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Books on the topic 'Iron deficiency diseases'

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Published: 4 June 2021
Last updated: 2 February 2022

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1

Dincer, Yildiz. Iron deficiency and its complications. Hauppauge, N.Y: Nova Science Publishers, 2011.

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2

Yehuda, Shlomo. Iron deficiency and overload: From basic biology to clinical medicine. New York, N.Y: Humana Press, 2010.

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3

Reddy, M. Ramakrishna. Prevalence of iron deficiency anaemia and malnuitrition in India. Bangalore: Institute for Social and Economic Change, 2004.

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4

Ruel, Marie T. Can food-based strategies help reduce vitamin A and iron deficiencies?: A review of recent evidence. Washington, D.C: International Food Policy Research Institute, 2001.

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5

Nils-Georg, Asp, Hallberg Leif, Berzelius Symposium, Stiftelsen Svensk näringsforskning, and Svenska läkaresällskapet, eds. Iron Nutrition in Health and Disease: The Swedish Nutrition Foundation 20th International Symposium; the Swedish Society of Medicine Berzelius Symposium XXXI. London: John Libbey, 1996.

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6

Thom, Ellen. A baseline survey on the prevalence of anaemia among antenatal women attending antenatal clinics in Balaka District. [Lilongwe: s.n., 1999.

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7

Dow, A. I. Iron chlorosis in Washington orchards and vineyards. Pullman Wash: Cooperative Extension, College of Agriculture & Home Economics, Washington State University, 1985.

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8

F, Waters William, and Boy Erick, eds. Fortificación en casa con micronutrientes de los alimentos de los niños y niñas de 6 a 59 meses de edad para combatir la anemia por falta de hierro y otras deficiencias: Una estrategia familiar efectiva al nivel local para disminuir la alta prevalencia de anemia nutricional, usando chis paz de salud. Quito, Ecuador: Aliméntate Ecuador, 2008.

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9

International Symposium on Iron Nutrition and Interactions in Plants (7th 1993 Zaragoza, Spain). Iron nutrition in soils and plants: Proceedings of the Seventh International Symposium on Iron Nutrition and Interactions in Plants, June 27-July 2, 1993, Zaragoza, Spain. Dordrecht: Kluwer Academic Publishers, 1995.

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10

International Symposium on Iron Nutrition and Interactions in Plants (5th 1989 Jerusalem). Iron nutrition and interactions in plants: Proceedings of the Fifth International Symposium on Iron Nutrition and Interactions in Plants, 11-17 June 1989, Jerusalem, Israel, 1989. Dordrecht: Kluwer Academic, 1991.

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11

translator, Yi Chu-gwan, and Pak Hyŏn-a. translator, eds. Manhwa ro ihae sik'inda uulchŭng mŏgŭmyŏnsŏ t'alch'ul: Chŏngsinkwa ŭisa 'maŭm ŭi pyŏng' hoebok p'ŭrojekt'ŭ. Sŏul-si: Ch'ŏnghong, 2019.

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12

Yehuda, Shlomo, and David I. Mostofsky. Iron Deficiency and Overload. Springer, 2011.

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13

Iodine deficiency disorders in Namibia and data on the status of vitamin A and iron. Win[d]hoek: The Ministry, 1992.

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14

Yehuda, Shlomo, and David I. Mostofsky. Iron Deficiency and Overload: From Basic Biology to Clinical Medicine. Humana, 2012.

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15

Ziauddin, Hyder S. M., BRAC. Research and Evaluation Division., and Umeå universitet. Institutionen för folkhälsa och klinisk medicin., eds. Anaemia and iron deficiency in women: Impact of iron supplementation during pregnancy in rural Bangladesh. [Umeå]: Epidemiology, Dept. of Public Health and Clinical Medicine, Umeå University, Sweden, 2002.

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16

Ruel, Marie T. Can Food-Based Strategies Help Reduce Vitnam A and Iron Deficiencies?: A Review of Recent Evidence (Food Policy Review, 5). Intl Food Policy Research Inst, 2002.

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17

Serge, Hercberg, Galan P, and Dupin Henri professeur, eds. Aspects actuels des carences en fer et en folates dans le monde: Colloque international, Paris 11-13 juillet 1989. Paris: Editions de l'Institut national de la santé et de la recherche médicale, 1990.

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18

Chen, Y., and Y. Hadar. Iron Nutrition and Interactions in Plants. Springer, 2012.

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19

Malyszko, Jolanta, and Iain C. Macdougall. Iron metabolism in chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0125.

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While whole-body (‘absolute’) iron deficiency is common and probably increased in frequency in chronic kidney disease (CKD), functional iron deficiency is a particular problem in CKD. Absolute iron deficiency is likely to be present in advanced CKD when the ferritin falls below 100 ng/mL and the TSAT falls below 20%. Functional iron deficiency is characterized by the presence of adequate iron stores (as defined by conventional criteria), but with an inability to mobilize this iron rapidly enough to adequately support erythropoiesis with the administration of erythropoietin. Among such patients, the serum ferritin level is either normal or elevated (usually between 100 and 800 ng/mL), with a TSAT typically ≤20%. Hepcidin, a novel peptide discovered at the turn of the twenty-first century, is an iron gatekeeper that plays a key role in functional iron deficiency, and the ‘anaemia of chronic disease’. The main function of hepcidin is homeostatic regulation of iron metabolism and mediation of host defence and inflammation. Hepcidin is the predominant negative regulator of iron absorption in the small intestine, iron transport across the placenta, and iron release from the macrophages. Novel strategies that modulate hepcidin and its target ferroportin for the treatment of anaemia of chronic diseases are currently undergoing extensive research.
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20

B, Mason John, International Development Research Centre (Canada), and Micronutrient Initiative, eds. The micronutrient report: Current progress and trends in the control of vitamin A, iron, and iodine deficiencies. Ottawa: International Development Research Centre, 2001.

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21

(Editor), John B. Mason, Mahshid Lotfi (Editor), Nita Dalmiya (Editor), Kavita Sethuraman (Editor), and Megan Deitchler (Editor), eds. The Micronutrient Report: Current Progress and Trends in the Control of Vitamin A, Iron, and Iodine Deficiences (Micronutrient Initiative Series). International Development Research Centre, 2001.

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22

Alaoui, Larbi. Evaluation of the iron status of a population of adults in Morocco: Influence of dietary intake. 1991.

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23

1954-, Hemantaranjan A., ed. Advancements in iron nutrition research. Jodhpur: Scientific Publishers, 1995.

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24

H, Youdim Moussa B., ed. Brain iron: Neurochemical and behavioural aspects. London: Taylor & Francis, 1988.

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25

Wick, M., W. Pinggera, and P. Lehmann. Clinical Aspects and Laboratory. Iron Metabolism, Anemias: Novel concepts in the anemias of malignancies and renal and rheumatoid diseases. 5th ed. Springer, 2003.

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26

O, Earl Robert, Woteki Catherine E, Calloway Doris Howes, Institute of Medicine (U.S.). Committee on the Prevention, Detection, and Management of Iron Deficiency Anemia among U.S. Children and Women of Childbearing Age., and Institute of Medicine (U.S.). Food and Nutrition Board., eds. Iron deficiency anemia: Recommended guidelines for the prevention, detection, and management among U.S. children and women of childbearing age. Washington, DC: National Academy Press, 1993.

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27

(Editor), Robert Earl, and Catherine E. Woteki (Editor), eds. Iron Deficiency Anemia: Recommended Guidelines for the Prevention, Detection, and Management Among U.S. Children and Women of Childbearing Age. National Academies Press, 1994.

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28

P, Vijayalakshmi, ed. Enhanced bioavailability of iron from mungbeans and its effects on health of schoolchildren. Taiwan: AVRDC-the World Vegetable Center, 2003.

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29

1938-, Lönnerdal Bo, ed. Iron metabolism in infants. Boca Raton, Fla: CRC Press, 1990.

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30

Milton, Joan Elisabeth. Predicting hematopoetic response to iron supplementation in nursing home geriatric patients. 1992.

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31

John, Dobbing, ed. Brain, behaviour, and iron in the infant diet. London: Springer-Verlag, 1990.

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32

Dietary Iron: Birth to Two Years. Raven Pr, 1989.

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33

Puntis, John. Iron deficiency. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198759928.003.0009.

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Iron deficiency is the most common nutritional deficiency in the world, affecting around 5 billion people mostly in developing countries. Risk factors in infants include low birthweight, high cow milk consumption, low intake of iron containing complementary foods, low socioeconomic status, and immigrant status. Developmental delay and poor educational achievement are among the long-term complications. Preventative strategies include promotion of breastfeeding, use of iron-fortified formula if breast milk not available, encouraging intake of iron-rich foods, vitamin C-rich drinks with meals to promote iron absorption, and avoiding whole cow’s milk in the first year of life. Poor response to oral iron treatment is most likely due to poor compliance (iron ingestion may cause abdominal pain diarrhoea or constipation) but should also raise the possibility of underlying disease causing inflammation, malabsorption, or blood loss.
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34

Keshav, Satish, and Alexandra Kent. Diagnosis in suspected gastrointestinal disease. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0194.

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The most frequent presenting complaints suggesting gastrointestinal disease are diarrhoea, constipation, nausea, vomiting, anorexia, and abdominal pain, which can localize to any of the quadrants of the abdomen observed from the front. Loss of weight is a feature of some gastrointestinal diseases, and general symptoms such as fever, malaise, and arthralgia may also occur. According to the National Institute for Clinical Excellence (NICE), alarm symptoms include unintentional weight loss, dysphagia, chronic gastrointestinal bleeding, iron deficiency anaemia, an abdominal mass, and/or persistent vomiting.
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35

Keshav, Satish, and Palak Trivedi. Genetic liver disease. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0214.

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This chapter discusses three of the major inherited forms of liver disease (all autosomal recessive): hereditary haemochromatosis, Wilson’s disease, and alpha-1-antitrypsin deficiency. Hereditary haemochromatosis is characterized by excessive absorption of dietary iron, with a pathological increase in total body iron that accumulates in tissues and organs, disrupting their function. Wilson’s disease (hepatolenticular degeneration) is an autosomal recessive genetic disorder in which copper accumulates in tissues. Alpha-1-antitrypsin deficiency is characterized by reduced circulating levels of alpha-1-antitrypsin, a liver-derived protease inhibitor, and accumulation within the hepatocytes of the abnormal, poorly degraded protein; the consequent excessive activity of proteases such as elastase in pulmonary alveoli, unopposed by protease inhibitors, leads to emphysema, and the accumulation of alpha-1-antitrypsin in hepatocytes causes liver dysfunction.
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36

Bowker, Lesley K., James D. Price, Ku Shah, and Sarah C. Smith. Haematology. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198738381.003.0016.

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This chapter provides information on the ageing haematopoietic system, investigating anaemia in older people, diagnosis of iron deficiency anaemia, treatment of iron deficiency anaemia, macrocytic anaemia, anaemia of chronic disease, paraproteinaemias, multiple myeloma, myelodysplasia and myelodysplastic syndrome, and chronic lymphocytic leukaemia.
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37

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.

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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
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38

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.

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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
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39

Carton, James. Haematopathology. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199591633.003.0014.

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Iron deficiency anaemia 256Anaemia of chronic disease 257Megaloblastic anaemias 258Hereditary spherocytosis 259Glucose-6-phosphate dehydrogenase deficiency 260Thalassaemias 261Sickle cell disorders 262Idiopathic thrombocytopenic purpura 264Thrombotic thrombocytopenic purpura 265von Willebrand disease 266Haemophilia 267Thrombophilia 268Acute B-lymphoblastic leukaemia 269...
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40

Lewis, Mary E. Disease and Trauma in the Children from Roman Britain. Edited by Sally Crawford, Dawn M. Hadley, and Gillian Shepherd. Oxford University Press, 2018. http://dx.doi.org/10.1093/oxfordhb/9780199670697.013.25.

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This chapter explores our current knowledge of pathology and trauma in Romano-British non-adult samples focusing on the children from the late Roman cemetery of Poundbury Camp, Dorset. Evidence for metabolic diseases (rickets, scurvy, iron deficiency anaemia), fractures, thalassemia, congenital disorders and tuberculosis, are presented with emphasis on what their presence tells us about the impact of the Romans in Britain. Many of the large Roman sites from the UK were excavated long before diagnostic criteria for recognizing pathology in child remains were fully developed, and European studies tend only to focus on anaemia and its link to malaria. A lack of environmental evidence for the sites from which our skeletal remains are derived is also problematic, and this chapter hopes to set the agenda for future research into the health and life of children living in the Roman World.
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41

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.

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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.
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42

E.D., Ph.D. Weinberg and Cheryl D. Garrison. Exposing the Hidden Dangers of Iron: What Every Medical Professional Should Know About the Impact of Iron on the Disease Process. Cumberland House Publishing, 2004.

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43

1951-, Stuart-Macadam Patricia, and Kent Susan 1952-, eds. Diet, demography, and disease: Changing perspectives on anemia. New York: Aldine de Gruyter, 1992.

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44

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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45

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).
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46

Ferini-Strambi, Luigi, and Sara Marelli. Restless legs syndrome/Willis–Ekbom disease. Edited by Sudhansu Chokroverty, Luigi Ferini-Strambi, and Christopher Kennard. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199682003.003.0024.

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Restless legs syndrome (RLS)/Willis–Ekbom disease (WED), is a common neurological disorder characterized by uncomfortable and unpleasant sensations in the legs, with an urge to move. The general population prevalence has been estimated at approximately 5%. In 1995, the International RLS/WED Study Group established four clinical criteria for RLS/WED diagnosis, and in 2012 introduced a fifth (that symptoms are not due to another medical or behavioral condition) to improve differential diagnosis. Periodic leg movements causing sleep fragmentation may be observed in almost 80% of RLS/WED patients. Genetics, central nervous system dopamine dysregulation, and brain iron deficiency seem to be the primary involved factors, but peripheral phenomena may also contribute to the pathophysiology. Several medications have demonstrated efficacy in treating RLS/WED, including dopaminergic agents, alpha-2-delta ligands, and opioids. Pharmacological therapy should be limited to those patients who suffer from clinically relevant symptoms with impaired sleep quality or quality of life.
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47

(Editor), Susan Kent, and Patricia Stuart-Macadam (Editor), eds. Diet, Demography, and Disease: Changing Perspectives on Anemia (Foundations of Human Behavior). Aldine Transaction, 1992.

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48

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.

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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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49

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.

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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.
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50

Zhu, Nancy Y., and Cynthia Wu. Anaemia, cytopenias, and thrombosis in palliative medicine. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199656097.003.0083.

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Many haematological issues can complicate end-of-life care, including cytopenias and venous thromboembolism (VTE). Anaemia is very common and can significantly impact quality of life; causes include haemorrhage, iron deficiency, nutritional deficiencies, and bone marrow infiltration. Neutropenia from bone marrow failure as a result of disease infiltration or from chemotherapy effects can result in life-threatening infections. Finally, VTE is commonly seen in cancer patients as well as those who require prolonged hospitalization. Symptoms can cause discomfort, mortality is increased, and treatment is associated with major bleeding. Understanding the therapeutic options and their adverse side effects is essential in the management of these complex problems. Despite the presence of effective therapies, it is also important to realize that events such as febrile neutropenia and pulmonary embolism are often seen at the end of life and intervention may not always impact prognosis. The risks of intervention should be weighed against expected benefits when developing appropriate palliative care plans.
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