an association of Glanzmann's disease and venous thrombosis have been published previously. One case was a young individual developing superficial thrombophlebitis [4]; another patient had a documented pulmonary embolism after a long air flight [5]. Animal studies have yielded conflicting data regarding the role of platelets in venous thrombosis. In stasis-dependent models, severe thrombocytopenia did not influence venous thrombosis [6]. When stasis was combined with a low dose of thromboplastin, the presence of severe thrombocytopenia markedly reduced thrombosis of the caval vein, while this protective effect vanished at higher thromboplastin concentrations. In a modified venous pouch model in rats, and in combination with stasis, neither severe thrombocytopenia, nor aspirin prevented thrombosis [7]. In contrast, ticlopedine, blocking platelet aggregation by a non prostaglandin-dependent pathway, had a limited antithrombotic activity [7]. The glycoprotein (Gp)IIb–IIIa antagonist SR 121566 A significantly inhibited venous thrombosis induced by a combination of stasis and a thrombotic challenge in rabbits, while aspirin was ineffective [8]. The antihuman von Willebrand factor antibody AJVW-2, which impairs ristocetin-induced platelet aggregation, prevented venous thrombosis in the injured femoral vein in hamsters [9]. Platelets may indeed show a more distinct role in thrombosis associated with vessel wall damage. In a model of venous thrombosis induced by a standardized pinch trauma of the femoral vein in rats or mice, thrombi were rich in platelets [10]. Upon vessel wall injury subendothelial collagen and other adhesive proteins may catalyze thrombus development. In the absence of such injury the role of platelets may be limited to accelerating procoagulant reactions in the static blood. Strong challenge with tissue factor may overrule the contribution of platelets, while lower challenges depend on platelets to some extent, for instance in their effect on tissue factor production by monocytes [11]. Our case report supports the notion that platelets play a limited role in the pathogenesis of venous thrombosis, at least in situations of immobilization." @default.
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• W2010809596 title "The role of platelets in venous thrombosis: a patient with Glanzmann's thrombasthenia and a factor V Leiden mutation suffering from deep venous thrombosis" @default.
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• W2010809596 doi "https://doi.org/10.1046/j.1538-7836.2003.00041.x" @default.
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