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Books on the topic 'Von Willebrand disease (vWD)'

Author: Grafiati

Published: 4 June 2021

Last updated: 3 February 2022

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1

Federici, Augusto B., Christine A. Lee, Erik E. Berntorp, David Lillicrap, and Robert R. Montgomery, eds. Von Willebrand Disease. Oxford, UK: Wiley-Blackwell, 2011. http://dx.doi.org/10.1002/9781444329926.

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2

James, Andra H. 100 questions & answers about Von Willebrand disease. Sudbury, Mass: Jones and Bartlett, 2009.

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3

Shapiro, Jane. Diane Dino's dilemma: Diane's story of von Willebrand Disease. Collegeville, PA (500 Arcola Road, Collegville 19426-0107): Armour Pharmaceutical Co., Educational Publications, 1994.

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4

Jones, Nicola Louise. An investigation of genetic defects in type 1 and type 3 Von Willebrand Disease. Wolverhampton: University of Wolverhampton, 2002.

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5

1935-, Lusher Jeanne M., and Kessler Craig M, eds. Hemophilia and von Willebrand's disease in the 1990s: A new decade of hopes and challenges : proceedings of the XIX Congress of the World Federation of Hemophilia, Washington, D.C., 14-19 August 1990. Amsterdam: Excerpta Medica, 1991.

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6

Downey, Laura A., and Nina A. Guzzetta. Von Willebrand Disease. Edited by Kirk Lalwani, Ira Todd Cohen, Ellen Y. Choi, and Vidya T. Raman. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190685157.003.0059.

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Von Willebrand disease (vWD) is the most common bleeding disorder in humans. It is the result of an abnormality in the amount, structure, or function of von Willebrand factor (vWF), a glycoprotein important in maintaining normal hemostasis.. In children with vWD, the most frequent presentation is easy bruising and epistaxis. Other symptoms include hematomas, menorrhagia, and bleeding from minor wounds. Although intraarticular bleeding may occur, especially in certain subtypes, it is much more commonly seen with hemophilia. There are several subtypes of vWD based on the underlying defect in vWF, but, in general, they may be categorized as quantitative (types 1 and 3) or qualitative (all types 2). If vWD is suspected, consultation with a hematologist to establish the correct diagnosis and perioperative approach to hemostasis is essential. Avoidance of medications that interfere with coagulation, anticipation of intraoperative and postoperative bleeding, and an appropriate hemostatic treatment plan should be addressed.

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7

Global Von Willebrand Disease (VWD) Treatment Market 2022 – Industry Analysis, Market Size, Competitive Trends: Credence Research: Von Willebrand Disease (VWD) Treatment Market. Serena Peter, 2016.

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8

I, Barnhart Marion, and Lusher Jeanne M. 1935-, eds. Factor VIII/vWF and platelet formation and function in health and disease: A tribute to Marion I. Barnhart. New York, N.Y: New York Academy of Sciences, 1987.

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9

Von Willebrand factor and Von Willebrand disease. London: Baillière Tindall, 2001.

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10

Jaques, Michiels Jan, ed. Von Willebrand factor and von Willebrand disease. London: Baillière Tindall, 2001.

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11

Von Willenbrand Disease. Wiley-Blackwell, 2011.

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12

Hemophilia and Von Willebrand Disease. Elsevier, 2018. http://dx.doi.org/10.1016/c2016-0-04171-2.

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13

Green, David. Hemophilia and Von Willebrand Disease: Factor VIII and Von Willebrand Factor. Elsevier Science & Technology, 2018.

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14

Cain, Grant F., and Cesar R. Massin. Von Willebrand Disease: Diagnosis and Management. Nova Science Publishers, Incorporated, 2012.

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15

Lee, Christine A., Erik E. Berntorp, David Lillicrap, Augusto B. Federici, and Robert R. Montgomery. Von Willebrand Disease: Basic and Clinical Aspects. Wiley & Sons, Incorporated, John, 2011.

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16

Lee, Christine A., Erik E. Berntorp, David Lillicrap, Augusto B. Federici, and Robert R. Montgomery. Von Willebrand Disease: Basic and Clinical Aspects. Wiley & Sons, Incorporated, John, 2011.

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17

Lee, Christine A., Erik E. Berntorp, David Lillicrap, Augusto B. Federici, and Robert R. Montgomery. Von Willebrand Disease: Basic and Clinical Aspects. Wiley & Sons, Incorporated, John, 2011.

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18

Lee, Christine A., Erik E. Berntorp, David Lillicrap, Augusto B. Federici, and Robert R. Montgomery. Von Willebrand Disease: Basic and Clinical Aspects. Wiley & Sons, Limited, John, 2011.

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19

Moser, Janet. Von Willebrand factor: Measurement, changes during pregnancy, and inheritance of von Willebrand factor deficiency. 1994.

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20

J, Seghatchian M., and Savidge G. F, eds. Factor VIII-von Willebrand factor. Boca Raton, Fla: CRC Press, 1989.

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21

Seghatchian, M. J., and G. F. Savidge. Factor VIII - von WIllebrand Factor, Volume I. CRC, 1989.

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22

Seghatchian, M. J., and G. F. Savidge. Factor VIII - von Willebrand Factor, Volume II. CRC, 1989.

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23

Meinkoth, James Harold. Storage and release of von Willebrand factor by endothelial cells of Doberman pinscher dogs with type I von Willebrand disease. 1993.

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24

Noris, Marina, and Tim Goodship. The patient with haemolytic uraemic syndrome/thrombotic thrombocytopenic purpura. Edited by Giuseppe Remuzzi. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0174.

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The patient who presents with microangiopathic haemolytic anaemia, thrombocytopenia, and evidence of acute kidney injury presents a diagnostic and management challenge. Haemolytic uraemic syndrome (HUS) and thrombotic thrombocytopenic purpura (TTP) are two of the conditions that frequently present with this triad. They are characterized by low platelet count with normal or near-normal coagulation tests, anaemia, and signs of intravascular red cell fragmentation on blood films, and high LDH levels.HUS associated with shiga-like toxins produced usually by E.coli (typically O157 strains) may occur in outbreaks or sporadically, with geographical variations in incidence. It is predominantly a disease of young children in which painful blood diarrhoea in a minority of infected patients is succeeded by microangiopathy and acute kidney injury. Management is supportive and recovery is usual, although permanent renal damage may lead to later deterioration. Older patients may be affected and tend to have worse outcomes. Neuraminidase-producing Streptococcus pneumoniae infections (usually pneumonia) very rarely cause a similar HUS.Atypical HUS occurs sporadically and is increasingly associated with defects in the regulation of the complement pathway, either genetic or autoimmune-caused. It may respond to plasma exchange for fresh frozen plasma. Recurrences are common, including after transplantation.TTP is associated with more neurological disease and less renal involvement, but HUS and TTP overlap substantially in their manifestations. The underlying problem is in von Willebrand factor (vWF) cleavage. The plasma metalloprotease ADAMTS13 is responsible for cleaving vWF multimers, a process that is important to prevent thrombosis in the microvasculature. Autoantibodies or rarely genetic deficiency may impair this process. Plasma exchange may remove antibodies and replenish the protease.

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25

Yvonne Nerene Li Hsin Ching. Treatment of canine type I von Willebrand factor deficiency with DDAVP, canine plasma and cryoprecipitate: Effects on Von Willebrand factor multimers and bleeding time. 1990.

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26

G, Westphal Robert, Smith Dennis M, and American Association of Blood Banks., eds. Treatment of hemophilia and von Willebrand's disease: New developments. Arlington, Va: American Association of Blood Banks, 1989.

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27

Karen, Bellenir, ed. Genetic disorders sourcebook: Basic information about heritable diseases and disorders such as Down syndrome, PKU, hemophilia, Von Willebrand disease, Gaucher disease, Tay-Sachs disease, and sickle cell disease ... Detroit, MI: Omnigraphics, 1996.

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28

Bellenir, Karen. Genetic Disorders Sourcebook: Basic Information About Heritable Diseases and Disorders Such As Down Synd Rome, Pku, Hemophilia, Von Willebrand Disease, ... Tay-Sachs d (Health Reference Series). Omnigraphics, 1996.

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29

Carton, James. Haematopathology. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198759584.003.0015.

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This chapter discusses haematopathology, including iron deficiency anaemia, anaemia of chronic disease, megaloblastic anaemias, hereditary spherocytosis, glucose-6-phosphate dehydrogenase deficiency, thalassaemias, sickle-cell disorders, idiopathic thrombocytopenic purpura (ITP), thrombotic thrombocytopenic purpura (TTP), von Willebrand disease, haemophilia, thrombophilia, acute B-lymphoblastic leukaemia, acute myeloid leukaemias, chronic lymphocytic leukaemia (CLL), chronic myelogenous leukaemia, polycythaemia vera (PV), essential thrombocythaemia (ET), primary myelofibrosis (PMF), myelodysplastic syndromes (MDS), follicular lymphoma, diffuse large B-cell lymphoma, Burkitt’s lymphoma (BL), extranodal marginal zone lymphoma of mucosa-associated lymphoid tissue (MALT lymphoma), mantle cell lymphoma, classical Hodgkin’s lymphoma (cHL), lymphoplasmacytic lymphoma (LPL), plasma cell myeloma, primary amyloidosis, and mature T-cell non-Hodgkin’s lymphomas.

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30

Provan, Drew, Trevor Baglin, Inderjeet Dokal, and Johannes de Vos. Haemostasis and thrombosis. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199683307.003.0010.

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Assessing haemostasis - The coagulation system - Laboratory tests - Platelets - Bleeding - Bleeding: laboratory investigations - Bleeding: therapeutic products - von Willebrand disease - Haemophilia A and B - Rare congenital coagulation disorders - Congenital thrombocytopenias - Congenital platelet function defects - Congenital vascular disorders - Haemorrhagic disease of the newborn - Thrombocytopenia (acquired) - Specific thrombocytopenic syndromes - Disseminated intravascular coagulation - Liver disease - Renal disease - Acquired anticoagulants and inhibitors - Treatment of spontaneous FVIII inhibitor - Acquired disorders of platelet function - Henoch–Schönlein purpura - Perioperative bleeding and massive blood loss - Massive blood loss - Heparin - Heparin induced thrombocytopenia/with thrombosis (HIT/T) - Oral anticoagulant therapy (warfarin, VKAs) - New oral anticoagulant drugs - Thrombosis - Risk assessment and thromboprophylaxis - Example of VTE risk assessment - Heritable thrombophilia - Acquired thrombophilia - Thrombotic thrombocytopenic purpura (TTP) - Haemolytic uraemic syndrome (HUS) - Heparin-induced thrombocytopenia (HIT)

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31

Provan, Drew, Trevor Baglin, Inderjeet Dokal, Johannes de Vos, and Angela Theodoulou. Haemostasis and thrombosis. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199683307.003.0010_update_001.

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Assessing haemostasis - The coagulation system - Laboratory tests - Platelets - Bleeding - Bleeding: laboratory investigations - Bleeding: therapeutic products - von Willebrand disease - Haemophilia A and B - Rare congenital coagulation disorders - Congenital thrombocytopenias - Congenital platelet function defects - Congenital vascular disorders - Haemorrhagic disease of the newborn - Thrombocytopenia (acquired) - Specific thrombocytopenic syndromes - Disseminated intravascular coagulation - Liver disease - Renal disease - Acquired anticoagulants and inhibitors - Treatment of spontaneous FVIII inhibitor - Acquired disorders of platelet function - Henoch–Schönlein purpura - Perioperative bleeding and massive blood loss - Massive blood loss - Heparin - Heparin induced thrombocytopenia/with thrombosis (HIT/T) - Oral anticoagulant therapy (warfarin, VKAs) - New oral anticoagulant drugs - Thrombosis - Risk assessment and thromboprophylaxis - Example of VTE risk assessment - Heritable thrombophilia - Acquired thrombophilia - Thrombotic thrombocytopenic purpura (TTP) - Haemolytic uraemic syndrome (HUS) - Heparin-induced thrombocytopenia (HIT)

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32

Argote-Romero, Graciela. Wilms Tumor. Edited by Kirk Lalwani, Ira Todd Cohen, Ellen Y. Choi, and Vidya T. Raman. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190685157.003.0041.

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Wilms tumor, known as well as nephroblastoma, is the most common primary malignant renal tumor in children. Over 95% of all renal tumors in patients under the age of 15 are Wilms tumors. The mean age at the time of diagnosis is 3.5 years. Wilms tumors are usually an incidental finding, a large abdominal mass discovered by a family member or pediatrician. Hematuria and hypertension can be present at the time of initial diagnosis. Up to 8% of the patients will have von Willebrand disease; therefore, all patients should have baseline coagulation studies. All patients should have either computed tomography of the abdomen and pelvis with oral and intravenous contrast or magnetic resonance imaging of the abdomen and pelvis with gadolinium. Treatment includes radical nephrectomy, chemotherapy, and, in some cases, radiotherapy. Emergency surgery is rarely. The disease-free survival rate is 86% for favorable-histology tumors and 64% for anaplastic tumors.

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33

Badimon, Lina, Felix C. Tanner, Giovanni G. Camici, and Gemma Vilahur. Pathophysiology of thrombosis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0018.

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Ischaemic heart disease and stroke are major causes of death and morbidity worldwide. Coronary and cerebrovascular events are mainly a consequence of a sudden thrombotic occlusion of the vessel lumen. Arterial thrombosis usually develops on top of a disrupted atherosclerotic plaque because of the exposure of thrombogenic material, such as collagen fibrils and tissue factor (TF), to the flowing blood. TF, either expressed by subendothelial cells, macrophage- and/or vascular smooth muscle-derived foam-cells in atherosclerotic plaques, is a key element in the initiation of thrombosis due to its ability to induce thrombin formation (a potent platelet agonist) and subsequent fibrin deposition at sites of vascular injury. Adhered platelets at the site of injury also play a crucial role in the pathophysiology of atherothrombosis. Platelet surface receptors (mainly glycoproteins) interact with vascular structures and/or Von Willebrand factor triggering platelet activation signalling events, including an increase in intracellular free Ca2+, exposure of a pro-coagulant surface, and secretion of platelet granule content. On top of this, interaction between soluble agonists and platelet G-coupled protein receptors further amplifies the platelet activation response favouring integrin alpha(IIb)beta(3) activation, an essential step for platelet aggregation. Blood-borne TF and microparticles have also been shown to contribute to thrombus formation and propagation. As thrombus evolves different circulating cells (red-blood cells and leukocytes, along with occasional undifferentiated cells) get recruited in a timely dependent manner to the growing thrombus and further entrapped by the formation of a fibrin mesh.

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