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Books on the topic 'Iron absorption'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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1

Sattarzadeh, Masoud. Determination of iron & iodine absorption from iron and iodine double-fortified salt. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1999.

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2

Swindell, Tina E. Dietary and physiological factors influencing iron absorption in the rat. Norwich: University of East Anglia, 1988.

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3

Lay, Deborah M. Determination of iron absorption in very low birthweight premature infants using two stable isotopes of iron. Ottawa: National Library of Canada, 1993.

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4

Cornelis, Pierre, and Simon C. Andrews. Iron uptake and homeostasis in microorganisms. Norfolk, UK: Caister Academic Press, 2010.

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5

Taylor, Peter. Adsorption of aqueous silicate on hematite. Pinawa, Man: Whiteshell Laboratories, 1997.

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6

Garrison, Cheryl D. The hemochromatosis cookbook: Recipes and meals for reducing the absorption of iron in your diet. Nashville: Cumberland House, 2008.

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7

McGarvey, G. B. Interactions between iron oxides and copper oxides under hydrothermal conditions. Pinewa, Man: Research Chemistry Branch, Whiteshell Laboratories, 1995.

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8

Siwka, Jerzy. Azot w ciekłych stopach żelaza. Częstochowa: Wydawn. Politechniki Częstochowskiej, 2006.

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9

Taylor, Peter. Interactions of silica with iron oxides: Effects on oxide transformations and sorption properties. Pinawa, Man: AECL, Whiteshell Laboratories, 1995.

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10

Peter, Taylor. Interactions of silica wity iron oxides: Effects on oxide transformations and sorption properties. Pinawa, Man: Whiteshell Laboratories, 1995.

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11

Tondeur, Mélody Christina. Determination of iron absorption from intrinsically labeled microencapsulated ferrous fumarate (sprinkles) in infants with 'low' versus 'high' hemoglobin using a dual stable isotope method. Ottawa: National Library of Canada, 2003.

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12

Wallace, Janae. The potential impact of septic tank soil-absorption systems on water quality in the principal valley-fill aquifer, Cedar Valley, Iron County, Utah: Assessment and guidelines. [Salt Lake City, Utah]: Utah Geological Survey, 1998.

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13

1932-, Forth Wolfgang, ed. Iron: Bioavailability, absorption, utilization. Mannheim: B.I. Wissenschaftsverlag, 1993.

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14

Nom Absorption Onto Iron Oxide Coated Sand (#90632). Amer Water Works Assn, 1993.

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15

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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16

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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17

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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18

Bunch, Chris. Deficiency anaemias. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0279.

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This chapter addresses the diagnosis, investigation, and management of anaemia due to a deficiency in iron, vitamin B12, or folate. Erythropoiesis requires an adequate supply of iron for haem formation, as well as vitamin B12 and folic acid (folate) to support high levels of DNA synthesis, and a lack of any of these will result in anaemia. Iron-deficient anaemias are typically microcytic, while a deficiency in vitamin B12 or folate results in megaloblastic haemopoiesis and a macrocytic anaemia. Iron deficiency results from poor dietary iron intake, poor absorption, increased demands, blood loss, or combinations of these. The usual cause of severe vitamin B12 deficiency in Western countries is an autoimmune atrophic gastritis, in which there is a loss of gastric parietal cell numbers and an absence of intrinsic factor production, which effectively prevents vitamin B12 absorption. This is the classical pernicious anaemia, and it is often seen in association with other autoimmune disorders. Folate deficiency may result from poor diet, malabsorption, or when demand for folate is increased, for example, during pregnancy, or with increased haemopoiesis in haemolytic anaemias or myeloproliferative disorders.

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19

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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20

Great Britain. Standing Committee of Analysts., ed. Methods for the determination of the metals aluminium, cadmium, chromium, cobalt, copper, iron, lead, manganese, nickel, uranium, vanadium, and zinc in marine, estuarine, and other waters by stripping voltammetry or concentration and atomic absorption spectrophotometry, 1987: With notes on other metals and related techniques. London: H.M.S.O., 1988.

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21

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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22

The potential impact of septic tank soil-absorption systems on water quality in the principal valley-fill aquifer, Cedar Valley, Iron County, Utah : assessment and guidelines. Utah Geological Survey, 1998. http://dx.doi.org/10.34191/ri-239.

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23

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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