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Pieter Willem Kamphuisen

Researcher at University of Amsterdam

Publications -  100
Citations -  7028

Pieter Willem Kamphuisen is an academic researcher from University of Amsterdam. The author has contributed to research in topics: Pulmonary embolism & Thrombosis. The author has an hindex of 36, co-authored 100 publications receiving 6411 citations. Previous affiliations of Pieter Willem Kamphuisen include Radboud University Nijmegen Medical Centre & University of Perugia.

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Plasma HDL cholesterol and risk of myocardial infarction: A mendelian randomisation study

Benjamin F. Voight, +140 more
TL;DR: In this paper, a Mendelian randomisation analysis was performed to compare the effect of HDL cholesterol, LDL cholesterol, and genetic score on risk of myocardial infarction.
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Reversal of rivaroxaban and dabigatran by prothrombin complex concentrate: a randomized, placebo-controlled, crossover study in healthy subjects.

TL;DR: In this article, the authors evaluated the potential of prothrombin complex concentrate (PCC) to reverse the anticoagulant effect of Rivaroxaban and dabigatran.
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Elevated factor VIII levels and the risk of thrombosis.

TL;DR: Despite growing insight in the pathogenesis of thrombophilia, the cause of manyThrombotic episodes remains unknown and genetic risk factors involved are still uncertain.
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Increased levels of factor VIII and fibrinogen in patients with venous thrombosis are not caused by acute phase reactions.

TL;DR: Results show that although systemic inflammation may be present in some of the patients, elevated levels of factor VIII:C and fibrinogen were in general not caused by acute phase reactions, which further supports a causal relationship between both high factor VIII-C levels and fibinogen levels and venous thrombosis.
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Association of V617F Jak2 mutation with the risk of thrombosis among patients with essential thrombocythaemia or idiopathic myelofibrosis: A systematic review

TL;DR: V617F Jak-2 increases the risk of thrombosis in essentialThrombocythaemia patients by about two fold while its role in idiopathic myelofibrosis patients is uncertain.