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

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Hypercogulable States. IN: Nilsson, K.R.; Piccini, J.P., eds. Osler Medical Handbook. Philadelphia, PA: Saunders. 2006. pp. 526-536.

This chapter on hypercoagulable states is from a handbook that provides the essentials of diagnosis and treatment, as well as the latest in evidence-based medicine, for residents working bedside, in-patient care. The chapter begins with a presentation of essential Fast Facts and concludes with Pearls and Pitfalls useful to the practicing internist. The body of the chapter is divided into sections: Epidemiology, Clinical Presentation, Diagnosis, and Management. Specific topics covered in this chapter include the most important primary (factor V Leiden and prothrombin gene mutation) and secondary (surgery, malignancy, peripartum state) hypercoagulable states; the causes of most thrombotic events, which in most patients require the presence of both a primary and secondary stimulus (such as surgery in patients with inherited thrombophilia); the risk of venous thrombosis in hypercoagulable states; conditions that predispose to both venous and arterial thrombosis, including antiphospholipid antibody syndrome, hyperhomocysteinemia, malignancy, heparin-induced thrombocytopenia and thrombotic syndrome (HIT-TS), and dysfibrinogenemia; and the management of thrombotic events, generally with anticoagulation for at least 3 months. The chapter concludes with a list of references, each labeled with a 'strength of evidence' grade to help readers determine the type of research available in that reference source. 3 figures. 3 tables. 26 references.

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Neonatal Kidney Problems. IN: Hogg, R., ed. Kidney Disorders in Children and Adolescents: A Global Perspective of Clinical Practice. New York, NY: Informa Healthcare USA. 2006. pp 53-66.

This chapter about neonatal kidney problems is from a textbook that presents a global perspective of clinical practice regarding kidney disorders in children and adolescents. The author reviews maturation during fetal life, postnatal maturation, symptoms and signs of renal disease in the neonate, gross hematuria, malformation syndromes, diagnostic tests used to confirm kidney and urologic disorders in the neonate, blood pressure and hypertension, renal function during neonatal respiratory disorders, acute renal failure (ARF), acquired diseases, and drugs and the neonatal kidney, including drugs administered to the mother during pregnancy. Acquired diseases discussed include urinary tract infection; renal venous thrombosis; cortical, medullary, and papillary necrosis; Bartter’s syndrome; nephrogenic diabetes insipidus; and oligonephropathy. The chapter includes black-and-white illustrations and photographs and concludes with an extensive list of references. 6 figures. 16 tables. 24 references.

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New Insights into Paroxysmal Nocturnal Hemoglobinuria. IN: Hematology 2006. Washington, DC: American Society of Hematology. 2006. pp. 24-28.

This article brings readers up-to-date on paroxysmal nocturnal hemoglobinuria (PNH), an uncommon intravascular hemolytic anemia that results from the clonal expansion of hematopoietic stem cells harboring somatic mutations in an X-linked gene, termed PIG-A. PIG-A mutations block glycosylphosphatidylinositol (GPI) anchor biosynthesis, resulting in a deficiency or absence of all GPI-anchored proteins on the cell surface. Intravascular hemolysis leads to release of free hemoglobin, which contributes to many of the clinical manifestations of PNH including fatigue, pain, esophageal spasm, erectile dysfunction and possibly thrombosis. The author also reports on the recent development of a humanized monoclonal antibody directed against the terminal complement protein C5 that has been shown to reduce hemolysis and greatly improve symptoms and quality of life for PNH patients. 2 figures. 40 references.

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Obesity, Diabetes and Endothelial Dysfunction. IN: Obesity and Diabetes. Totowa, NJ: Humana Press. 2006. pp. 213-220.

The prevalence of obesity is increasing globally and is associated with an increased risk of coronary artery disease (CAD), hypertension, dyslipidemia, and type 2 diabetes, all of which combine to an increased risk for cardiovascular disease (CVD). Endothelial dysfunction is an early event in atherogenesis and has been shown to precede by several years the development of clinically detectable atherosclerotic plaques in the coronary arteries. This chapter on obesity, diabetes, and endothelial dysfunction is from a comprehensive textbook on obesity and diabetes. The authors note that the vascular endothelium is no longer viewed as an inert lining of blood vessels, rather, it plays a vital role in vascular homeostasis, vascular tone regulation, vascular smooth muscle cell proliferation, leukocyte migration, thrombosis, and thrombolysis. Endothelial dysfunction is described as a state in which factors that favor a vasoconstrictive, growth-promoting, procoagulant, and proinflammatory state become predominant. Research shows that exercise improves endothelial function; in individuals with risk factors for CVD, exercise appears to be even more beneficial. The authors conclude with a brief discussion on the potential impact of macronutrient modifications (such as the use of olive oil or soy protein) on endothelial function. 56 references.

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Pregnancy and Neonatal Haematology. IN: Hoffbrand, A.V.; Moss, P.A.H.; Pettit, J.E. Essential Haematology. 5th ed. Williston, VT: Blackwell Publishing Inc. 2006. pp. 352-359.

Pregnancy places extreme stresses on the hematological system, thus an understanding of the physiological changes of pregnancy is essential to best care for pregnant women. This chapter on pregnancy and neonatal hematology is from a hematology textbook that offers a comprehensive look at the biochemical, physiological, and immunological processes involved in normal blood cell formation and function and the disturbances that may occur in different diseases. The first section discusses physiological anemia, iron deficiency anemia, folate deficiency, thrombocytopenia, hemostasis and thrombosis, and the treatment of thrombosis in the mother. The neonatal hematology section covers normal blood count, anemia in the neonate, anemia of prematurity, neonatal polycythemia, fetomaternal alloimmune thrombocytopenia, and coagulation. The final section considers hemolytic disease of the newborn (HDN), notably Rh HDN, which occurs when an Rh D-negative woman has a pregnancy with an Rh D-positive fetus. The chapter features full-color photographs and illustrations. 7 figures. 6 references.

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Renal Transplantation in Childhood. IN: Hogg, R., ed. Kidney Disorders in Children and Adolescents: A Global Perspective of Clinical Practice. New York, NY: Informa Healthcare USA. 2006. pp 243-252.

This chapter about renal transplantation in childhood is from a textbook that presents a global perspective of clinical practice regarding kidney disorders in children and adolescents. The author notes that in recent years, graft and patient survival have increased due to improvements in the care of young patients and advances in pharmacologic immunosuppression. The author focuses on providing information for primary care physicians on the care of a child who has received a kidney transplant for end-stage renal disease (ESRD). Topics include the results of transplantation with a living related donor versus a cadaveric donor; graft survival; antirejection medications, including corticosteroids, azathioprine, mycophenolate mofetil, cyclosporine, tacrolimus, rapamycin, and antilymphocyte antibodies; complications of renal transplantation, including delayed graft function, vascular thrombosis, rejection, hypertension, infections, recurrence of primary disease, malignancy, and noncompliance with treatment; growth after renal transplantation; and preparation for renal transplantation. 33 references.

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Role of JAK-STAT Signaling in the Pathogenesis of Myeloproliferative Disorders. IN: Hematology 2006. Washington, DC: American Society of Hematology. 2006. pp 233-239.

This article outlines the role of JAK–STAT signaling in the pathogenesis of myeloproliferative disorders (MPD). The authors contend that the identification of JAK2V617F mutations in polycythemia vera (PV), essential thrombocytosis (ET), and myelofibrosis (MF) represents an important advance in our understanding of these myeloproliferative disorders (MPD). Most, if not all, patients with PV and a significant number of patients with ET and MF are JAK2V617F positive, and the mutation likely arises in the hematopoietic stem cell compartment. The authors review animal studies that support the central role of JAK2V617F in the pathogenesis of MPD. They conclude that, despite these advances, many questions remain regarding the role of a single disease allele in three phenotypically distinct MPD and the potential clinical efficacy of JAK2 inhibitors. 1 table. 58 references.

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Think of HIT. Washington, DC: American Society of Hematology. 2006. pp. 408-414.

This article reviews the condition of heparin-induced thrombocytopenia (HIT), a problem that can present in many ways, ranging from isolated thrombocytopenia, venous thromboembolism, or acute limb ischemia to less common but specific presentations such as necrotizing skin lesions at heparin injection sites, post-bolus acute systemic reactions, and adrenal hemorrhagic necrosis—secondary to adrenal vein thrombosis. HIT is an acquired, transient, prothrombotic disorder that, ironically, is caused by the anticoagulant heparin and is characterized by mild or moderate thrombocytopenia. HIT that begins after stopping heparin—"delayed-onset HIT"—is increasingly recognized. The author reviews factors influencing the risk of HIT include type of heparin—unfractionated heparin holds a greater risk than low-molecular-weight heparin, type of patient—surgical patients have a greater risk than medical patients, and gender—females have a greater risk than males. Since timely diagnosis and treatment of HIT may reduce the risk of adverse outcomes, the author focuses on those clinical circumstances that should prompt the clinician to consider the presence of HIT. The author cautions that coumarin anticoagulants such as warfarin are ineffective in acute HIT and can even be deleterious by predisposing to micro-thrombosis via protein C depletion. Thus, it is important to avoid or postpone coumarin while managing HIT hypercoagulability, using instead agents that inhibit thrombin directly—lepirudin, algarroba—or that inhibit its generation—danaparoid, fondaparinux. 4 figures. 3 tables. 40 references.

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Thrombosis and Antithrombotic Therapy. IN: Hoffbrand, A.V.; Moss, P.A.H.; Pettit, J.E. Essential Haematology. 5th ed. Williston, VT: Blackwell Publishing Inc. 2006. pp. 303-319.

This chapter on thrombosis and antithrombotic therapy is from a hematology textbook that offers a comprehensive look at the biochemical, physiological, and immunological processes involved in normal blood cell formation and function and the disturbances that may occur in different diseases. Thrombi are solid masses or plugs formed in the circulation from blood components, primarily platelets and fibrin. Symptoms arising from these clots result from ischemia, or lack of blood flow, from either local vascular obstruction or distant embolization. Thrombosis, both arterial and venous, is more common as age increases and is associated with certain risk factors such as surgery or pregnancy. The authors discuss arterial thrombosis, venous thrombosis, investigation of thrombophilia, diagnosis of venous thrombosis, anticoagulant drugs, heparin, oral anticoagulants, graduated compression stockings, inferior vena cava filter, fibrinolytic agents, and antiplatelet drugs. The chapter features full-color illustrations. 8 figures. 10 tables. 27 references.

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Thrombosis in Infants and Children. IN: Hematology 2006. Washington, DC: American Society of Hematology. 2006. pp 86-96.

This article reviews thromboembolism (TE) in childhood, still considered a rare event. During the last decade much progress has been made toward better understanding of the underlying reasons causing thromboembolism in children, and better understanding of diagnostics and therapy has followed suit. A considerable number of acquired and hereditary thrombotic risk factors have been identified which may also have an impact on therapeutic decisions and prognosis concerning outcome and the risk of a second event. However, indications for therapeutic interventions, such as thrombolysis and prophylactic anticoagulation with respect to the different clinical conditions and their combination with other risk factors, are not yet well defined. The authors describe the causes, epidemiology, clinical presentation, and management of thrombosis in neonates, infants, and older children, focusing on the most clinically relevant conditions, including the management of thrombosis in children with cancer. 2 figures. 5 tables. 65 references.

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