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Your search term(s) "Thrombocytosis or thrombosis" returned 95 results.

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Chronic Myeloproliferative Diseases. IN: Sekeres, M.; Kalaycio, M.; Bolwell, B., eds. Clinical Malignant Hematology. Columbus, OH: McGraw Hill. 2007. pp 445-502.

This section about chronic myeloproliferative disorders (CMPDs) is from a comprehensive reference book that covers the full spectrum of cancers in the blood, bone marrow, and lymphatic system, including leukemia, lymphoma, and myeloma. CMPDs are characterized by the chronic proliferation of one or more of the three hematopoietic cell lines or by marrow stromal cells, in various proportions. The CMPDs include polycythemia vera, idiopathic myelofibrosis, chronic myelogenous leukemia (CML), and essential thrombocytosis (ET). This section offers six chapters: epidemiology, risk factors, and classification; molecular biology, pathology, and cytogenetics; clinical features and making the diagnosis; the recommended treatment approach to polycythemia vera and essential thrombocythemia; the recommended approach to chronic idiopathic myelofibrosis, with extramedullary hematopoiesis; and the management of chronic myelomonocytic leukemia and other rare myeloproliferative disorders. The chapters are illustrated with black-and-white clinical pictures and photomicrographs. Each chapter concludes with an extensive list of references.

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Coagulation in the Pathophysiology of Hemolytic Anemias. IN: Hematology 2007. Washington, DC: American Society of Hematology.2007. pp 74-78.

This chapter, from the Hematology 2007 monograph, reviews coagulation in the pathophysiology of hemolytic anemias (HA). The author focuses on three hemolytic disorders: sickle cell disease and beta-thalassemia, paroxysmal nocturnal hemoglobinuria (PNH), and thrombotic microangiopathies (TMA). In sickle cell disease and in ß-thalassemia, a thrombophilic status has been well documented as multifactorial involving hemostatic changes and activation of the coagulation cascade. Other evidence points to the involvement of endothelial activation in vascular occlusion. The main clinical manifestation of paroxysmal nocturnal hemoglobinuria (PNH) is HA, and the most common complications are thrombosis, pancytopenia, and myelodysplastic syndrome or acute leukemia. The author notes that the mechanism responsible for the increased incidence of thrombotic events in PNH remains unclear. Recent advances have been made in understanding the coagulation involvement TMA, a heterogeneous group of diseases characterized by microangiopathic HA and thrombocytopenia due to platelet clumping in the microcirculation, leading to ischemic organ dysfunction with neurologic symptoms and renal impairment. The author concludes by discussing the three ways that hemolysis contributes to coagulation abnormalities in HA: red blood cell membrane alterations, erythrocyte/endothelium interaction, and nitric oxide (NO) deficiency. 1 figure. 38 references.

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Double Hazard of Thrombophilia And Bleeding in Leukemia. IN: Hematology 2007. Washington, DC: American Society of Hematology. 2007. pp.151-157.

This chapter, from the annual Hematology 2007, considers the association between thrombosis and cancer, notably the incidence of thrombosis in malignant hematologic disorders such as leukemia. The author notes that thrombotic, or clotting, complications in acute leukemia are often overlooked because bleeding complications generally dominate the clinical picture. Yet, the patient is at risk for both. The factors in patients with leukemia that may contribute to thrombosis include hyperleukocytosis, increased expression of tissue factor and its activation in leukemic cells, and the prothrombotic adverse effects of therapeutic agents and vascular access catheters. In addition, comorbid conditions including hereditary thrombophilia, infection, endothelial cell activation by cytokines, antiphospholipid syndrome and acquired activated protein C resistance are major contributory factors. Factors that increase the bleeding risk include thrombocytopenia, disseminated intravascular coagulation, and excessive fibrinolysis, which is enhanced by increased expression of annexin II by leukemic cells. The author concludes by cautioning readers to keep these factors in mind and to consider earlier application of prophylactic measures for patients at risk. 1 figure. 3 tables. 44 references.

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Growth Factors in Short-Bowel Syndrome Patients. Gastroenterology Clinics of North America. 36(1): 109-122. 2007.

This article, from a special issue of Gastroenterology Clinics of North America that covers nutrition in gastrointestinal illness, discusses growth factors in patients with short-bowel syndrome. The author notes that malabsorption of nonessential and essential nutrients, fluids, and electrolytes, if not compensated for by increased intake, is a key finding in patients with short-bowel syndrome. Dependence on parenteral nutritional (PN) support significantly impairs the quality of life in these patients and is associated with complications, including recurrent infections, increased risk of venous thrombosis, and PN-associated liver failure. The author focuses on selected factors responsible for the morphologic and functional changes in the adaptive processes and presents results of clinical trials that use either growth hormone or glucagon-like peptide (GLP)-2 to facilitate a condition of hyperadaptation in short-bowel patients. Intestinal adaptation refers to the progressive recovery from intestinal insufficiency or failure that follows a loss of intestinal length. The author concludes that the effects of high doses of growth hormone are related to the wet-weight absorption (or fluid retention) and mainly in patients with a preserved colon, whereas the effects on energy absorption are minimal. 1 figure. 1 table. 54 references.

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Haematological Disorders at the Extremes of Life. IN: Provan, D., ed. ABC of Clinical Haematology. Williston, VT: Blackwell Publishing Inc. 2007. pp. 72-77.

This chapter about hematological disorders at infancy and old age is from a book on clinical hematology, written by specialists for nonspecialists. The book is designed to be easy to use and covers the symptoms, investigations, treatment, and management of conditions presenting in day-to-day practice. In this chapter, the authors first discuss hematological disorders in infants, including anemia, hemolytic disease of the fetus and newborn, hemoglobinopathies, thalassemia, sickle cell disease, enzyme deficiencies, membrane defects, sepsis, bleeding and thrombotic disorders, prematurity, thrombocytopenia, neonatal alloimmune thrombocytopenia, transfusion in this age group, neutropenia, polycythemia, and leukemia. A final section covers iron deficiency anemia, megaloblastic anemia, anemia of chronic disease, and malignancies of the blood in people older than 70 years. The authors caution that anemia in the neonate results in reduced tissue oxygenation, metabolic acidosis, and ultimately growth retardation and many other sequelae. Neonatal thrombosis and thrombocytopenia are potentially lethal and prompt diagnosis and management are essential. At the other end of life, elderly people are more susceptible to the effects of anemia, which is often multifactorial and should be investigated and treated appropriately. The chapter is illustrated with full-color photographs, drawings, and charts. 4 figures. 14 tables. 8 references.

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Haemophilia and Haemostasis: A Case-Based Approach to Management. Williston, VT: Blackwell Publishing Inc. 2007. 229 p.

This book compiles a breadth of questions relating to perplexing or complicated management questions in the fields of hemophilia and hemostasis. The contributing authors have provided practical, hands-on answers to the questions sent in by practitioners in the field. The book is organized into seven sections: hemophilia A and hemophilia B, Von Willebrand disease, factor deficiencies, rare platelet and coagulation disorders, acquired bleeding diatheses, miscellaneous questions, and thrombotic disorders. Specific topics covered include the hemophilic ankle and knee, hemophilia with HIV, pregnancy in women with hemophilia, hemophilia and scuba diving, hemodialysis, hepatitis in people with hemophilia, VWD and pregnancy, Factor VIII deficiency, Factor X deficiency, Gardner-Diamond syndrome, cocaine and DDAVP, selective serotonin reuptake inhibitors (SSRIs) and clotting disturbances, the work-up for children with intracranial bleeding, treatment of antithrombin deficiency, recurrent thrombosis, and thromboembolic disease. Most sections include references, and a detailed subject index concludes the volume.

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Management of Pregnant Women With Thrombophilia or a History of Venous Thromboembolism. IN: Hematology 2007. Washington, DC: American Society of Hematology. 2007. pp.143-150.

This chapter, from the annual Hematology 2007, considers the management of pregnant women with thrombophilia or a history of venous thromboembolism. The author reminds readers that pregnancy is associated with an increased risk of venous thromboembolism (VTE), and this condition remains an important cause of maternal morbidity and mortality. Recent studies suggest there is a link between thrombophilia and pregnancy loss, as well as with other gestational vascular complications. The author reviews the management and prevention of VTE and other complications related to the heritable thrombophilias during pregnancy. This area remains particularly challenging because of the potential for anticoagulant-related fetal as well as maternal complications and the paucity of good-quality data upon which to base clinical decisions. The author concludes that treatment that prevents fetal loss may not prevent other complications and, at present, data on the effect of antithrombotic interventions in other adverse pregnancy outcomes in women with hereditary thrombophilia are insufficient to provide any recommendations. 6 tables. 53 references.

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Management of Thrombohemorrhagic Syndromes (THS) in Hematologic Malignancies. IN: Hematology 2007. Washington, DC: American Society of Hematology. 2007. pp. 165-171.

This chapter, from the annual Hematology 2007, describes the recommended management of thrombohemorrhagic syndromes (THS) in patients with hematologic malignancies such as leukemia or lymphoma. The authors caution that chemotherapy and antiangiogenic drugs increase the thrombotic risk in patients with lymphomas, acute leukemias, and multiple myeloma (MM). Patients with hematologic malignancies often present with a hypercoagulable state or chronic disseminated intravascular coagulation (DIC) in the absence of active thrombosis and/or bleeding. Some of the factors for clotting activation in hematologic malignancies include malignant cell procoagulant properties, cytotoxic therapies, and concomitant infections. In acute leukemia, clinical manifestations range from localized venous or arterial thrombosis to a diffuse, life-threatening THS. Randomized controlled trials (RCTs) of different prophylactic regimens to prevent VTE or THS in hematologic malignancies are urgently needed, particularly in patients with lymphoma or MM during chemotherapy and in patients with acute promyelocytic leukemia (APL). The authors stress that anticoagulant therapy is a particular challenge in patients with hematologic malignancies because these patients are at very high risk for hemorrhage. No guidelines are presently available for the prophylaxis or treatment of VTE.

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Pathophysiologic Changes Occur in Women Years Before Clinical Diagnosis of Type 2 Diabetes. Review of Endocrinology. 1(3): 40-44. July 2007.

This article explores the traditional and emerging cardiovascular risk factors that may predict the progression from normoglycemia to prediabetes, as well as any gender differences in the risk factor distributions. The authors briefly report on their epidemiologic case-control study of alcohol intake patterns and risk of cardiovascular disease (CVD); the full report was published previously (Stranges, S., et al. Hypertension. 2005). Compared with controls, the prediabetic women were older and had a higher mean waist circumference after adjustment for age, ethnicity, and year of study enrollment. The results demonstrated higher levels of markers of endothelial dysfunction and thrombosis as well as hypertension in women who progressed from normoglycemia to prediabetes. The authors conclude that this shows pathophysiologic changes begin long before the clinical diagnosis of diabetes is made. Clinicians are encouraged to assess each patient’s risk for developing diabetes and coronary artery disease and implement interventions as early as possible with lifestyle modification to prevent or delay type 2 diabetes and CVD. 4 tables. 23 references.

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Platelet Disorders. IN: Provan, D., ed. ABC of Clinical Haematology. Williston, VT: Blackwell Publishing Inc. 2007. pp. 33-39.

Platelets, produced from bone marrow megakaryocytes, are important in the formation of platelet plugs during normal hemostasis. This chapter about platelet disorders is from a book on clinical hematology, written by specialists for nonspecialists. The book is designed to be easy to use and covers the symptoms, investigations, treatment, and management of conditions presenting in day-to-day practice. In this chapter, the authors first review normal hemostasis and then discuss congenital abnormalities, including Fanconi’s anemia, thrombocytopenia with absent radii (TAR syndrome), Wiskott-Aldrich syndrome, MYH9-related thrombocytopenias, disorders of the surface membrane, and platelet storage pool diseases; acquired abnormalities, including decreased production of platelets, increased consumption of platelets, idiopathic thrombocytopenic purpura, post-transfusion purpura, neonatal alloimmune thrombocytopenia, heparin-induced thrombocytopenia, thrombotic thrombocytopenic purpura, microangiopathic thrombocytopenia, disseminated intravascular coagulation, massive blood transfusion, massive splenomegaly, drug-induced platelet disorders, bleeding in patients with uremia, and thrombocytosis; diagnostic tests used to confirm a suspected platelet disorder; and the management of congenital and acquired disorders. The chapter is illustrated with full-color photographs, drawings, and charts. 9 figures. 5 tables. 7 references.

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