Latent iron deficiency

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Latent Iron Deficiency
Other namesIron-deficient erythropoiesis
Specialty Endocrinology   OOjs UI icon edit-ltr-progressive.svg

Latent iron deficiency (LID), also called iron-deficient erythropoiesis, [1] is a medical condition in which there is evidence of iron deficiency without anemia (normal hemoglobin level). [2] It is important to assess this condition because individuals with latent iron deficiency may develop iron-deficiency anemia. Additionally, there is some evidence of a decrease in vitality and an increase in fatigue among individuals with LID. [3]

Contents

Diagnosis

Diagnostic tests for latent iron deficiency LID

Note: Iron therapy must be suspended 48 hours beforehand to ensure valid test results. [4]

The normal range for hemoglobin is 13.8 to 17.2 grams per deciliter (g/dL) for men and 12.1 to 15.1 g/dL for women. [6] Low hemoglobin indicates anemia but will be normal for LID. [5]

Normal serum iron is between 60 and 170 micrograms per deciliter (μg/dL). [7] Normal total iron-binding capacity for both sexes is 240 to 450 μg/dL. [6] Total iron-binding capacity increases when iron deficiency exists. [4]

Serum ferritin levels reflect the iron stores available in the body. [4] The normal range is 20 to 200 ng/mL for men and 15 to 150 ng/mL for women. [8] Low levels (< 12 ng/mL) are specific for iron deficiency. [4] However, inflammatory and neoplastic disorders can cause ferritin levels to increase – this may be seen in cases of hepatitis, leukemia, Hodgkin lymphoma, and GI tract tumors. [4]

The most sensitive and specific criterion for iron-deficient erythropoiesis is depleted iron stores in the bone marrow. However, in practice, a bone marrow examination is rarely needed. [4]

Interpretation of diagnostic test results in terms of stage of iron deficiency

LID is present in stage 1 and 2, before anemia occurs in stage 3. These first two stages can be interpreted as depletion of iron stores and reduction of effective iron transport. [4]

Stage 1 is characterized by loss of bone marrow iron stores while hemoglobin and serum iron levels remain normal. Serum ferritin falls to less than 20 ng/mL. Increased iron absorption, a compensatory change, results in an increased amount of transferrin and consequent increased iron-binding capacity. [4]

Stage 2 – Erythropoiesis is impaired. In spite of an increased level of transferrin, serum iron level is decreased along with transferrin saturation. Erythropoiesis impairment begins when the serum iron level falls to less than 50 μg/dL and transferrin saturation is less than 16%. [4]

In stage 3, anemia (reduced hemoglobin levels) is present but red blood cell appearance remains normal. [4]

Changes in the appearance of red blood cells are the hallmark of stage 4; first microcytosis and then hypochromia develop. [4]

Iron deficiency begins to affect tissues in stage 5, manifesting as symptoms and signs. [4]

Treatment

There is no consensus on how to treat LID but one option is to treat it as an iron-deficiency anemia with ferrous sulfate (Iron(II) sulfate) at a dose of 100 mg x day in two doses (one at breakfast and the other at dinner) [9] or 3 mg x Kg x day in children (also in two doses) [10] for two or three months. The ideal is to increase the body's iron deposits, measured as levels of ferritin in serum, with the aim of reaching a ferritin value between 30 and 100 ng/mL. Another clinical study has shown an increase in ferritin levels in those taking iron compared with others receiving a placebo from persons with LID. [11] With ferritin levels higher than 100 ng/mL an increase in infections has been reported. [12] Another way to treat LID is with an iron-rich diet and additionally ascorbic acid or vitamin C, contained in many types of fruits as oranges, kiwifruits, etc. which will increase iron absorption 2 to 5-fold. [13] [14]

Epidemiology

Many studies have been done on LID; its frequency varies according to country of origin, diet, pregnancy status age, gender, etc. Depending on these previous conditions, the frequency can vary from 11% in male athletes (Poland) to 44.7% in children less than one year old (China):

Frequency of LID in different countries and populations:

Related Research Articles

<span class="mw-page-title-main">Anemia</span> Medical condition

Anemia or anaemia is a blood disorder in which the blood has a reduced ability to carry oxygen due to a lower than normal number of red blood cells, or a reduction in the amount of hemoglobin. When anemia comes on slowly, the symptoms are often vague, such as tiredness, weakness, shortness of breath, headaches, and a reduced ability to exercise. When anemia is acute, symptoms may include confusion, feeling like one is going to pass out, loss of consciousness, and increased thirst. Anemia must be significant before a person becomes noticeably pale. Symptoms of anemia depend on how quickly hemoglobin decreases. Additional symptoms may occur depending on the underlying cause. Preoperative anemia can increase the risk of needing a blood transfusion following surgery. Anemia can be temporary or long term and can range from mild to severe.

<span class="mw-page-title-main">Iron deficiency</span> State in which a body lacks enough iron to supply its needs

Iron deficiency, or sideropenia, is the state in which a body lacks enough iron to supply its needs. Iron is present in all cells in the human body and has several vital functions, such as carrying oxygen to the tissues from the lungs as a key component of the hemoglobin protein, acting as a transport medium for electrons within the cells in the form of cytochromes, and facilitating oxygen enzyme reactions in various tissues. Too little iron can interfere with these vital functions and lead to morbidity and death.

<span class="mw-page-title-main">Ferritin</span> Iron-carrying protein

Ferritin is a universal intracellular protein that stores iron and releases it in a controlled fashion. The protein is produced by almost all living organisms, including archaea, bacteria, algae, higher plants, and animals. It is the primary intracellular iron-storage protein in both prokaryotes and eukaryotes, keeping iron in a soluble and non-toxic form. In humans, it acts as a buffer against iron deficiency and iron overload.

<span class="mw-page-title-main">Transferrin</span> Mammalian protein found in Homo sapiens

Transferrins are glycoproteins found in vertebrates which bind to and consequently mediate the transport of iron (Fe) through blood plasma. They are produced in the liver and contain binding sites for two Fe3+ ions. Human transferrin is encoded by the TF gene and produced as a 76 kDa glycoprotein.

<span class="mw-page-title-main">Iron-deficiency anemia</span> Medical condition

Iron-deficiency anemia is anemia caused by a lack of iron. Anemia is defined as a decrease in the number of red blood cells or the amount of hemoglobin in the blood. When onset is slow, symptoms are often vague such as feeling tired, weak, short of breath, or having decreased ability to exercise. Anemia that comes on quickly often has more severe symptoms, including confusion, feeling like one is going to pass out or increased thirst. Anemia is typically significant before a person becomes noticeably pale. Children with iron deficiency anemia may have problems with growth and development. There may be additional symptoms depending on the underlying cause.

<span class="mw-page-title-main">Erythropoiesis</span> Process which produces red blood cells

Erythropoiesis is the process which produces red blood cells (erythrocytes), which is the development from erythropoietic stem cell to mature red blood cell.

<span class="mw-page-title-main">Microcytic anemia</span> Medical condition

Microcytic anaemia is any of several types of anemia characterized by smaller than normal red blood cells. The normal mean corpuscular volume is approximately 80–100 fL. When the MCV is <80 fL, the red cells are described as microcytic and when >100 fL, macrocytic. The MCV is the average red blood cell size.

Anemia of chronic disease (ACD) or anemia of chronic inflammation is a form of anemia seen in chronic infection, chronic immune activation, and malignancy. These conditions all produce elevation of interleukin-6, which stimulates hepcidin production and release from the liver. Hepcidin production and release shuts down ferroportin, a protein that controls export of iron from the gut and from iron storing cells. As a consequence, circulating iron levels are reduced. Other mechanisms may also play a role, such as reduced erythropoiesis. It is also known as anemia of inflammation, or anemia of inflammatory response.

<span class="mw-page-title-main">Sideroblastic anemia</span> Medical condition

Sideroblastic anemia, or sideroachrestic anemia, is a form of anemia in which the bone marrow produces ringed sideroblasts rather than healthy red blood cells (erythrocytes). In sideroblastic anemia, the body has iron available but cannot incorporate it into hemoglobin, which red blood cells need in order to transport oxygen efficiently. The disorder may be caused either by a genetic disorder or indirectly as part of myelodysplastic syndrome, which can develop into hematological malignancies.

Serum iron is a medical laboratory test that measures the amount of circulating iron that is bound to transferrin (90%) and serum ferritin (10%). Clinicians order this laboratory test when they are concerned about iron deficiency, which can cause anemia and other problems. 65% of the iron in the body is bound up in hemoglobin molecules in red blood cells. About 4% is bound up in myoglobin molecules. Around 30% of the iron in the body is stored as ferritin or hemosiderin in the spleen, the bone marrow and the liver. Small amounts of iron can be found in other molecules in cells throughout the body. None of this iron is directly accessible by testing the serum.}

<span class="mw-page-title-main">Total iron-binding capacity</span>

Total iron-binding capacity (TIBC) or sometimes transferrin iron-binding capacity is a medical laboratory test that measures the blood's capacity to bind iron with transferrin. Transferrin can bind two atoms of ferric iron (Fe3+) with high affinity. It means that transferrin has the capacity to transport approximately from 1.40 to 1.49 mg of iron per gram of transferrin present in the blood.

Transferrin saturation (TS), measured as a percentage, is a medical laboratory value. It is the value of serum iron divided by the total iron-binding capacity of the available transferrin, the main protein that binds iron in the blood, this value tells a clinician how much serum iron is bound. For instance, a value of 15% means that 15% of iron-binding sites of transferrin are being occupied by iron. The three results are usually reported together. A low transferrin saturation is a common indicator of iron deficiency anemia whereas a high transferrin saturation may indicate iron overload or hemochromatosis. Transferrin saturation is also called transferrin saturation index (TSI) or transferrin saturation percentage (TS%)

<span class="mw-page-title-main">Human iron metabolism</span> Iron metabolism in the body

Human iron metabolism is the set of chemical reactions that maintain human homeostasis of iron at the systemic and cellular level. Iron is both necessary to the body and potentially toxic. Controlling iron levels in the body is a critically important part of many aspects of human health and disease. Hematologists have been especially interested in systemic iron metabolism, because iron is essential for red blood cells, where most of the human body's iron is contained. Understanding iron metabolism is also important for understanding diseases of iron overload, such as hereditary hemochromatosis, and iron deficiency, such as iron-deficiency anemia.

<span class="mw-page-title-main">Beta thalassemia</span> Thalassemia characterized by the reduced or absent synthesis of the beta globin chains of hemoglobin

Beta thalassemias are a group of inherited blood disorders. They are forms of thalassemia caused by reduced or absent synthesis of the beta chains of hemoglobin that result in variable outcomes ranging from severe anemia to clinically asymptomatic individuals. Global annual incidence is estimated at one in 100,000. Beta thalassemias occur due to malfunctions in the hemoglobin subunit beta or HBB. The severity of the disease depends on the nature of the mutation.


Anemia is a deficiency in the size or number of red blood cells or in the amount of hemoglobin they contain.This deficiency limits the exchange of O2 and CO2 between the blood and the tissue cells.Globally, young children, women, and older adults are at the highest risk of developing anemia. Anemia can be classified based on different parameters, and one classification depends on whether it is related to nutrition or not so there are two types: nutritional anemia and non-nutritional anemia. Nutritional anemia refers to anemia that can be directly attributed to nutritional disorders or deficiencies. Examples include Iron deficiency anemia and pernicious anemia. It is often discussed in a pediatric context.

Sideropenic hypochromic anemia is primarily characterized by low serum iron concentration. Non-sideropenic hypochromic anemia is the ineffective utilisation of iron stores, usually from chronic infection/inflammation. It is very important to distinguish iron deficit anemia from the anemia of chronic disorders so as to ensure specific treatment.

Clement Alfred Finch, often deemed "The Iron Man", was a Physician specializing in Hematology whose research on iron metabolization in the bloodstream at the University of Washington led to significant advancements in accurately diagnosing and treating anemia during a time period in which little was known about this aspect of the body. Finch was distinctively noted for using himself as a test subject by taking blood and bone marrow from his own bones before conducting similar tests on patients. He graduated in 1941 from the University of Rochester Medical School and a year later was married to the first of three wives. He experienced a 60-year tenure at the University of Washington, and has published many scholarly articles pertaining to iron in the bloodstream and is the author of three books entitled: Iron Metabolism (1962) Red Cell Manual (1969) and Fulfilling the Dream: A History of the University of Washington School of Medicine 1946 to 1988 (1990). Clement Finch was elected as a Fellow of the National Academy of Sciences in 1974, and elected as a Fellow of the American Academy of Arts and Sciences in 1976.

Iron(III)-hydroxide polymaltose complex is a medication used to treat iron deficiency / iron deficiency anemia and belongs to the group of oral iron preparations. The preparation is a macromolecular complex, consisting of iron(III) hydroxide (trivalent iron, Fe3+, Fe(OH)3·H2O) and the carrier polymaltose and is available in solid form as a film-coated or chewable tablet and in liquid form as a syrup, drinkable solution, or drops. It is used for treating iron deficiency without anemia (latent iron deficiency) or with anemia (apparent iron deficiency). Prior to administration, the iron deficiency should be diagnostically established and verified via laboratory tests (e.g., low ferritin concentration, low transferrin saturation).

Anemia is a condition in which blood has a lower-than-normal amount of red blood cells or hemoglobin. Anemia in pregnancy is a decrease in the total red blood cells (RBCs) or hemoglobin in the blood during pregnancy. Anemia is an extremely common condition in pregnancy world-wide, conferring a number of health risks to mother and child. While anemia in pregnancy may be pathologic, in normal pregnancies, the increase in RBC mass is smaller than the increase in plasma volume, leading to a mild decrease in hemoglobin concentration referred to as physiologic anemia. Maternal signs and symptoms are usually non-specific, but can include: fatigue, pallor, dyspnea, palpitations, and dizziness. There are numerous well-known maternal consequences of anemia including: maternal cardiovascular strain, reduced physical and mental performance, reduced peripartum blood reserves, increased risk for peripartum blood product transfusion, and increased risk for maternal mortality.

Iron preparation is the formulation for iron supplements indicated in prophylaxis and treatment of iron-deficiency anemia. Examples of iron preparation include ferrous sulfate, ferrous gluconate, and ferrous fumarate. It can be administered orally, and by intravenous injection, or intramuscular injection.

References

  1. ↑ Suominen, P; Punnonen, K; Rajamäki, A; Irjala, K (October 1998). "Serum transferrin receptor and transferrin receptor-ferritin index identify healthy subjects with subclinical iron deficits". Blood. 92 (8): 2934–9. doi:10.1182/blood.V92.8.2934. PMID   9763580.
  2. ↑ Yehuda, Shlomo; Mostofsky, David I. (2010-03-10). Iron Deficiency and Overload: From Basic Biology to Clinical Medicine. Springer Science & Business Media. p. 302. ISBN   9781597454629.
  3. ↑ Patterson, A. J.; Brown, W. J.; Roberts, D. C. (August 2001). "Dietary and supplement treatment of iron deficiency results in improvements in general health and fatigue in Australian women of childbearing age". Journal of the American College of Nutrition. 20 (4): 337–42. doi:10.1080/07315724.2001.10719054. PMID   11506061. S2CID   1886582.
  4. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 "Iron Deficiency Anemia". Merck Manuals Professional Edition. Retrieved 2016-06-22.
  5. 1 2 "Iron deficiency anemia - Mayo Clinic". www.mayoclinic.org. Retrieved 2016-06-22.
  6. 1 2 "Hemoglobin: MedlinePlus Medical Encyclopedia". www.nlm.nih.gov. Retrieved 2016-06-22.
  7. ↑ "Serum iron test: MedlinePlus Medical Encyclopedia". www.nlm.nih.gov. Retrieved 2016-06-22.
  8. ↑ "Ferritin blood test: MedlinePlus Medical Encyclopedia". www.nlm.nih.gov. Retrieved 2016-06-22.
  9. ↑ Norrby, A (1974). "Iron absorption studies in iron deficiency". Scandinavian Journal of Haematology. Supplementum. 20: 1–125. PMID   4526330.
  10. ↑ Dallman, P. R.; Siimes, M. A.; Stekel, A (January 1980). "Iron deficiency in infancy and childhood". The American Journal of Clinical Nutrition. 33 (1): 86–118. doi:10.1093/ajcn/33.1.86. PMID   6986756.
  11. ↑ Leonard, A. J.; Chalmers, K. A.; Collins, C. E.; Patterson, A. J. (April 2014). "Comparison of two doses of elemental iron in the treatment of latent iron deficiency: efficacy, side effects and blinding capabilities". Nutrients. 6 (4): 1394–405. doi: 10.3390/nu6041394 . PMC   4011041 . PMID   24714351.
  12. ↑ Weiss, G; Goodnough, L. T. (March 2005). "Anemia of chronic disease". The New England Journal of Medicine. 352 (10): 1011–23. doi:10.1056/NEJMra041809. PMID   15758012.
  13. ↑ Sayers, M. H.; Lynch, S. R.; Charlton, R. W.; Bothwell, T. H.; Walker, R. B.; Mayet, F (May 1974). "Iron absorption from rice meals cooked with fortified salt containing ferrous sulphate and ascorbic acid". The British Journal of Nutrition. 31 (3): 367–75. doi: 10.1079/BJN19740045 . PMID   4835790.
  14. ↑ Sayers, M. H.; Lynch, S. R.; Charlton, R. W.; Bothwell, T. H.; Walker, R. B.; Mayet, P (December 1974). "The fortification of common salt with ascorbic acid and iron". British Journal of Haematology. 28 (4): 483–95. doi:10.1111/j.1365-2141.1974.tb06667.x. PMID   4455301. S2CID   5516683.
  15. ↑ Malczewska, J; Szczepańska, B; Stupnicki, R; Sendecki, W (March 2001). "The assessment of frequency of iron deficiency in athletes from the transferrin receptor-ferritin index". International Journal of Sport Nutrition and Exercise Metabolism. 11 (1): 42–52. doi:10.1123/ijsnem.11.1.42. PMID   11255135.
  16. ↑ Mehta, B. C. (September 2004). "Iron deficiency amongst nursing students". Indian Journal of Medical Sciences. 58 (9): 389–93. PMID   15470280.
  17. ↑ Capel-Casbas, Maria J.; Duran, Jose J.; Diaz, Jorge; Ruiz, Gerardo; Simon, Ramon; Rodriguez, Francisco; Piqueras, Josep; Pelegri, Dolors; Pujol-Moix, Nuria (2005). "Latent Iron Metabolism Disturbances in Fertile Women and Its Detection with the Automated Hematology Instrument LH750®". Blood. 106 (11): 3707. doi:10.1182/blood.V106.11.3707.3707.
  18. ↑ Liao, Q. K.; Chinese Children, Pregnant Women & Premenopausal Women Iron Deficiency Epidemiological Survey Group (November 2004). "[Prevalence of iron deficiency in pregnant and premenopausal women in China: a nationwide epidemiological survey]". Zhonghua Xue Ye Xue Za Zhi (in Chinese). 25 (11): 653–7. PMID   15634568.
  19. ↑ Zhu, Y. P.; Liao, Q. K.; Collaborative Study Group for "The Epidemiological Survey of Iron Deficiency in Children in China" (December 2004). "[Prevalence of iron deficiency in children aged 7 months to 7 years in China]". Zhonghua Er Ke Za Zhi (in Chinese). 42 (12): 886–91. PMID   15733354.
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