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Latest revision as of 22:26, 29 July 2020

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Shyam Patel [2]

Overview

Iron is needed for haemoglobin synthesis which is essential for oxygen transport in the body. Iron is stored as ferritin in the body and transported as transferrin. The source of iron is diet and recycling iron from reticuloendothelial cells. The absorption of iron is highly regulated by hepcidin. Loss of iron from the body, inadequate intake or increased hepcidin can lead to iron deficiency anemia.

Pathophysiology

Physiology

Iron is needed for the synthesis of haemoglobin and new DNA. It is a major component of oxidation and reduction enzymes (cytochromes)^[1]

In the human body, iron mainly exists as bound to protein (hemoprotein), as heme compounds (hemoglobin or myoglobin), heme enzymes, or nonheme compounds (flavin-iron enzymes, transferrin, and ferritin).^[2]

The body requires iron for the synthesis of its oxygen transport proteins, (hemoglobin and myoglobin), and for the formation of heme enzymes and other iron-containing enzymes involved in electron transfer and oxidation-reductions.

Human iron metabolism is controlled by various factors.

60% of the body iron is found in the hemoglobin present in circulating erythrocytes, 25% is contained in transferrin and ferritin, and the remaining 15% is bound to myoglobin in muscle tissue and in a variety of enzymes involved in the oxidative metabolism and many other cell functions.^[3]

Iron is bound and transported in the body via transferrin and stored in ferritin molecules.

Iron is delivered to tissues by circulating transferrin, a transporter that captures iron released into the plasma from intestinal enterocytes or reticuloendothelial macrophages.^[4]
The binding of transferrin to the cell-surface transferrin receptor (TfR) 1 results in endocytosis and uptake of iron.
Internalized iron is transported to mitochondria for the synthesis of heme or other iron containing enzymes.
Excess iron is stored in cytosolic ferritin.

Absorption of iron

Iron absorption occurs by the enterocytes in the duodenum and upper jejunum.^[5]^[6]^[7]
Dietary iron occurs in two forms: heme and non-heme. The primary sources of heme iron are hemoglobin and myoglobin from consumption of meat, poultry, and fish, whereas non-heme iron is obtained from cereals, pulses, legumes, fruits, and vegetables.^[8]
In the blood, it is transported by transferrin to the cells or the bone marrow for erythropoiesis.^[9]
Iron absorption is controlled by ferroportin on the basolateral surface of the cell. Ferroportin allows or does not allow iron from the mucosal cell into the plasma.
Iron is absorbed in Fe⁺² (ferric) state.
The iron is consumed in Fe+3 (ferrous) state and is reduced to Fe+2 state by the acidic gastric pH by enzyme ferric reductase.^[10]
Fe+2 is absorbed by the enterocytes and exported across the basolateral membrane into the bloodstream via Fe+2 transporter ferroportin.
The ferroportin-mediated efflux of Fe+2 is coupled by its reoxidation to Fe+3, catalyzed by ferroxidase hephaestin that interacts with ferroportin.^[11]
The total iron content of transferrin is dynamic and undergoes changes to sustain erythropoiesis.
Senescent RBCs are cleared by reticuloendothelial macrophages, which metabolize hemoglobin and heme and release iron into the bloodstream.
The transferrin iron pool is replenished by iron recycled from RBCs and by newly absorbed dietary iron.
Macrophages export Fe+2 from their plasma membrane via ferroportin, in a process coupled by reoxidation of Fe+2 to Fe+3 by ceruloplasmin and followed by the loading of Fe+3 to transferrin.

Regulation of iron homeostasis

Iron balance is mainly regulated at the point of absorption.^[12]
Hepcidin is a circulating peptide hormone secreted by the liver that plays a central role in the regulation of iron homeostasis. Inflammatory conditions lead to increased IL-6 production, which stimulates hepcidin production.
This hormone is produced by hepatocytes and is a negative regulator of iron entry into plasma. Hepcidin acts by binding to ferroportin.^[13]^[14]^[15]
Binding of hepcidin induces ferroportin degradation.
The loss of ferroportin from the cell surface prevents iron entry into plasma and decreased iron levels in the body.^[16]
Decreased expression of hepcidin leads to increased cell surface ferroportin and increased iron absorption.
Plasma hepcidin levels are regulated by cytokines, plasma iron, anemia, and hypoxia.
Overexpression of hepcidin leads to the anemia of chronic disease, while low hepcidin production results in hereditary hemochromatosis (HFE).

Storage

Ferritin concentration together with that of hemosiderin reflects the body iron stores.^[17]^[18]^[19]^[20]^[21]^[21]
They store iron in an insoluble form and are present primarily in the liver, spleen, and bone marrow.
Serum ferritin is the most convenient laboratory test to estimate iron stores.

Factors effecting iron absorption

Factors that enhance iron uptake are:
- Ascorbate and citrate increase iron uptake by acting as weak chelators^[22]^[23].
- Iron is readily transferred from these compounds into the mucosal lining cells.

Factors inhibiting iron absorption are:
- Phytate (myo-inositol hexakisphosphate) is the main inhibitor of iron absorption^[24]^[25]^[26].
- Calcium
- Animal proteins such as milk proteins, egg proteins, and albumin, have been shown to inhibit iron absorption.
- Proteins from soybean also decrease iron absorption.
- Suppresion of gastric acid such as use of antacids suprress iron absorption.
- Lead competes with iron for the absorption and blocks its absorption by competetive inhibition.

Iron requirement

Recommended Dietary Allowances (RDAs) for Iron
Age	Male	Female	Pregnancy	Lactation
Birth to 6 months	0.27 mg*	0.27 mg*
7–12 months	11 mg	11 mg
1–3 years	7 mg	7 mg
4–8 years	10 mg	10 mg
9–13 years	8 mg	8 mg
14–18 years	11 mg	15 mg	27 mg	10 mg
19–50 years	8 mg	18 mg	27 mg	9 mg
51+ years	8 mg	8 mg

Pathogenesis

Iron deficiency anemia occurs when there is^[27]^[28]:
- Low dietary intake
- Increased demands of iron
- Impaired absorption of iron
- Excessive loss of iron (blood loss)
- Increased hepcidin (chronic inflammation)
Low dietary intake:
- Iron is obtained from foods such as:
  - meat, such as lamb, pork, chicken, and beef
  - beans
  - pumpkin and squash seeds
  - leafy greens, such as spinach
  - raisins and other dried fruit
  - eggs
  - seafood, such as clams, sardines, shrimp, and oysters
  - Iron-fortified dry and instant cereals Foods high in vitamin C include:
  - Fruits such as oranges, grapefruits, strawberries, kiwis, guavas, papayas, pineapples, melons, and mangoes
  - Red and green bell peppers
  - Brussels sprouts
  - Cauliflower
  - Tomatoes
  - Leafy greens
- Increased demands of iron
  - Growth, the requirement of iron increases during the developmental period from infancy to adolescence and during adolescence.
  - Pregnancy, during pregnancy the demand for iron is increased.
- Impaired absorption of iron:
  - Malabsorption
  - Deficiency of vitamin C in diet
- Excessive loss of iron (blood loss)
  - The only means of excretion for iron is through blood loss
  - Any source of external and internal bleeding can cause iron deficiency depending on the blood loss
- Increased hepcidin
  - In chonric inflammatory conditions, the levels of hepcidin increase
  - Increased hepcidin causes ferriportin degeneration and impaired iron absorption
Iron is required for haemoglobin synthesis, so deficiency of iron leads to depletion of haemoglobin
Decrease in haemoglobin leads to anemia
Due to low haemoglobin, oxygen is not tranported effectively to cells and results in hypoxia

Population	Hb Diagnostic of anaemia (g/dL)
Children aged 6 months to 6 years old	<11.0
Children aged 6-14 years old	<12.0
Adult men	<13.0
Adult non-pregnant women	<12.0
Adult pregnant women	<11.0

Histology

(Images shown below are courtesy of Melih Aktan MD, Istanbul Medical Faculty - Turkey)

Iron deficiency anemia
Iron deficiency anemia
Iron deficiency anemia

Video

External Link

Center for disease control and prevention

References

↑ Brissot P, Troadec MB, Loréal O, Brissot E (2018). "Pathophysiology and classification of iron overload diseases; update 2018". Transfus Clin Biol. doi:10.1016/j.tracli.2018.08.006. PMID 30173950.
↑ Murray-Kolb LE (2018). "Examining Consequence of Brain Iron Deficiency in the Absence of Anemia". J Nutr. doi:10.1093/jn/nxy186. PMID 30169646.
↑ Ghaffari S, Pourafkari L (2018). "Koilonychia in Iron-Deficiency Anemia". N Engl J Med. 379 (9): e13. doi:10.1056/NEJMicm1802104. PMID 30157401.
↑ Kassebaum NJ, Jasrasaria R, Naghavi M, Wulf SK, Johns N, Lozano R; et al. (2014). "A systematic analysis of global anemia burden from 1990 to 2010". Blood. 123 (5): 615–24. doi:10.1182/blood-2013-06-508325. PMC 3907750. PMID 24297872.
↑ Price EA, Mehra R, Holmes TH, Schrier SL (2011). "Anemia in older persons: etiology and evaluation". Blood Cells Mol Dis. 46 (2): 159–65. doi:10.1016/j.bcmd.2010.11.004. PMID 21208814.
↑ Mast AE, Bialkowski W, Bryant BJ, Wright DJ, Birch R, Kiss JE; et al. (2016). "A randomized, blinded, placebo-controlled trial of education and iron supplementation for mitigation of iron deficiency in regular blood donors". Transfusion. 56 (6 Pt 2): 1588–97. doi:10.1111/trf.13469. PMC 4905782. PMID 26813849.
↑ Shams S, Asheri H, Kianmehr A, Ziaee V, Koochakzadeh L, Monajemzadeh M; et al. (2010). "The prevalence of iron deficiency anaemia in female medical students in Tehran". Singapore Med J. 51 (2): 116–9. PMID 20358149.
↑ Fonseca C, Marques F, Robalo Nunes A, Belo A, Brilhante D, Cortez J (2016). "Prevalence of anaemia and iron deficiency in Portugal: the EMPIRE study". Intern Med J. 46 (4): 470–8. doi:10.1111/imj.13020. PMID 26841337.
↑ Cook JD, Skikne BS (1989). "Iron deficiency: definition and diagnosis". J Intern Med. 226 (5): 349–55. PMID 2681511.
↑ Annibale B, Capurso G, Chistolini A, D'Ambra G, DiGiulio E, Monarca B; et al. (2001). "Gastrointestinal causes of refractory iron deficiency anemia in patients without gastrointestinal symptoms". Am J Med. 111 (6): 439–45. PMID 11690568.
↑ Lopez A, Cacoub P, Macdougall IC, Peyrin-Biroulet L (2016). "Iron deficiency anaemia". Lancet. 387 (10021): 907–16. doi:10.1016/S0140-6736(15)60865-0. PMID 26314490.
↑ Khadem G, Scott IA, Klein K (2012). "Evaluation of iron deficiency anaemia in tertiary hospital settings: room for improvement?". Intern Med J. 42 (6): 658–64. doi:10.1111/j.1445-5994.2012.02724.x. PMID 22288902.
↑ Ioannou GN, Rockey DC, Bryson CL, Weiss NS (2002). "Iron deficiency and gastrointestinal malignancy: a population-based cohort study". Am J Med. 113 (4): 276–80. PMID 12361812. Review in: ACP J Club. 2003 May-Jun;138(3):80
↑ Unsworth DJ, Lock FJ, Harvey RF (1999). "Iron-deficiency anaemia in premenopausal women". Lancet. 353 (9158): 1100. PMID 10199377.
↑ Corazza GR, Valentini RA, Andreani ML, D'Anchino M, Leva MT, Ginaldi L; et al. (1995). "Subclinical coeliac disease is a frequent cause of iron-deficiency anaemia". Scand J Gastroenterol. 30 (2): 153–6. PMID 7732338.
↑ Unsworth DJ, Lock RJ, Harvey RF (2000). "Improving the diagnosis of coeliac disease in anaemic women". Br J Haematol. 111 (3): 898–901. PMID 11122153.
↑ Camaschella C (2015). "Iron deficiency: new insights into diagnosis and treatment". Hematology Am Soc Hematol Educ Program. 2015: 8–13. doi:10.1182/asheducation-2015.1.8. PMID 26637694.
↑ Hershko C, Hoffbrand AV, Keret D, Souroujon M, Maschler I, Monselise Y; et al. (2005). "Role of autoimmune gastritis, Helicobacter pylori and celiac disease in refractory or unexplained iron deficiency anemia". Haematologica. 90 (5): 585–95. PMID 15921373.
↑ Kalantar-Zadeh K, Höffken B, Wünsch H, Fink H, Kleiner M, Luft FC (1995). "Diagnosis of iron deficiency anemia in renal failure patients during the post-erythropoietin era". Am J Kidney Dis. 26 (2): 292–9. PMID 7645533.
↑ Eschbach JW, Cook JD, Scribner BH, Finch CA (1977). "Iron balance in hemodialysis patients". Ann Intern Med. 87 (6): 710–3. PMID 931207.
↑ ^21.0 ^21.1 Hershko C, Camaschella C (2014). "How I treat unexplained refractory iron deficiency anemia". Blood. 123 (3): 326–33. doi:10.1182/blood-2013-10-512624. PMID 24215034.
↑ Iolascon A, d'Apolito M, Servedio V, Cimmino F, Piga A, Camaschella C (2006). "Microcytic anemia and hepatic iron overload in a child with compound heterozygous mutations in DMT1 (SCL11A2)". Blood. 107 (1): 349–54. doi:10.1182/blood-2005-06-2477. PMID 16160008.
↑ Coates A, Mountjoy M, Burr J (2017). "Incidence of Iron Deficiency and Iron Deficient Anemia in Elite Runners and Triathletes". Clin J Sport Med. 27 (5): 493–498. doi:10.1097/JSM.0000000000000390. PMID 27606953.
↑ Thomas DW, Hinchliffe RF, Briggs C, Macdougall IC, Littlewood T, Cavill I; et al. (2013). "Guideline for the laboratory diagnosis of functional iron deficiency". Br J Haematol. 161 (5): 639–48. doi:10.1111/bjh.12311. PMID 23573815.
↑ Simpson E, Mull JD, Longley E, East J (2000). "Pica during pregnancy in low-income women born in Mexico". West J Med. 173 (1): 20–4, discussion 25. PMC 1070964. PMID 10903283.
↑ Rector WG (1989). "Pica: its frequency and significance in patients with iron-deficiency anemia due to chronic gastrointestinal blood loss". J Gen Intern Med. 4 (6): 512–3. PMID 2585159.
↑ Reynolds RD, Binder HJ, Miller MB, Chang WW, Horan S (1968). "Pagophagia and iron deficiency anemia". Ann Intern Med. 69 (3): 435–40. PMID 5244572.
↑ Trost LB, Bergfeld WF, Calogeras E (2006). "The diagnosis and treatment of iron deficiency and its potential relationship to hair loss". J Am Acad Dermatol. 54 (5): 824–44. doi:10.1016/j.jaad.2005.11.1104. PMID 16635664.

Template:WH Template:WS

[pmid30173950-1] Brissot P, Troadec MB, Loréal O, Brissot E (2018). "Pathophysiology and classification of iron overload diseases; update 2018". Transfus Clin Biol. doi:10.1016/j.tracli.2018.08.006. PMID 30173950.

[pmid30169646-2] Murray-Kolb LE (2018). "Examining Consequence of Brain Iron Deficiency in the Absence of Anemia". J Nutr. doi:10.1093/jn/nxy186. PMID 30169646.

[pmid30157401-3] Ghaffari S, Pourafkari L (2018). "Koilonychia in Iron-Deficiency Anemia". N Engl J Med. 379 (9): e13. doi:10.1056/NEJMicm1802104. PMID 30157401.

[pmid24297872-4] Kassebaum NJ, Jasrasaria R, Naghavi M, Wulf SK, Johns N, Lozano R; et al. (2014). "A systematic analysis of global anemia burden from 1990 to 2010". Blood. 123 (5): 615–24. doi:10.1182/blood-2013-06-508325. PMC 3907750. PMID 24297872.

[pmid21208814-5] Price EA, Mehra R, Holmes TH, Schrier SL (2011). "Anemia in older persons: etiology and evaluation". Blood Cells Mol Dis. 46 (2): 159–65. doi:10.1016/j.bcmd.2010.11.004. PMID 21208814.

[pmid26813849-6] Mast AE, Bialkowski W, Bryant BJ, Wright DJ, Birch R, Kiss JE; et al. (2016). "A randomized, blinded, placebo-controlled trial of education and iron supplementation for mitigation of iron deficiency in regular blood donors". Transfusion. 56 (6 Pt 2): 1588–97. doi:10.1111/trf.13469. PMC 4905782. PMID 26813849.

[pmid20358149-7] Shams S, Asheri H, Kianmehr A, Ziaee V, Koochakzadeh L, Monajemzadeh M; et al. (2010). "The prevalence of iron deficiency anaemia in female medical students in Tehran". Singapore Med J. 51 (2): 116–9. PMID 20358149.

[pmid26841337-8] Fonseca C, Marques F, Robalo Nunes A, Belo A, Brilhante D, Cortez J (2016). "Prevalence of anaemia and iron deficiency in Portugal: the EMPIRE study". Intern Med J. 46 (4): 470–8. doi:10.1111/imj.13020. PMID 26841337.

[pmid2681511-9] Cook JD, Skikne BS (1989). "Iron deficiency: definition and diagnosis". J Intern Med. 226 (5): 349–55. PMID 2681511.

[pmid11690568-10] Annibale B, Capurso G, Chistolini A, D'Ambra G, DiGiulio E, Monarca B; et al. (2001). "Gastrointestinal causes of refractory iron deficiency anemia in patients without gastrointestinal symptoms". Am J Med. 111 (6): 439–45. PMID 11690568.

[pmid26314490-11] Lopez A, Cacoub P, Macdougall IC, Peyrin-Biroulet L (2016). "Iron deficiency anaemia". Lancet. 387 (10021): 907–16. doi:10.1016/S0140-6736(15)60865-0. PMID 26314490.

[pmid22288902-12] Khadem G, Scott IA, Klein K (2012). "Evaluation of iron deficiency anaemia in tertiary hospital settings: room for improvement?". Intern Med J. 42 (6): 658–64. doi:10.1111/j.1445-5994.2012.02724.x. PMID 22288902.

[pmid12361812-13] Ioannou GN, Rockey DC, Bryson CL, Weiss NS (2002). "Iron deficiency and gastrointestinal malignancy: a population-based cohort study". Am J Med. 113 (4): 276–80. PMID 12361812. Review in: ACP J Club. 2003 May-Jun;138(3):80

[pmid10199377-14] Unsworth DJ, Lock FJ, Harvey RF (1999). "Iron-deficiency anaemia in premenopausal women". Lancet. 353 (9158): 1100. PMID 10199377.

[pmid7732338-15] Corazza GR, Valentini RA, Andreani ML, D'Anchino M, Leva MT, Ginaldi L; et al. (1995). "Subclinical coeliac disease is a frequent cause of iron-deficiency anaemia". Scand J Gastroenterol. 30 (2): 153–6. PMID 7732338.

[pmid11122153-16] Unsworth DJ, Lock RJ, Harvey RF (2000). "Improving the diagnosis of coeliac disease in anaemic women". Br J Haematol. 111 (3): 898–901. PMID 11122153.

[pmid26637694-17] Camaschella C (2015). "Iron deficiency: new insights into diagnosis and treatment". Hematology Am Soc Hematol Educ Program. 2015: 8–13. doi:10.1182/asheducation-2015.1.8. PMID 26637694.

[pmid15921373-18] Hershko C, Hoffbrand AV, Keret D, Souroujon M, Maschler I, Monselise Y; et al. (2005). "Role of autoimmune gastritis, Helicobacter pylori and celiac disease in refractory or unexplained iron deficiency anemia". Haematologica. 90 (5): 585–95. PMID 15921373.

[pmid7645533-19] Kalantar-Zadeh K, Höffken B, Wünsch H, Fink H, Kleiner M, Luft FC (1995). "Diagnosis of iron deficiency anemia in renal failure patients during the post-erythropoietin era". Am J Kidney Dis. 26 (2): 292–9. PMID 7645533.

[pmid931207-20] Eschbach JW, Cook JD, Scribner BH, Finch CA (1977). "Iron balance in hemodialysis patients". Ann Intern Med. 87 (6): 710–3. PMID 931207.

[pmid24215034-21] 21.0 ^21.1 Hershko C, Camaschella C (2014). "How I treat unexplained refractory iron deficiency anemia". Blood. 123 (3): 326–33. doi:10.1182/blood-2013-10-512624. PMID 24215034.

[pmid16160008-22] Iolascon A, d'Apolito M, Servedio V, Cimmino F, Piga A, Camaschella C (2006). "Microcytic anemia and hepatic iron overload in a child with compound heterozygous mutations in DMT1 (SCL11A2)". Blood. 107 (1): 349–54. doi:10.1182/blood-2005-06-2477. PMID 16160008.

[pmid27606953-23] Coates A, Mountjoy M, Burr J (2017). "Incidence of Iron Deficiency and Iron Deficient Anemia in Elite Runners and Triathletes". Clin J Sport Med. 27 (5): 493–498. doi:10.1097/JSM.0000000000000390. PMID 27606953.

[pmid23573815-24] Thomas DW, Hinchliffe RF, Briggs C, Macdougall IC, Littlewood T, Cavill I; et al. (2013). "Guideline for the laboratory diagnosis of functional iron deficiency". Br J Haematol. 161 (5): 639–48. doi:10.1111/bjh.12311. PMID 23573815.

[pmid10903283-25] Simpson E, Mull JD, Longley E, East J (2000). "Pica during pregnancy in low-income women born in Mexico". West J Med. 173 (1): 20–4, discussion 25. PMC 1070964. PMID 10903283.

[pmid2585159-26] Rector WG (1989). "Pica: its frequency and significance in patients with iron-deficiency anemia due to chronic gastrointestinal blood loss". J Gen Intern Med. 4 (6): 512–3. PMID 2585159.

[pmid5244572-27] Reynolds RD, Binder HJ, Miller MB, Chang WW, Horan S (1968). "Pagophagia and iron deficiency anemia". Ann Intern Med. 69 (3): 435–40. PMID 5244572.

[pmid16635664-28] Trost LB, Bergfeld WF, Calogeras E (2006). "The diagnosis and treatment of iron deficiency and its potential relationship to hair loss". J Am Acad Dermatol. 54 (5): 824–44. doi:10.1016/j.jaad.2005.11.1104. PMID 16635664.

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@@ Line 1: / Line 1: @@
 __NOTOC__
 {{Iron deficiency anemia}}
+{{CMG}} {{shyam}}
-Please help WikiDoc by adding more content here.  It's easy!  Click  [[Help:How_to_Edit_a_Page|here]]  to learn about editing.
+==Overview==
+Iron is needed for [[Hemoglobin|haemoglobin]] synthesis which is essential for oxygen transport in the body. Iron is stored as [[ferritin]] in the body and transported as [[transferrin]]. The source of iron is diet and recycling iron from [[Reticuloendothelial system|reticuloendothelial]] cells. The absorption of iron is highly regulated by [[hepcidin]]. Loss of iron from the body, inadequate intake or increased hepcidin can lead to iron deficiency anemia.
+==Pathophysiology==
+===Physiology===
+*Iron is needed for the synthesis of [[Hemoglobin|haemoglobin]] and new [[DNA]]. It is a major component of oxidation and reduction enzymes ([[Cytochrome)|cytochromes]])<ref name="pmid30173950">{{cite journal| author=Brissot P, Troadec MB, Loréal O, Brissot E| title=Pathophysiology and classification of iron overload diseases; update 2018. | journal=Transfus Clin Biol | year= 2018 | volume=  | issue=  | pages=  | pmid=30173950 | doi=10.1016/j.tracli.2018.08.006 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=30173950  }} </ref>
+*In the human body, iron mainly exists as bound to protein (hemoprotein), as heme compounds (hemoglobin or myoglobin), heme enzymes, or nonheme compounds (flavin-iron enzymes, [[transferrin]], and [[ferritin]]).<ref name="pmid30169646">{{cite journal| author=Murray-Kolb LE| title=Examining Consequence of Brain Iron Deficiency in the Absence of Anemia. | journal=J Nutr | year= 2018 | volume=  | issue=  | pages=  | pmid=30169646 | doi=10.1093/jn/nxy186 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=30169646  }} </ref>
-{{CMG}}
+*The body requires iron for the synthesis of its oxygen transport proteins, ([[hemoglobin]] and [[Myoglobin|myoglobin)]], and for the formation of heme enzymes and other iron-containing enzymes involved in electron transfer and oxidation-reductions.
-==Overview==
+*Human iron metabolism is controlled by various factors.
+*60% of the body iron is found in the hemoglobin present in circulating [[Red blood cell|erythrocytes]], 25% is contained in transferrin and ferritin, and the remaining 15% is bound to [[myoglobin]] in muscle tissue and in a variety of enzymes involved in the oxidative metabolism and many other cell functions.<ref name="pmid30157401">{{cite journal| author=Ghaffari S, Pourafkari L| title=Koilonychia in Iron-Deficiency Anemia. | journal=N Engl J Med | year= 2018 | volume= 379 | issue= 9 | pages= e13 | pmid=30157401 | doi=10.1056/NEJMicm1802104 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=30157401  }} </ref>
+*Iron is bound and transported in the body via transferrin and stored in ferritin molecules.
+*Iron is delivered to tissues by circulating transferrin, a transporter that captures iron released into the plasma from intestinal enterocytes or reticuloendothelial [[Macrophage|macrophages]].<ref name="pmid24297872">{{cite journal| author=Kassebaum NJ, Jasrasaria R, Naghavi M, Wulf SK, Johns N, Lozano R et al.| title=A systematic analysis of global anemia burden from 1990 to 2010. | journal=Blood | year= 2014 | volume= 123 | issue= 5 | pages= 615-24 | pmid=24297872 | doi=10.1182/blood-2013-06-508325 | pmc=3907750 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24297872  }} </ref>
+*The binding of transferrin to the cell-surface transferrin receptor (TfR) 1 results in [[endocytosis]] and uptake of iron.
+*Internalized iron is transported to [[Mitochondrion|mitochondria]] for the synthesis of heme or other iron containing enzymes.
+*Excess iron is stored in cytosolic ferritin.
+====Absorption of iron====
+*Iron absorption occurs by the [[Enterocyte|enterocytes]] in the [[duodenum]] and upper [[jejunum]].<ref name="pmid21208814">{{cite journal| author=Price EA, Mehra R, Holmes TH, Schrier SL| title=Anemia in older persons: etiology and evaluation. | journal=Blood Cells Mol Dis | year= 2011 | volume= 46 | issue= 2 | pages= 159-65 | pmid=21208814 | doi=10.1016/j.bcmd.2010.11.004 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21208814  }} </ref><ref name="pmid26813849">{{cite journal| author=Mast AE, Bialkowski W, Bryant BJ, Wright DJ, Birch R, Kiss JE et al.| title=A randomized, blinded, placebo-controlled trial of education and iron supplementation for mitigation of iron deficiency in regular blood donors. | journal=Transfusion | year= 2016 | volume= 56 | issue= 6 Pt 2 | pages= 1588-97 | pmid=26813849 | doi=10.1111/trf.13469 | pmc=4905782 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26813849  }} </ref><ref name="pmid20358149">{{cite journal| author=Shams S, Asheri H, Kianmehr A, Ziaee V, Koochakzadeh L, Monajemzadeh M et al.| title=The prevalence of iron deficiency anaemia in female medical students in Tehran. | journal=Singapore Med J | year= 2010 | volume= 51 | issue= 2 | pages= 116-9 | pmid=20358149 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20358149  }} </ref>
+*Dietary iron occurs in two forms: heme and non-heme. The primary sources of heme iron are hemoglobin and myoglobin from consumption of meat, poultry, and fish, whereas non-heme iron is obtained from cereals, pulses, legumes, fruits, and vegetables.<ref name="pmid26841337">{{cite journal| author=Fonseca C, Marques F, Robalo Nunes A, Belo A, Brilhante D, Cortez J| title=Prevalence of anaemia and iron deficiency in Portugal: the EMPIRE study. | journal=Intern Med J | year= 2016 | volume= 46 | issue= 4 | pages= 470-8 | pmid=26841337 | doi=10.1111/imj.13020 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26841337  }} </ref>
+*In the blood, it is transported by transferrin to the cells or the [[bone marrow]] for [[erythropoiesis]].<ref name="pmid2681511">{{cite journal| author=Cook JD, Skikne BS| title=Iron deficiency: definition and diagnosis. | journal=J Intern Med | year= 1989 | volume= 226 | issue= 5 | pages= 349-55 | pmid=2681511 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2681511  }} </ref>
+*Iron absorption is controlled by ferroportin on the basolateral surface of the cell. Ferroportin allows or does not allow iron from the mucosal cell into the plasma.
+*Iron is absorbed in Fe<sup>+2</sup> (ferric) state.
+*The iron is consumed in Fe+3 (ferrous) state and is reduced to Fe+2 state by the acidic [[Stomach|gastric]] pH by enzyme ferric reductase.<ref name="pmid11690568">{{cite journal| author=Annibale B, Capurso G, Chistolini A, D'Ambra G, DiGiulio E, Monarca B et al.| title=Gastrointestinal causes of refractory iron deficiency anemia in patients without gastrointestinal symptoms. | journal=Am J Med | year= 2001 | volume= 111 | issue= 6 | pages= 439-45 | pmid=11690568 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11690568  }} </ref>
+*Fe+2 is absorbed by the enterocytes and exported across the basolateral membrane into the bloodstream via Fe+2 transporter [[ferroportin]].
+*The ferroportin-mediated efflux of Fe+2 is coupled by its reoxidation to Fe+3, catalyzed by ferroxidase hephaestin that interacts with ferroportin.<ref name="pmid26314490">{{cite journal| author=Lopez A, Cacoub P, Macdougall IC, Peyrin-Biroulet L| title=Iron deficiency anaemia. | journal=Lancet | year= 2016 | volume= 387 | issue= 10021 | pages= 907-16 | pmid=26314490 | doi=10.1016/S0140-6736(15)60865-0 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26314490  }} </ref>
+*The total iron content of transferrin is dynamic and undergoes changes to sustain [[erythropoiesis]].
+*Senescent RBCs are cleared by reticuloendothelial macrophages, which metabolize hemoglobin and heme and release iron into the bloodstream.
+*The transferrin iron pool is replenished by iron recycled from RBCs and by newly absorbed dietary iron.
+*Macrophages export Fe+2 from their plasma membrane via ferroportin, in a process coupled by reoxidation of Fe+2 to Fe+3 by [[ceruloplasmin]] and followed by the loading of Fe+3 to transferrin.
+====Regulation of iron homeostasis====
+*Iron balance is mainly regulated at the point of absorption.<ref name="pmid22288902">{{cite journal| author=Khadem G, Scott IA, Klein K| title=Evaluation of iron deficiency anaemia in tertiary hospital settings: room for improvement? | journal=Intern Med J | year= 2012 | volume= 42 | issue= 6 | pages= 658-64 | pmid=22288902 | doi=10.1111/j.1445-5994.2012.02724.x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22288902  }} </ref>
+*[[Hepcidin]] is a circulating peptide [[hormone]] secreted by the liver that plays a central role in the regulation of iron homeostasis. Inflammatory conditions lead to increased IL-6 production, which stimulates hepcidin production.
+*This hormone is produced by [[Hepatocyte|hepatocytes]] and is a negative regulator of iron entry into plasma. Hepcidin acts by binding to ferroportin.<ref name="pmid12361812">{{cite journal| author=Ioannou GN, Rockey DC, Bryson CL, Weiss NS| title=Iron deficiency and gastrointestinal malignancy: a population-based cohort study. | journal=Am J Med | year= 2002 | volume= 113 | issue= 4 | pages= 276-80 | pmid=12361812 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12361812  }}  [https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=&cmd=prlinks&id=12725635 Review in: ACP J Club. 2003 May-Jun;138(3):80] </ref><ref name="pmid10199377">{{cite journal| author=Unsworth DJ, Lock FJ, Harvey RF| title=Iron-deficiency anaemia in premenopausal women. | journal=Lancet | year= 1999 | volume= 353 | issue= 9158 | pages= 1100 | pmid=10199377 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10199377  }} </ref><ref name="pmid7732338">{{cite journal| author=Corazza GR, Valentini RA, Andreani ML, D'Anchino M, Leva MT, Ginaldi L et al.| title=Subclinical coeliac disease is a frequent cause of iron-deficiency anaemia. | journal=Scand J Gastroenterol | year= 1995 | volume= 30 | issue= 2 | pages= 153-6 | pmid=7732338 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7732338  }} </ref>
+*Binding of hepcidin induces ferroportin degradation.
+*The loss of ferroportin from the cell surface prevents iron entry into [[Blood plasma|plasma]] and decreased iron levels in the body.<ref name="pmid11122153">{{cite journal| author=Unsworth DJ, Lock RJ, Harvey RF| title=Improving the diagnosis of coeliac disease in anaemic women. | journal=Br J Haematol | year= 2000 | volume= 111 | issue= 3 | pages= 898-901 | pmid=11122153 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11122153  }} </ref>
+*Decreased expression of hepcidin leads to increased cell surface ferroportin and increased iron absorption.
+*Plasma hepcidin levels are regulated by [[Cytokine|cytokines]], plasma iron, [[anemia]], and [[Hypoxemia|hypoxia]].
+*Overexpression of hepcidin leads to the anemia of chronic disease, while low hepcidin production results in hereditary [[hemochromatosis]] (HFE).
+====Storage====
+*Ferritin concentration together with that of [[hemosiderin]] reflects the body iron stores.<ref name="pmid26637694">{{cite journal| author=Camaschella C| title=Iron deficiency: new insights into diagnosis and treatment. | journal=Hematology Am Soc Hematol Educ Program | year= 2015 | volume= 2015 | issue=  | pages= 8-13 | pmid=26637694 | doi=10.1182/asheducation-2015.1.8 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26637694  }} </ref><ref name="pmid15921373">{{cite journal| author=Hershko C, Hoffbrand AV, Keret D, Souroujon M, Maschler I, Monselise Y et al.| title=Role of autoimmune gastritis, Helicobacter pylori and celiac disease in refractory or unexplained iron deficiency anemia. | journal=Haematologica | year= 2005 | volume= 90 | issue= 5 | pages= 585-95 | pmid=15921373 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15921373  }} </ref><ref name="pmid7645533">{{cite journal| author=Kalantar-Zadeh K, Höffken B, Wünsch H, Fink H, Kleiner M, Luft FC| title=Diagnosis of iron deficiency anemia in renal failure patients during the post-erythropoietin era. | journal=Am J Kidney Dis | year= 1995 | volume= 26 | issue= 2 | pages= 292-9 | pmid=7645533 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7645533  }} </ref><ref name="pmid931207">{{cite journal| author=Eschbach JW, Cook JD, Scribner BH, Finch CA| title=Iron balance in hemodialysis patients. | journal=Ann Intern Med | year= 1977 | volume= 87 | issue= 6 | pages= 710-3 | pmid=931207 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=931207  }} </ref><ref name="pmid24215034">{{cite journal| author=Hershko C, Camaschella C| title=How I treat unexplained refractory iron deficiency anemia. | journal=Blood | year= 2014 | volume= 123 | issue= 3 | pages= 326-33 | pmid=24215034 | doi=10.1182/blood-2013-10-512624 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24215034  }} </ref><ref name="pmid24215034">{{cite journal| author=Hershko C, Camaschella C| title=How I treat unexplained refractory iron deficiency anemia. | journal=Blood | year= 2014 | volume= 123 | issue= 3 | pages= 326-33 | pmid=24215034 | doi=10.1182/blood-2013-10-512624 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24215034  }} </ref>
+*They store iron in an insoluble form and are present primarily in the liver, spleen, and bone marrow.
+*Serum ferritin is the most convenient laboratory test to estimate iron stores.
+====Factors effecting iron absorption====
+*Factors that enhance iron uptake are:
+**[[Vitamin C|Ascorbate]] and [[citrate]] increase iron uptake by acting as weak chelators<ref name="pmid16160008">{{cite journal| author=Iolascon A, d'Apolito M, Servedio V, Cimmino F, Piga A, Camaschella C| title=Microcytic anemia and hepatic iron overload in a child with compound heterozygous mutations in DMT1 (SCL11A2). | journal=Blood | year= 2006 | volume= 107 | issue= 1 | pages= 349-54 | pmid=16160008 | doi=10.1182/blood-2005-06-2477 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16160008  }} </ref><ref name="pmid27606953">{{cite journal| author=Coates A, Mountjoy M, Burr J| title=Incidence of Iron Deficiency and Iron Deficient Anemia in Elite Runners and Triathletes. | journal=Clin J Sport Med | year= 2017 | volume= 27 | issue= 5 | pages= 493-498 | pmid=27606953 | doi=10.1097/JSM.0000000000000390 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27606953  }} </ref>.
+**Iron is readily transferred from these compounds into the mucosal lining cells.
+*Factors inhibiting iron absorption are:
+**[[Phytic acid|Phytate]] (myo-inositol hexakisphosphate) is the main inhibitor of iron absorption<ref name="pmid23573815">{{cite journal| author=Thomas DW, Hinchliffe RF, Briggs C, Macdougall IC, Littlewood T, Cavill I et al.| title=Guideline for the laboratory diagnosis of functional iron deficiency. | journal=Br J Haematol | year= 2013 | volume= 161 | issue= 5 | pages= 639-48 | pmid=23573815 | doi=10.1111/bjh.12311 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23573815  }} </ref><ref name="pmid10903283">{{cite journal| author=Simpson E, Mull JD, Longley E, East J| title=Pica during pregnancy in low-income women born in Mexico. | journal=West J Med | year= 2000 | volume= 173 | issue= 1 | pages= 20-4; discussion 25 | pmid=10903283 | doi= | pmc=1070964 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10903283  }} </ref><ref name="pmid2585159">{{cite journal| author=Rector WG| title=Pica: its frequency and significance in patients with iron-deficiency anemia due to chronic gastrointestinal blood loss. | journal=J Gen Intern Med | year= 1989 | volume= 4 | issue= 6 | pages= 512-3 | pmid=2585159 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2585159  }} </ref>.
+**[[Calcium]]
+**Animal proteins such as milk proteins, egg proteins, and [[albumin]], have been shown to inhibit iron absorption.
+**Proteins from [[soybean]] also decrease iron absorption.
+**Suppresion of [[gastric acid]] such as use of [[Antacid|antacids]] suprress iron absorption.
+**Lead competes with iron for the absorption and blocks its absorption by competetive inhibition.
+====Iron requirement====
+{| class="wikitable"
+|+Recommended Dietary Allowances (RDAs) for Iron
+!Age
+!Male
+!Female
+!Pregnancy
+!Lactation
+|-
+|Birth to 6 months
+|0.27 mg*
+|0.27 mg*
+|
+|
+|-
+|7–12 months
+|11 mg
+|11 mg
+|
+|
+|-
+|1–3 years
+|7 mg
+|7 mg
+|
+|
+|-
+|4–8 years
+|10 mg
+|10 mg
+|
+|
+|-
+|9–13 years
+|8 mg
+|8 mg
+|
+|
+|-
+|14–18 years
+|11 mg
+|15 mg
+|27 mg
+|10 mg
+|-
+|19–50 years
+|8 mg
+|18 mg
+|27 mg
+|9 mg
+|-
+|51+ years
+|8 mg
+|8 mg
+|
+|
+|}
+===Pathogenesis===
+*Iron deficiency anemia occurs when there is<ref name="pmid5244572">{{cite journal| author=Reynolds RD, Binder HJ, Miller MB, Chang WW, Horan S| title=Pagophagia and iron deficiency anemia. | journal=Ann Intern Med | year= 1968 | volume= 69 | issue= 3 | pages= 435-40 | pmid=5244572 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=5244572  }} </ref><ref name="pmid16635664">{{cite journal| author=Trost LB, Bergfeld WF, Calogeras E| title=The diagnosis and treatment of iron deficiency and its potential relationship to hair loss. | journal=J Am Acad Dermatol | year= 2006 | volume= 54 | issue= 5 | pages= 824-44 | pmid=16635664 | doi=10.1016/j.jaad.2005.11.1104 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16635664  }} </ref>:
+**Low dietary intake
+**Increased demands of iron
+**Impaired absorption of iron
+**Excessive loss of iron ([[Bleeding|blood loss]])
+**Increased hepcidin (chronic [[inflammation]])
+*Low dietary intake:
+**Iron is obtained from foods such as:
+***meat, such as lamb, pork, chicken, and beef
+***beans
+***pumpkin and squash seeds
+***leafy greens, such as spinach
+***raisins and other dried fruit
+***eggs
+***seafood, such as clams, sardines, shrimp, and oysters
+***Iron-fortified dry and instant cereals Foods high in vitamin C include:
+***Fruits such as oranges, grapefruits, strawberries, kiwis, guavas, papayas, pineapples, melons, and mangoes
+***Red and green bell peppers
+***Brussels sprouts
+***Cauliflower
+***Tomatoes
+***Leafy greens
+**Increased demands of iron
+***Growth, the requirement of iron increases during the developmental period from [[Infant|infancy]] to [[adolescence]] and during adolescence.
+***[[Pregnancy]], during pregnancy the demand for iron is increased.
+**Impaired absorption of iron:
+***[[Malabsorption]]
+***Deficiency of vitamin C in diet
+**Excessive loss of iron (blood loss)
+***The only means of excretion for iron is through blood loss
+***Any source of external and internal bleeding can cause iron deficiency depending on the blood loss
+**Increased hepcidin
+***In chonric [[Inflammation|inflammatory]] conditions, the levels of hepcidin increase
+***Increased hepcidin causes ferriportin degeneration and impaired iron absorption
+*Iron is required for [[Hemoglobin|haemoglobin]] synthesis, so deficiency of iron leads to depletion of haemoglobin
+*Decrease in haemoglobin leads to [[anemia]]
+*Due to low haemoglobin, oxygen is not tranported effectively to cells and results in [[hypoxia]]
+{| class="wikitable"
+!Population
+!Hb Diagnostic of anaemia (g/dL)
+|-
+|Children aged 6 months to 6 years old
+|<11.0
+|-
+|Children aged 6-14 years old
+|<12.0
+|-
+|Adult men
+|<13.0
+|-
+|Adult non-pregnant women
+|<12.0
+|-
+|Adult pregnant women
+|<11.0
+|}
+===Histology===
+(Images shown below are courtesy of Melih Aktan MD, Istanbul Medical Faculty - Turkey)
-==Physiology==
+<div align="left">
-* In the human body, iron is present in all cells and has several vital functions such as:
+<gallery heights="175" widths="175">
-** A carrier of oxygen to the tissues from the lungs in the form of [[hemoglobin]] (Hb)
+Image:Iron deficiency anemia 0001.jpg|Iron deficiency anemia
-** Facilitator of oxygen use and storage in the muscles as [[myoglobin]]
+Image:Iron deficiency anemia 0002.jpg|Iron deficiency anemia
-** Transport medium for electrons within the cells in the form of [[cytochromes]]
+Image:Iron deficiency anemia 0003.jpg|Iron deficiency anemia
-** Integral part of enzyme reactions in various tissues.
+</gallery>
-* Total body iron averages approximately 3.8 g in men and 2.3 g in women.
-===Iron hemostasis (Absorption and bioavailability)===
+===Video===
-* There are several mechanisms that control [[human iron metabolism]] and safeguard against iron deficiency. The capacity of the body to absorb iron from the diet depends on the amount of iron in the body, the rate of red blood cell production, the amount and kind of iron in the diet, and the presence of absorption enhancers and inhibitors in the diet.
+{{#ev:youtube|7uDbu7esZik}}
-====Gastrointestinal tract====
-* Regulation of iron balance occurs mainly in the gastrointestinal tract through absorption.
-* When the absorptive mechanism is operating normally, a person maintains functional iron and tends to establish iron stores.
-* The percentage of iron absorbed (i.e., iron bioavailability) can vary from less than 1% to greater than 50%.
-* The main factor controlling iron absorption is the amount of iron stored in the body.
-* The gastrointestinal tract increases iron absorption when the body's iron stores are low and decreases absorption when stores are sufficient. An increased rate of red blood cell production can also stimulate iron uptake severalfold.
-* Among adults, absorption of dietary iron averages approximately 6% for men and 13% for nonpregnant women in their childbearing years.
-* The higher absorption efficiency of these women reflects primarily their lower iron stores as a result of menstruation and pregnancy.
-* Among iron-deficient persons, iron absorption is also high. Absorption of iron increases during pregnancy, but the amount of the increase is not well defined; as iron stores increase postpartum, iron absorption decreases.
-====Dietary composition====
-* Iron bioavailability also depends on dietary composition. Heme iron, which is found only in meat, poultry, and fish, is two to three times more absorbable than non-heme iron, which is found in plant-based foods and iron-fortified foods.
-* The bioavailability of non-heme iron is strongly affected by the kind of other foods ingested at the same meal.
-* Enhancers of iron absorption are heme iron (in meat, poultry, and fish) and [[vitamin C]]; inhibitors of iron absorption include polyphenols (in certain vegetables), tannins (in tea), phytates (in bran), and calcium (in dairy products).
-* Vegetarian diets, by definition, are low in [[heme]] iron. However, iron bioavailability in a vegeterian diet can be increased by careful planning of meals to include other sources of iron and enhancers of iron absorption.
-* In the diet of an infant, before the introduction of solid foods, the amount of iron absorbed depends on the amount and bioavailability of iron in breast milk or formula.
-====Iron turn over====
-* [[Red blood cell]] formation and destruction is responsible for most iron turnover in the body.
-* In adult men, approximately 95% of the iron required for the production of red blood cells is recycled from the breakdown of red blood cells and only 5% comes from dietary sources.
-* In contrast, an infant is estimated to derive approximately 70% of red blood cell iron from the breakdown of red blood cells and 30% from the diet.
-* In adults, approximately 1 mg of iron is lost daily through feces and desquamated mucosal and skin cells.
-* Women of childbearing age require additional iron to compensate for menstrual blood loss (an average of 0.3-0.5 mg daily during the childbearing years) and for tissue growth during pregnancy and blood loss at delivery and postpartum (an average of 3 mg daily over 280 days' gestation).
-* In all persons, a minute amount of iron is lost daily from physiological gastrointestinal blood loss.
-* Pathological gastrointestinal iron loss through gastrointestinal bleeding occurs in infants and children sensitive to cow's milk and in adults who have peptic ulcer disease, inflammatory bowel syndrome, or bowel cancer.
-* Hookworm infections, although not common in the United States, are also associated with gastrointestinal blood loss and iron depletion
-==External link==
+==External Link==
 [http://www.cdc.gov/mmwr/preview/mmwrhtml/00051880.htm Center for disease control and prevention]
 ==References==
-{{Reflist|2}}
+{{reflist|2}}
-[[Category:Needs content]]
 {{WH}}
 {{WS}}
+[[Category:Hematology]]
+[[Category:Gastroenterology]]
+[[Category:Endocrinology]]