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1
Bernhardt, Ingolf, and J. Clive Ellory, eds. Red Cell Membrane Transport in Health and Disease. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/978-3-662-05181-8.
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2
Bernhardt, Ingolf. Red Cell Membrane Transport in Health and Disease. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003.
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3
R, Bridges Kenneth, and Pearson Howard A, eds. Anemias and other red cell disorders. New York: McGraw-Hill, 2007.
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4
Tsuyoshi, Ohnishi S., and Ohnishi Tomoko, eds. Membrane abnormalities in sickle cell disease and in other red blood cell disorders. Boca Raton, Fla: CRC Press, 1994.
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5
Malaria resistance or susceptibility in red cells disorders. Hauppauge, NY: Nova Science, 2009.
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6
1949-, Agre Peter, and Cartron Jean Pierre, eds. Protein blood group antigens of the human red cell: Structure, function, and clinical significance. Baltimore: Johns Hopkins University Press, 1992.
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7
The match: "savior siblings" and one family's battle to heal their daughter. Boston: Beacon Press, 2010.
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8
Lichtman, Marshall A., and Josef T. Prchal. Red Cell and Its Diseases. McGraw-Hill Education, 2021.
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9
Provan, Drew, Trevor Baglin, Inderjeet Dokal, and Johannes de Vos. Red cell disorders. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199683307.003.0002.
Повний текст джерелаАнотація:
The peripheral blood film in anaemias - Anaemia in renal disease - Anaemia in endocrine disease - Anaemia in joint disease - Anaemia in gastrointestinal disease - Anaemia in liver disease - Iron (Fe) deficiency anaemia - Vitamin B12 deficiency - Folate deficiency - Other causes of megaloblastic anaemia - Anaemia in other deficiency states - Haemolytic syndromes - Genetic control of haemoglobin production - Sickling disorders - HbS—sickle-modifying therapies - Sickle cell trait (HbAS) - Other sickling disorders - Other haemoglobinopathies - Unstable haemoglobins - Thalassaemias - α thalassaemia - β thalassaemia - Other thalassaemias - Hereditary persistence of fetal haemoglobin - Hb patterns in haemoglobin disorders - Non-immune haemolysis - Hereditary spherocytosis - Hereditary elliptocytosis - Glucose-6-phosphate dehydrogenase (G6PD) deficiency - Pyruvate kinase deficiency - Other red cell enzymopathies - Drug-induced haemolytic anaemia - Methaemoglobinaemia - Microangiopathic haemolytic anaemia - Acanthocytosis - Autoimmune haemolytic anaemia - Cold haemagglutinin disease - Leucoerythroblastic anaemia - Aplastic anaemia - Paroxysmal nocturnal haemoglobinuria - Pure red cell aplasia - Iron (Fe) overload - Transfusion haemosiderosis
10
Provan, Drew, Trevor Baglin, Inderjeet Dokal, Johannes de Vos, Banu Kaya, and Angela Theodoulou. Red cell disorders. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199683307.003.0002_update_001.
Повний текст джерелаАнотація:
The peripheral blood film in anaemias - Anaemia in renal disease - Anaemia in endocrine disease - Anaemia in joint disease - Anaemia in gastrointestinal disease - Anaemia in liver disease - Iron (Fe) deficiency anaemia - Vitamin B12 deficiency - Folate deficiency - Other causes of megaloblastic anaemia - Anaemia in other deficiency states - Haemolytic syndromes - Genetic control of haemoglobin production - Sickling disorders - HbS—sickle-modifying therapies - Sickle cell trait (HbAS) - Other sickling disorders - Other haemoglobinopathies - Unstable haemoglobins - Thalassaemias - α thalassaemia - β thalassaemia - Other thalassaemias - Hereditary persistence of fetal haemoglobin - Hb patterns in haemoglobin disorders - Non-immune haemolysis - Hereditary spherocytosis - Hereditary elliptocytosis - Glucose-6-phosphate dehydrogenase (G6PD) deficiency - Pyruvate kinase deficiency - Other red cell enzymopathies - Drug-induced haemolytic anaemia - Methaemoglobinaemia - Microangiopathic haemolytic anaemia - Acanthocytosis - Autoimmune haemolytic anaemia - Cold haemagglutinin disease - Leucoerythroblastic anaemia - Aplastic anaemia - Paroxysmal nocturnal haemoglobinuria - Pure red cell aplasia - Iron (Fe) overload - Transfusion haemosiderosis
11
Clarke, Noel W. Metastatic disease in prostate cancer. Edited by James W. F. Catto. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199659579.003.0068.
Повний текст джерелаАнотація:
Metastases are the predominant cause of morbidity and death from prostate cancer (CaP). The tendency for cells to migrate from the primary site, enter the vascular/lymphatic circulation, and implant/grow at secondary sites is the principal discriminator of aggressive form indolent disease. But this process is poorly understood. Cells enter the circulation in increasing number as the disease progresses, impinging on endothelial surfaces, particularly in red bone marrow where they bind and transmigrate, forming early cell colonies. This requires chemo-attractants and nutrients enabling cellular survival. Established metastases thrive independently, disrupting local tissue, as characterized by progressive replacement of red bone marrow and disruption of skeletal architecture. Bone disruption includes massive overstimulation of both osteoblasts and osteoclasts, inducing synchronous over-production of abnormal bone and gross osteolysis.
12
Jain, Shilpa, and Mark T. Gladwin. Sickle crisis in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0275.
Повний текст джерелаАнотація:
Sickle cell disease crises are precipitated by an acute occlusion of microvessels, which can lead to end organ ischaemia reperfusion injury and acute haemolysis. Acute fat emboli syndrome, acute lung injury (the acute chest syndrome), acute pulmonary hypertension, and cor pulmonale, haemorrhagic and occlusive stroke, and systemic infection represent the most common life-threatening complications observed in current ICU practice. General principles of management in all patients admitted to the critical care unit are hydration, antibiotics, pain control, and maintenance of oxygenation and ventilation. Red blood cell transfusion therapy is the treatment of choice for most complications of sickle cell disease requiring intensive care management. Transfusion of sickle negative, leukoreduced red blood cells, phenotypically matched for Rhesus and Kell antigens is the minimum standard of care in sickle cell disease patients as they have a high incidence of red blood cell alloimmunization.
13
(Editor), I. Bernhardt, and J. C. Ellory (Editor), eds. Red Cell Membrane Transport in Health and Disease. Springer, 2003.
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14
Walsh, Timothy. Pathophysiology and management of anaemia in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0273.
Повний текст джерелаАнотація:
Anaemia is prevalent among the critically ill, with a multifactorial aetiology including haemodilution, iatrogenic blood loss, a reduced red cell lifespan, and especially decreased erythropoiesis. Acute inflammation probably has a major contribution to critical illness-induced anaemia, resulting in reduced iron absorption, sequestration of iron resulting in functional iron deficiency, relative erythropoietin deficiency, and impaired marrow red cell maturation. Anaemia during critical illness resembles the anaemia of chronic inflammatory disease, and probably results from similar pathophysiological processes. Current evidence does not support pharmacological manipulation of this process with iron or erythropoietin. Management should focus on minimization of blood loss and evidence-based use of red cells to maintain haemoglobin level.
15
Mutter, Walter P. Urinalysis. Edited by Christopher G. Winearls. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0006.
Повний текст джерелаАнотація:
Physicians have examined urine for over 6000 years. Urine microscopy was first employed to diagnose kidney disease in the seventeenth century and remains an indispensable tool. The value of urinalysis for diagnosis and management of renal and genitourinary disease is well accepted. Urinalysis aids in the diagnosis of renal disease especially in cases when a renal biopsy is not immediately available or is contraindicated. It is most informative when done by the treating physician with knowledge of the clinical context. Inspection is done by eye. Routine chemical analysis is done by dipstick but urine microscopy is essential for it may reveal abnormalities even when chemical evaluation is normal. Dysmorphic red cells, red cell casts, white blood cells, renal cells, and specific crystals may be diagnostically important. Urinalysis and microscopy can narrow the differential diagnosis faster than many more complex tests are able to.
16
Lance, Eboni I., and Andrew W. Zimmerman. Sickle Cell Anemia. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0079.
Повний текст джерелаАнотація:
Sickle cell disease is a genetic hematological disorder involving red blood cells that become deformed when stressed. Patients with homozygous hemoglobin SS disease often have multiple systemic and neurologic complications, particularly stroke. Intellectual disability is commonly seen in the population, in patients with and without a history of stroke, attributed to different underlying mechanisms of brain injury. Autism is rare and not described in sickle cell disease in the literature to date. Many treatments (chronic transfusion therapy, hydroxyurea, bone marrow transplant) are in trials at this time to see if risk of stroke and other neurologic complications can be reduced (ClinicalTrials.gov identifiers: NCT01425307, NCT01389024, NCT00152113).
17
Provan, Drew, Trevor Baglin, Inderjeet Dokal, and Johannes de Vos. Paediatric haematology. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199683307.003.0012.
Повний текст джерелаАнотація:
Blood counts in children - Red cell transfusion and blood component therapy—special considerations in neonates and children - Polycythaemia in newborn and childhood - Neonatal anaemia - Anaemia of prematurity - Haemolytic anaemia in the neonate - Congenital red cell defects - Acquired red cell defects - Haemolytic disease of the newborn - Hyperbilirubinaemia - Neonatal haemostasis - Neonatal alloimmune thrombocytopenia - Congenital dyserythropoietic anaemias - Congenital red cell aplasia - Acquired red cell aplasia - Fanconi anaemia - Rare congenital marrow failure syndromes - Neutropenia in childhood - Disorders of neutrophil function - Childhood immune (idiopathic) thrombocytopenic purpura - Haemolytic uraemic syndrome - Childhood cancer and malignant blood disorders - Childhood lymphoblastic leukaemia - Childhood lymphomas - Childhood acute myeloid leukaemia - Childhood myelodysplastic syndromes and chronic leukaemias - Histiocytic syndromes - Haematological effects of systemic disease in children
18
Provan, Drew, Trevor Baglin, Inderjeet Dokal, Johannes de Vos, and Angela Theodoulou. Paediatric haematology. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199683307.003.0012_update_001.
Повний текст джерелаАнотація:
Blood counts in children - Red cell transfusion and blood component therapy—special considerations in neonates and children - Polycythaemia in newborn and childhood - Neonatal anaemia - Anaemia of prematurity - Haemolytic anaemia in the neonate - Congenital red cell defects - Acquired red cell defects - Haemolytic disease of the newborn - Hyperbilirubinaemia - Neonatal haemostasis - Neonatal alloimmune thrombocytopenia - Congenital dyserythropoietic anaemias - Congenital red cell aplasia - Acquired red cell aplasia - Fanconi anaemia - Rare congenital marrow failure syndromes - Neutropenia in childhood - Disorders of neutrophil function - Childhood immune (idiopathic) thrombocytopenic purpura - Haemolytic uraemic syndrome - Childhood cancer and malignant blood disorders - Childhood lymphoblastic leukaemia - Childhood lymphomas - Childhood acute myeloid leukaemia - Childhood myelodysplastic syndromes and chronic leukaemias - Histiocytic syndromes - Haematological effects of systemic disease in children
19
Spinella, Philip C., and Jeffrey J. Bednarski. Hematology and Oncology. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199918027.003.0013.
Повний текст джерелаАнотація:
Coagulopathy, thrombosis, and other hematological abnormalities are common in the pediatric intensive care unit . Current guidelines recommend red blood cell transfusion for a hemoglobin concentration less than 7 g/dL in critically ill, hemodynamically stable patients; platelets for a concentration less than 10,000 in nonbleeding patients; and cryoprecipitate in bleeding patients for fibrinogen values less than 100 to 150 mg/dL. Massive transfusion protocols that push blood products to the bedside are more practical than reactive protocols. Transfusion reactions include transfusion-associated acute lung injury and transfusion-associated circulatory overload. Hematologic crises in the PICU are commonly complications of other primary disorders. Sickle cell disease may lead to acute chest syndrome, sequestration crisis, and stroke, and require aggressive intervention. Oncological diseases produce hyperleukocytosis, tumor lysis syndrome, veno-occlusive disease, graft-versus-host disease, and sepsis in association with leukopenia. A relatively newly recognized disorder, hemophagocytic lymphohistiocytosis, requires early recognition and treatment to avoid adverse outcomes.
20
Ajithkumar, Thankamma, Ann Barrett, Helen Hatcher, and Natalie Cook. Haematological malignancies. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199235636.003.0013.
Повний текст джерелаАнотація:
Hodgkin's lymphoma (HL), now called Hodgkin disease, is one of the neoplastic diseases of the lymphatic tissue. In 1832, Thomas Hodgkin first described the disease in his historic paper entitled ‘On Some Morbid Appearances of the Absorbant Glands and Spleen’. In 1898 and 1902 Carl Sternberg and Dorothy Reed contributed the first microscopic descriptions of the pathognomonic Hodgkin and Reed–Sternberg (H-RS) cells (...
21
Kesteven, Patrick. Haematology. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0061.
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This chapter describes the common haematological abnormalities seen in rheumatic conditions with special reference to laboratory findings and diagnostic traps. The chapter is organized into sections dealing with red cell abnormalities (and the distinction between anaemia of chronic disease and iron deficiency); white cell abnormalities (neutrophilia and neutropenia); platelets (thrombocytosis, idiopathic thrombocytopenic purpura and thrombotic thrombocytopenic purpura); and finally coagulation abnormalities (lupus anticoagulant).
22
Watkins, Neal, and Patti Harter. Announcing the Coming End of Biological Aging and Disease: Read about 24 Major Diseases Already Targeted with Regenerative Stem Cell Therapy! Independently Published, 2017.
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23
Neary, John, and Neil Turner. The patient with haematuria. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0046.
Повний текст джерелаАнотація:
Haematuria is a common presenting feature of diseases of the kidney or the renal tract. It is also common in screening tests, single dipstick tests being positive in perhaps 5% of individuals. Age and whether the blood is visible (macroscopic) or non-visible (microscopic) impact largely on whether the explanation is likely to be broadly urological or nephrological. Origins are most commonly simple or urological. Macroscopic bleeding is rare in renal disease, and urine colour is then usually more rather smoky than red except when there is very acute inflammation. The chief urological causes are neoplasia, infection, stones, and trauma. Some traditionally medical conditions may cause simple bleeding; examples include cystic kidney diseases, papillary necrosis and macro- or microvascular ischaemic lesions. The major concern to nephrologists is that even non-visible haematuria may be a pointer to inflammatory or destructive glomerular processes. The presence of casts or dysmorphic red cells is a pointer to glomerular disease; more important in clinical practice are the three other key markers of renal disease: proteinuria, renal impairment in the absence of urinary tract obstruction, and hypertension. In the general population, microscopic haematuria does associate with a long-term increased risk of end-stage renal failure, so after negative investigations, occasional long-term checks are indicated. The case for population screening for haematuria appears weak.
24
Macdougall, Iain C. Clinical aspects and overview of renal anaemia. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0123.
Повний текст джерелаАнотація:
Anaemia is an almost ubiquitous complication of chronic kidney disease, which has a number of implications for the patient. It is associated with adverse outcomes, an increased rate of red cell transfusions, poor quality of life, and reduced physical capacity. Severe anaemia also impacts on cardiac function, as well as on platelet function, the latter contributing to the bleeding diathesis of uraemia. Renal anaemia occurs mainly in the later stages of chronic kidney disease (stages 3B, 4, and 5), and up to 95% of patients on dialysis suffer from this condition. It is caused largely by inappropriately low erythropoietin levels, but other factors such as a shortened red cell survival also play a part. The anaemia is usually normochromic and normocytic, unless concomitant iron deficiency is present. The latter is also common in renal failure, partly due to low dietary iron intake and absorption, and partly due to increased iron losses. Prior to the 1990s, treatment options were limited, and many patients (particularly those on haemodialysis) required regular blood transfusions, resulting in iron overload and human leucocyte antigen sensitization. Correction of anaemia requires two main treatment strategies: increased stimulation of erythropoiesis, and maintenance of an adequate iron supply to the bone marrow. Ever since the introduction of recombinant human erythropoietin, it has been possible to boost erythropoietic activity, and both oral and intravenous iron products are available to provide supplemental iron. In dialysis patients, oral iron is usually poorly absorbed due to upregulation of hepcidin activity, and intravenous iron is often required. The physiological processes relevant to red cell production are described, as well as the prevalence, characteristics, pathogenesis, and physiological consequences of renal anaemia.
25
Grace, Rachael. Fast Facts : Pyruvate Kinase Deficiency for Patients and Supporters: A Rare Genetic Disease That Affects Red Blood Cells. Karger AG, S., 2019.
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26
Macdougall, Iain C. Erythropoiesis-stimulating agents in chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0124.
Повний текст джерелаАнотація:
The advent of recombinant human erythropoietin (epoetin) in the late 1980s transformed the management of renal anaemia, liberating many dialysis patients from lifelong regular blood transfusions, in turn causing severe iron overload and human leucocyte antigen sensitization. Epoetin can be administered either intravenously or subcutaneously, but the half-life of the drug is fairly short at around 6–8 hours, necessitating frequent injections. To circumvent this problem, two manipulations to the erythropoietin molecule were engineered. The first of these was to attach an extra two carbohydrate chains to the therapeutic protein hormone (to make darbepoetin alfa), and the second was to attach a large pegylation chain to make continuous erythropoietin receptor activator. Both of these strategies prolonged the circulating half-life of the erythropoietin analogue. The next erythropoietic agent to be produced was peginesatide, a peptide-based agent which had no structural homology with native or recombinant erythropoietin, but shared the same biological and functional characteristics. Future strategies include stabilization of hypoxia-inducible factor, by orally active inhibitors of the prolyl hydroxylase enzyme, and advanced clinical trials are underway. In the meantime, several large randomized controlled trials have highlighted the potential harm in targeting a near normal haemoglobin of 13–14 g/dL (with an increased risk of cardiovascular complications), and sub-normal correction of anaemia is now advised. Some patients may show mild or severe resistance to erythropoiesis-stimulating agent (ESA) therapy, and common causes include iron insufficiency, infection, and underlying inflammation. Very rarely, patients may produce antibodies against their ESA, which neutralize not only the ESA, but also endogenous erythropoietin, causing pure red cell aplasia.
27
Steensma, David P. Benign Hematology. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199755691.003.0294.
Повний текст джерелаАнотація:
The major forms of benign hematologic conditions are anemia, neutropenia, transfusion reactions, Gaucher disease, and porphyria. Anemia is a sign of disease rather than a disease itself. Anemia results from 1 or more of 3 pathologic mechanisms: inadequate production of red blood cells (RBCs) by the bone marrow, blood loss, or premature destruction of RBCs. The major causes of neutropenia include hematologic neoplasm, metastatic neoplasm involving the marrow, irradiation, vitamin B12 deficiency and folate deficiency, drugs, infections, congenital or acquired primary disorders of hematopoiesis, autoimmune neutropenia, hypersplenism, hemodilution, and benign idiopathic neutropenia. The porphyrias are enzyme disorders that are autosomal dominant with low disease penetrance, except for congenital erythropoietic porphyria, which is autosomal recessive, and porphyria cutanea tarda, which may be acquired and is associated with hepatitis C and hemochromatosis.
28
Protein Blood Group Antigens of the Human Red Cell: Structure, Function, and Clinical Significance (The Johns Hopkins Series in Hematology/Oncology). The Johns Hopkins University Press, 1992.
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29
Barros, Rodrigo José Saraiva de, Tereza Cristina de Brito Azevedo, Carla de Castro Sant’Anna, Marianne Rodrigues Fernandes, Leticia Martins Lamarão, and Rommel Mario Rodríguez Burbano. Grupos sanguíneos e anticorpos anti-eritrocitários de importância transfusional. Brazil Publishing, 2020. http://dx.doi.org/10.31012/978-65-5861-112-7.
Повний текст джерелаАнотація:
Immunohematology is an area dedicated to the study of the interactions of the immune system and blood cells in transfusion practice. Blood transfusion is a therapeutic technique that has been widely used since the 17th century. The transfusion medicine aims to repair the pathological needs of blood components in the living organism, be it red blood cells, plasma, platelets, clotting factors, among others. Despite being a therapeutic means, transfusion of blood components can be considered at risk because it is a biological material and due to the transfusion immunological reactions that can be caused during or after the moment of transfusion. In the surface structure of red blood cells, numerous molecules of a protein, glycoprotein or glycolipid nature are found, which are also called membrane antigens that make up structures and perform transport functions, as receptors, as adhesion, enzymatic and / or complement regulatory molecules. The formation of these antigens occurs by an approximate amount of 39 genes involved in their production, of which 282 different antigens are organized in more than 30 blood group systems. This antigenic diversity is a major cause of the formation of irregular anti-erythrocyte antibodies. Therefore, with the increase in blood transfusions in surgeries, transplants and clinical treatment of cancer and other chronic diseases, a significant increase in the occurrence of alloimmunizations in polytransfused patients began to be observed. Such biological phenomena motivated us to carry out this study and the antigenic diversity motivated us to elaborate this small compendium where we also describe the main blood groups.
30
Izzedine, Hassan, and Victor Gueutin. Drug-induced acute tubulointerstitial nephritis. Edited by Adrian Covic. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0084.
Повний текст джерелаАнотація:
Drug-induced acute tubulointerstitial nephritis (ATIN) is the most common aetiology of ATIN and a potentially correctable cause of acute kidney injury (AKI). An interval of 7–10 days typically exists between drug exposure and development of AKI, but this interval can be considerably shorter following re-challenge or markedly longer with certain drugs. It occurs in an idiosyncratic and non-dose-dependent manner. Antibiotics, NSAIDs, and proton pump inhibitors are the most frequently involved agents, but the list of drugs that can induce ATIN is continuously increasing. The mechanism of renal injury is postulated to involve cell-mediated immunity, supported by the observation that T cells are the predominant cell type comprising the interstitial infiltrate. A humoral response underlies rare cases of ATIN, in which a portion of a drug molecule (i.e. methicillin) may act as a hapten, bind to the tubular basement membrane (TBM), and elicit anti-TBM antibodies. The classic symptoms of fever, rash, and arthralgia may be absent in up to two-thirds of patients. Diagnostic studies, such as urine eosinophils and renal gallium-67 scanning provide only suggestive evidence. Renal biopsy remains the gold standard for diagnosis, but it may not be required in mild cases or when clinical improvement is rapid after removal of an offending medication. Pathologic findings include interstitial inflammation, oedema, and tubulitis. The time until removal of such agents and the severity of renal biopsy findings provide the best prognostic value for the return to baseline renal function. Poor prognostic indicators are the long duration of AKI (> 3 weeks), a patient’s advanced age, and the high degree of interstitial fibrosis. Early recognition and appropriate therapy are essential to the management of drug-induced ATIN, because patients can ultimately develop chronic kidney disease. The mainstay of therapy is timely discontinuation of the causative agent, whereas controversy persists about the role of steroids.
31
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.
Повний текст джерелаАнотація:
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.
32
El Kenz, Hanane, and Philippe Van der Linden. The physiology of blood in anaesthetic practice. Edited by Jonathan G. Hardman. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0011.
Повний текст джерелаАнотація:
Following the discovery of the ABO blood groups by Landsteiner in 1901, Albert Hustin described the first transfusion of a whole blood unit in 1914. The modern transfusion era really begins in 1916 with the discovery of sodium citrate as an anticoagulant by the same physician, allowing blood conservation in dedicated packs. Since that time, many advances have been made especially over the past two decades in the storage, the conservation, and the laboratory testing of blood components and in transfusion medicine practice. Transfusion of whole blood has been replaced by blood component therapy, which consists of the administration of packed red blood cells, fresh frozen plasma, or platelets. Although blood transfusion is safer than ever, the risk of complications will never reach zero. The risk of infectious transfusion-transmitted diseases has been markedly reduced by the implementation of extensive infectious disease testing, donor selection, and pathogen-inactivation procedures. In countries with a high human development index, the leading causes of allogeneic blood transfusion-related deaths actually resulted from immunological and septic complications. The first section of this chapter describes the structure, function, and immunological aspects of the different blood components that are routinely transfused today. The second section details the composition of the different blood components, their indications, the pre-transfusion compatibility tests, and the main adverse effects associated with their transfusion.
33
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.
Повний текст джерелаАнотація:
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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Cox, F. E. G. Babesiosis and malaria. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198570028.003.0055.
Повний текст джерелаАнотація:
Babesiosis and malaria are rare zoonoses that, with new developments in diagnosis and the application of molecular techniques, are becoming increasingly frequently recognised. Babesia species infect millions of cattle and unknown numbers of sheep, dogs, horses, and wildlife throughout the world but human infections are very uncommon. There are two distinct forms of human babesiosis. In Europe the causative agent is Babesia divergens, a natural parasite of cattle transmitted by the tick Ixodes ricinis. B. divergens infections in humans are extremely rare and nearly all have been recorded from asplenic or otherwise immunocompromised patients. In the USA, human babesiosis is more common than in Europe, although still very rare, and is not restricted to immunocompromised individuals. The causative agents are Babesia microti and B. duncani, common parasites of rodents, transmitted by the tick Ixodes scapularis. In addition there have been sporadic reports of human babesiosis from other parts of the world but in most cases the species of Babesia involved has not been characterised. Malaria parasites and Babesia both inhabit red blood cells during part of their life cycles and these stages cause the diseases, malaria and babesiosis, which are similar in many respects. The facts that humans can occasionally acquire malaria and babesiosis from animals, that both parasites appear similar when seen in blood films and that both cause similar symptoms can cause problems in diagnosis and these rare infections are, therefore, of interest to clinicians and epidemiologists.
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Barsoum, Rashad S. Schistosomiasis. Edited by Neil Sheerin. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0181_update_001.
Повний текст джерелаАнотація:
AbstractSchistosomes are blood flukes that parasitize humans, apes, cattle, and other animals. In these definitive hosts they are bisexual, and lay eggs which are shed to fresh water where they complete an asexual cycle in different snails, ending in the release of cercariae which infect the definitive hosts to complete the life cycle.Seven of over 100 species of schistosomes are human pathogens, causing disease in different organs depending on the parasite species. Racial and genetic factors are involved in susceptibility, severity, and sequelae of infection.Morbidity is induced by the host’s immune response to schistosomal antigens. The latter include tegument, microsomal, gut, and oval antigens. The former are important in the process of invasion and establishment of infection, oval antigens in formation of granulomata which lead to fibrosis in different sites, and the gut antigens constitute the main circulating antigens in established infection, leading to immune-complex disease, particularly in the kidneys. The host immunological response includes innate and adaptive mechanisms, the former being the front line responsible for removing 90% of the infecting cercarial load. Adaptive immunity includes a Th1 phase, dominated by activation of an acute inflammatory response, followed by a prolonged Th2 phase which is responsible for immunity to re-infection as well as progression of tissue injury. Switching from Th1 to Th2 phases is controlled by functional and morphological change in the antigen-presenting cells, which is achieved by molecules of host as well as parasitic origin.Many cells participate in parasite killing, but also in the induction of tissue injury. The most potent of these is the eosinophil, which by binding antibodies to the parasite, particularly immunoglobulin E, facilitates parasite elimination. However, this process is complex, including agonist as well as antagonist pathways, which provide escape mechanisms for the parasite to survive, thereby achieving a delicate balance that permits schistosomes to live for decades in the infected host.
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Macdougall, Iain C. Iron management in renal anaemia. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0126.
Повний текст джерелаАнотація:
Although erythropoiesis-stimulating agent therapy is the mainstay of renal anaemia management, maintenance of an adequate iron supply to the bone marrow is also pivotal in the process of erythropoiesis. Thus, it is important to be able to detect iron insufficiency, and to treat this appropriately. Iron deficiency may be absolute (when the total body iron stores are exhausted) or functional (when the total body iron stores are normal or increased, but there is an inability to release iron from the stores rapidly enough to provide a ready supply of iron to the bone marrow). Several markers of iron status have been tested, but those of the greatest utility are the serum ferritin, transferrin saturation, and percentage of hypochromic red cells. Measurement of serum hepcidin, which is the master regulator of iron homoeostasis, has to date proved disappointing as a means of detecting iron insufficiency, and none of the available iron markers reliably exclude the need for supplemental iron. Iron may be replaced by either the oral or the intravenous route. In the advanced stages of chronic kidney disease, however, hepcidin is upregulated, and this powerfully inhibits the absorption of iron from the gut. Thus, such patients often require intravenous iron, particularly those on dialysis. Several intravenous (IV) iron preparations are available, and they have in common a core containing an iron salt, surrounded by a carbohydrate shell. The IV iron preparations differ in their kinetics of iron release from the iron–carbohydrate complex. In recent times, several new IV iron preparations have become available, and these allow a greater amount of iron to be given more rapidly as a single administration, without the need for a test dose.
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Lee, Olivia T., Jennifer N. Wu, Frederick J. Meyers, and Christopher P. Evans. Genitourinary aspects of palliative care. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199656097.003.0084.
Повний текст джерелаАнотація:
Genitourinary tract diseases in the palliative care setting most commonly involve urinary tract obstruction, intractable bleeding, fistulae, and bladder-associated pain. Sources of obstruction in the lower urinary tract include benign prostatic hyperplasia, invasive prostate or bladder cancer, urethral stricture, or bladder neck contracture. Upper tract obstruction includes intraluminal or extraluminal blockage of the renal collecting system and ureters, such as transitional cell carcinoma, fibroepithelial polyps, stricture, stones, pelvic or retroperitoneal malignancy, fibrosis, or prior radiation. Untreated, obstructive uropathy leads to elevated bladder, ureter, and kidney pressures, bladder dysfunction, urolithiasis, renal failure, pyelonephritis, or urosepsis. Intractable haematuria can cause problematic anaemia, frequent transfusions, clot retention, haemorrhagic shock, and death. In addition, urinary tract fistulae such as vesicovaginal and vesicoenteric fistulae are common in patients who have had prior pelvic surgery or radiation especially in the setting of immunocompromise, poor nutrition, and infection. Untreated, these symptoms lead to rash, skin breakdown, ulcers, chronic infection, and sepsis. Lastly, pelvic and bladder pain, depending on aetiology can be treated with oral medications, intravesical therapies, or surgical therapies such as palliative resection or urinary diversion. Selection of tests and treatment modalities in the palliative care setting should be based on using the least invasive means to achieve the most relief in suffering. Some genitourinary conditions are potentially fatal, and in the acute or subacute setting, require re-evaluation of the end-of-life goals and wishes of the patient and family.
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Alexander, D. J., N. Phin, and M. Zuckerman. Influenza. Edited by I. H. Brown. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198570028.003.0037.
Повний текст джерелаАнотація:
Influenza is a highly infectious, acute illness which has affected humans and animals since ancient times. Influenza viruses form the Orthomyxoviridae family and are grouped into types A, B, and C on the basis of the antigenic nature of the internal nucleocapsid or the matrix protein. Infl uenza A viruses infect a large variety of animal species, including humans, pigs, horses, sea mammals, and birds, occasionally producing devastating pandemics in humans, such as in 1918 when it has been estimated that between 50–100 million deaths occurred worldwide.There are two important viral surface glycoproteins, the haemagglutinin (HA) and neuraminidase (NA). The HA binds to sialic acid receptors on the membrane of host cells and is the primary antigen against which a host’s antibody response is targeted. The NA cleaves the sialic acid bond attaching new viral particles to the cell membrane of host cells allowing their release. The NA is also the target of the neuraminidase inhibitor class of antiviral agents that include oseltamivir and zanamivir and newer agents such as peramivir. Both these glycoproteins are important antigens for inducing protective immunity in the host and therefore show the greatest variation.Influenza A viruses are classified into 16 antigenically distinct HA (H1–16) and 9 NA subtypes (N1–9). Although viruses of relatively few subtype combinations have been isolated from mammalian species, all subtypes, in most combinations, have been isolated from birds. Each virus possesses one HA and one NA subtype.Last century, the sudden emergence of antigenically different strains in humans, termed antigenic shift, occurred on three occasions, 1918 (H1N1), 1957 (H2N2) and 1968 (H3N2), resulting in pandemics. The frequent epidemics that occur between the pandemics are as a result of gradual antigenic change in the prevalent virus, termed antigenic drift. Epidemics throughout the world occur in the human population due to infection with influenza A viruses, such as H1N1 and H3N2 subtypes, or with influenza B virus. Phylogenetic studies have led to the suggestion that aquatic birds that show no signs of disease could be the source of many influenza A viruses in other species. The 1918 H1N1 pandemic strain is thought to have arisen as a result of spontaneous mutations within an avian H1N1 virus. However, most pandemic strains, such as the 1957 H2N2, 1968 H3N2 and 2009 pandemic H1N1, are considered to have emerged by genetic re-assortment of the segmented RNA genome of the virus, with the avian and human influenza A viruses infecting the same host.Influenza viruses do not pass readily between humans and birds but transmission between humans and other animals has been demonstrated. This has led to the suggestion that the proposed reassortment of human and avian influenza viruses takes place in an intermediate animal with subsequent infection of the human population. Pigs have been considered the leading contender for the role of intermediary because they may serve as hosts for productive infections of both avian and human viruses, and there is good evidence that they have been involved in interspecies transmission of influenza viruses; particularly the spread of H1N1 viruses to humans. Apart from public health measures related to the rapid identification of cases and isolation. The main control measures for influenza virus infections in human populations involves immunization and antiviral prophylaxis or treatment.