Iron deficiency anemia

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:

Iron deficiency anemia occurs when body iron stores are inadequate to meet normal metabolic demands of the body. It is the most common cause of microcytic anemia.

Iron deficiency anemia occurs in the setting of blood loss, insufficient dietary intake or poor oral absorption of iron from food. Symptoms of iron deficiency anemia including fatigue, weakness, shortness of breath, lightheadedness, and pallor. Twenty percent of all women of childbearing age have iron deficiency anemia, compared with only 2% of adult men. The principal cause of iron deficiency anemia in premenopausal women is excessive blood loss during menses. In post menopausal women and men, the main cause of iron deficiency are digestive tract diseases.

Iron deficiency anemia is the final stage of iron deficiency. When the body has sufficient iron to meet its needs (functional iron), the remainder is stored for later use in the bone marrow, liver, and spleen. Iron deficiency ranges from iron depletion, which yields little physiological damage, to iron deficiency anemia, which can affect the function of numerous organ systems. Iron depletion causes the amount of stored iron to be reduced, but has no effect on the functional iron. However, a person with no stored iron has no reserves to use if the body requires more iron. In essence, the amount of iron absorbed by the body is not adequate for growth and development or to replace the amount lost.

Iron deficiency anemia was discovered in 1852 by Karl Vierordt and his student H. Welcher.

There is no established system for the classification of iron deficiency. However, based on the pathology, it can be divided into functional and absolute iron deficiency.

Iron homeostasis is maintained by a balance of iron absorption and iron loss. Iron absorption is a more active process and is mainly responsible for regulation of iron balance. The absorption of iron is highly regulated by hepcidin, a protein secreted by hepatocytes.

Iron is absorbed in ferrous form (Fe2+) in the small intestine via divalent metal transporter (DMT1). After absorption, depending on iron levels in the body, iron can be sequestered in ferritin or bound to transferrin by ferroportin. Once bound to transferrin, iron is transported to cells that require iron. Iron enters cells when transferrin binds to transferrin receptor (TfR).

Iron deficiency occurs in three stages. In the prelatent stage, ferritin is low but serum iron levels are normal. In the latent stage, transferrin saturation and serum iron are also low in addition to low ferritin. In the last stage, hemoglobin level is below normal along with depletion of iron stores and drop in serum iron and transferrin saturation.

In developed nations, the main cause of iron deficiency anemia is blood loss. Bleeding from any source can cause iron deficiency anemia. Obvious causes of blood loss like menorrhagia, hematemesis, melena, hematuria, multiple child births, frequent blood donations can be easily recognized with history alone. Occult blood loss from causes like GI bleeding, parasitic infestations etc may be overlooked.

Inadequate dietary iron is the most common cause of iron deficiency anemia in resource poor countries. It is also the most common cause of iron deficiency anemia in toddlers. In toddlers, poor nutritional practices like excessive cow milk intake or snacking contribute to iron deficiency.

Malabsorption due to celiac disease, atrophic gastritis, Helicobacter pylori infection, post-bariatric surgery can also cause iron deficiency.

Drugs which suppress gastric acid can also impair absorption of iron as iron requires an acidic medium for absorption. Certain antibiotics like quinolones, doxycyline, chrloramphenicol etc also diminish the absorption of iron.^[1]

Chronic conditions like chronic heart failure, CKD, inflammatory bowel disease, malignancy, rheumatoid arthritis are also associated with iron deficiency anemia.

Other less common cause of iron deficiency include urinary and pulmonary hemosiderosis and genetic conditions like IRIDA due to TMPRSS6 mutations.

Iron deficiency anemia and Thalassemia Minor present with many of the same lab results. It is very important not to treat a patient with Thalassemia with an iron supplement as this can lead to hemochromatosis (accumulation of iron in the liver) A hemoglobin electrophoresis would provide useful evidence in distinguishing these two conditions, along with iron studies.

According to WHO’s Global Burden of Disease Project 2000 (GBD 2000), iron deficiency is responsible for 841,000 deaths worldwide with the major burden of mortality seen in Africa and parts of Asia.

In the US, iron deficiency is seen in 9% of toddlers between age 1 and 2 years. Compared to white toddlers, Hispanic toddlers are twice as likely to have iron deficiency.^[2]

The prevalence in adolescent girls and women in reproductive age group is between 9% to 11%. It is most commonly seen in multiparous women from low income minority populations. In males, it is seen in around 1% of population with slightly high prevalence of 2 – 4% in middle aged and older men.

There is a positive correlation between obesity and the risk of developing iron deficiency.^[3]

Risk of iron deficiency anemia is more in those individuals who consume less iron in diet and who are at increased risk of bleeding.

Screening is recommended in women of reproductive age and toddlers.

Untreated iron deficiency anemia is associated with significant cognitive impairment and decreased work capacity and quality of life.

During pregnancy, untreated iron deficiency can affect fetal brain maturation and predispose the newborn to iron deficiency and low birth weight. Maternal adverse outcomes include depression, increase risk of sepsis and maternal mortality.

In patients undergoing cardiac or abdominal surgery, pre operative iron deficiency is associated with poor outcomes. In patients with heart failure, untreated iron deficiency can cause an increase in mortality.

If treated with iron supplementation, the prognosis is excellent.

Iron deficiency anemia is diagnosed on the basis of results of CBC, peripheral blood film and iron studies. A normal hemoglobin does not rule out iron deficiency. Iron deficiency is diagnosed when serum ferritin is < 30ng/mL.

Majority of symptoms are non specific and include weakness, fatigue, dyspnea on exertion, irritability, poor concentration and decreased exercise capacity. These are attributable to low oxygen delivery to tissues and decreased activity of iron containing enzymes.

Pica occurs in approximately half of these patients and pagophagia (craving for ice) is quite specific for iron deficiency.^[4]

Patients may have a history of dry mouth, hair loss, dysphagia, brittle fingernails and restless leg syndrome

Beeturia is a finding which is not specific for iron deficiency but is increased in these individuals. It is the result of a change in GI function due to severe Iron deficiency. The urine turns red following ingestion of beets.

Physical examination can be normal or show dry skin, atrophic glossitis, cheilosis, pallor and koilonychia(spoon shaped nails). Cardiac auscultation may reveal systolic murmur.

Physical examination may reveal pallor, koilonychia (spoon shaped nails), cheilosis, atrophic glossitis, dry skin and systolic murmur on cardiac auscultation.

The first step in diagnosis is ordering a CBC, peripheral smear and serum ferritin. Low serum ferritin is only seen in iron deficiency anemia but high ferritin can be seen in many chronic disorders. Absolute iron deficiency is diagnosed with a serum ferritin of < 30ng/mL. A normal hemoglobin does not exclude iron deficiency as hemoglobin does not become low till a significant percentage of body iron is depleted.

Uncomplicated iron deficiency can be diagnosed by assessing standard iron parameters, such as serum ferritin and transferrin saturation.

Serum iron varies during the day and is influenced by diet. A fasting sample should be obtained in the morning. Plasma iron is reduced as the iron in the body is exhausted. Total iron binding capacity (TIBC) is elevated in iron deficiency anemia.

Serum transferrin is raised in iron deficiency anemia. Transferrin saturation index (TSAT) is the ratio of serum iron to TIBC. It is one of the earliest biomarker of ID and is useful when serum ferritin is unequivocal. A decrease (< 20%) indicates ID, either absolute or functional.^[5]

Soluble transferrin receptor (sTfR) is a fragment of membrane receptor for transferrin. It is elevated in iron deficiency because of upregulation of transferrin receptors. It can help differentiate between absolute(increased sTfR) and functional ID( normal sTfR).

sTfR–Ferritin index is the ratio of sTfR to serum ferritin. It is also considered a good indicator for evaluation of iron deficiency.

Other tests available for evaluating iron status include Zinc protoporphyrin/heme ratio and reticulocyte hemoglobin content.

Iron supplementation is available in oral and IV forms. Oral iron is readily available, inexpensive, effective, safe, and convenient. Some of the available formulations include ferrous sulfate, ferrous fumarate, and ferrous gluconate. GI side effects are seen in up to 70% of the patients taking oral iron, leading to noncompliance with treatment. GI symptoms can be minimized by the use of chelated forms of iron. Enteric-coated tablets lead to poor absorption and should not be used.^[6]

Intravenous iron is available in many forms, such as ferric carboxymaltose, ferric gluconate, ferric/iron sucrose, ferumoxytol, and low-molecular-weight iron dextran. Response to IV iron should be checked to establish the need for further supplementation six to eight weeks after initial iron replacement.^[7]

There is a very low risk of allergic reactions with all IV iron formulations. Premedication with antihistamines does not prevent infusion reactions and should not be given. Patients with a history of asthma or drug allergies should receive steroids prior to infusion.

In pregnancy, oral iron is given during the first trimester as the safety of IV iron in the first trimester has not been established.

Generally, oral iron is given to pregnant women if it can be tolerated. Exceptions include women with severe anemia, women with IBD, and those who have undergone bariatric surgery. In these patients, IV iron is preferred. All IV forms have equal efficacy and safety except for some formulations of ferric gluconate which contain benzyl alcohol as a preservative. These are avoided because of the possibility of harm to the fetus.

In developing countries, patients should be advised to consume iron rich foods and fruits and vegetables high in Vitamin C. In babies born to iron deficient mothers, delayed umbilical cord clamping can be helpful in preventing iron deficiency in newborns.^[8]

In infants, iron should be supplemented after 6 months of breastfeeding. Iron fortified cereal and formula should be given. Anti helminthic drugs should be given to children with parasitic infections. In areas where prevalence of iron deficiency is high, women of reproductive age group should take daily iron supplements.

References

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Shyam Patel [2]; Associate Editor(s)-in-Chief: Jogeet Singh Sekhon, M.D. [3]

Iron deficiency anemia was discovered in 1852 by Karl Vierordt and his student H. Welcher. Over the next century, the details of iron regulation were elucidated.

• In 1852, Karl Vierordt and his student H. Welcher discovered iron deficiency anemia.

• In 1949, Finch and colleagues showed that reticulocytes (precursors of red blood cells) can incorporate iron from the plasma to make hemoglobin.^[1]

• In 1969, Evan Morgan and colleagues showed internalization of transferrin (the carrier of iron) by cells.^[1] This was one of the first demonstrations that the internalization of a membrane protein was important for iron regulation.

• In 1979, Bothwell published a monograph about early iron homeostasis. By this time, iron regulation was well understood.^[1]

• In 1990, Donnall Thomas received the Nobel Prize for his discoveries about bone marrow transplantation.^[1]

• Between 1990 and 2010, the prevalence of anemia worldwide decreased from 40.2% to 32.9%.^[2]

• In 2000, Breton-Gorius and Bessis showed via electron micrography that there were erythroblastic islands (locations of red blood cell production) in the bone marrow, and they showed that iron (in the form of ferritin) could be transferred between the erythroblasts and surrounding cells.^[1]

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Shyam Patel [2]; Associate Editor(s)-in-Chief: Jogeet Singh Sekhon, M.D. [3]

There is no established system for the classification of iron deficiency anemia. However, based on the pathology it can be divided into 2 types on the basis of cause of iron deficiency into absolute iron deficiency and functional iron deficiency.

Iron deficiency anemia can be classified into^[1].

• Absolute iron deficiency arising due to the lowered or exhausted level of total body iron stores.
• Functional iron deficiency wherein the total body iron stores are normal or increased, with the insufficient iron supply to the bone marrow. Functional iron deficiency is present in many acute and chronic inflammatory states. In this case, the problem lies within utilization of iron stores.

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

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.

• 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.

• 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.

• 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).

• 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 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 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

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

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:

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Iron deficiency anemia causes can be broadly divided into physiological causes as that seen during growth and pregnancy and due to pathological process. The pathological process could be further divided based on blood loss and inadequate iron absorption.

• Severe blood loss such as traumatic haemorrhage, haemetemesis, haemoptysis or uncontrolled bleeding from any body part can result in death from hypovolemic shock^[1][2][3][4]

^{[5][6][7][8][9][10][11][12][13]} .

• Growth
• Pregnancy
• Malnutrition
• Malabsorption
• Blood loss
• Chronic Kidney disease
• Anemia of chronic disease
• Myeloproliferative disorders

• Erythrpoetin/eryhtropoetin stimulating drugs
• Leflunomide
• Pramipexole
• Trientine

• IRIDA- iron referactory iron deficiency anemia due to TMPRSS6 mutation
• SLC11A-2 mutation
• Iron-refractory iron deficiency anaemia •
• Divalent metal transporter deficiency anaemia, •
• Fanconianaemia
• Pyruvate kinase deficiency

• Menstruation
• Gastrointestinal tract (Bleeding from the gastrointestinal tract (ulcers, hemorrhoids, Esophageal varices, The use of aspirin, ibuprofen, or arthritis medicines for a long time, Cancer in the esophagus, stomach, or colon)
  • Food sensitivity
  • Hookworms
• Genitourinary tract
• Respiratory tract (Rarely laryngological bleeding or from the respiratory tract)
• Blood donation

• Dietary deficiency
• Impaired absorption (Celiac disease, Crohn’s disease)
  • Intestinal malabsorption
  • Gastric surgery
  • Hypochorhydria
• Taking too many antacids that contain calcium

Center for disease control and prevention

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Iron deficiency anemia and Thalassemia Minor present with many of the same lab results. It is very important not to treat a patient with Thalassemia with an iron supplement as this can lead to hemochromatosis (accumulation of iron in the liver) A hemoglobin electrophoresis would provide useful evidence in distinguishing these two conditions, along with iron studies.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Jogeet Singh Sekhon, M.D. [2]

Iron deficiency anemia can occur in any age group, region, gender but there are some factors that predispose individuals of some groups to develop iron deficiency.

• The incidence/prevalence of iron deficicency anemia is approximately 720-1360 per 100,000 individuals worldwide.^[1]

• Patients of all age groups may develop iron deficiency anemia^[2][3][4][5].
• Older individuals are more commonly affected.
• Children aged 6 months to 24 months are also at risk.

• African Americans have more risk of developing iron deficiency anemia.

• Iron deficiency anemia develops more commonly in females than males.

• Iron deficiency anemia is more common in regions where meat is consumed in small quantities.

Center for disease control and prevention

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Jogeet Singh Sekhon, M.D. [2]

Risk of iron deficiency anemia is more in those individuals who consume less iron in diet and who are at increased risk of bleeding.

• Women of childbearing age.
• Pregnant women.
• People with poor diets.
• People who donate blood frequently.
• Infants and children, especially those born prematurely or experiencing a growth spurt.
• Vegetarians who don’t replace meat with another iron-rich food.
• Infants who drink cow’s milk rather than breast milk or iron-fortified formula.

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Screening is recommended in pregnant women and new borns.

• Screening is recommended in pregnant women and new borns^[1][2].

• CBC is the initial test.
• If microcytic hypochromic anemia is seen, then iron studies are done.

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The symptoms of iron deficiency are similar as in any other case of anemia. Iron deficiency anemia has age specific presentations. Iron deficiency anemia can lead to severe complications if not treated. The prognosis of iron deficiency anemia is good if iron supplementation is started.

• The symptoms of iron deficiency are similar as in any other case of anemia^{[1][2][3][4][5][6][7]}

• .The stage of anemia develops when there is chronic deficiency of iron and all the iron stores of body are used up.

• Initially in iron defiicency, no symptoms develop as body has sufficient store of iron in the form of ferritin.
• Normal ferittin levels are 20 to 300 ng/mL. This level denotes suffiicient iron levels in the body.
• Ferittin levels between 20-40 ng/ml denotes iron deficiency without anemia.
• Ferittin levels <20 ng/ml denotes iron deficency with anemia and signs and symptoms of anemia develop at this stage.
• Iron deficiency anemia has age specific presentations:
  • Infants (age 0-12 months) and Preschool Children (age 1-5 years)
    • Iron-deficiency anemia is defined as a Hb concentration of less than or equal to 10.0 g/dL .
    • Developmental delays.
    • Behavioral disturbances (e.g., decreased motor activity, social interaction, and attention to tasks)
    • Iron-deficiency anemia also contributes to lead poisoning in children by increasing the gastrointestinal tract’s ability to absorb heavy metals, including lead.
    • Psychiatric illnesses such as unipolar disorder, bipolar disorder and autism spectrum disorder in adolescense.
  • Adults (persons aged greater than or equal to 18 years)
    • Decreased functional capacity
    • Signs of hypoxia due to low oxygen delivery to the tissues.
  • Pregnant Female
    • Increased chances of pre term labor
    • Low birth weight baby

• Iron deficiency anemia can lead to severe complications if not treated^{[8][9][10][11][12][13][14][15]}.

• Severe iron deficiency (ferittin <10 ng/mL (<10 mcg/L; <22.5 picoM/L) can lead to severe complications.
• Exercise:
  • Fatigue
  • Low stamina
  • Muscle atrophy
  • Decreased aerobic capacity
  • Decreased endurance ability
• Heart
  • Irregular heart beat
  • Cardiac failure
  • Dilated cardiomyopathy
  • Systolic flow murmur
  • Myocardial ischemia
  • Angina pectoris
  • Haemodynamic instability
• Lungs
  • Pulmonary edema
  • Dyspnea
• Development delay in children
  • Mental retardation
  • Behavioral differences
  • Psychiatric illness
  • Shortened attention span
  • Neurocognitive delay
• Pregnancy
  • Preterm labor
  • Low birth weight baby
  • Postpartum depression
• Restless leg syndrome
• Atrophic glossitis
• Alopecia
• Immune system weakness
• Syncope
• Plummer Vinson syndrome

• The prognosis of iron deficiency anemia is good if iron supplementation is started.
• Serum iron levels improve within 2 months of starting treatment.
• Severe iron defiicency is present when ferritin <10 ng/mL and Hb <7mg/dl. At this stage severe complications may start developing.
• The severity of iron deficiency anemia depends on:
  • Level of severity.
  • Age of onset.
  • Presence of chronic disease.
  • Speed of onset.
  • Cause of iron deficiency.
• In cases like chronic diseases, restoring iron stores will not treat the anemia unless the disease is treated as cause of anemia is not decreased iron deficiency but iron trapped in its storage form.
• Reversible causes like bleeding can be managed with blood transfusion and have a good prognosis if blood can be restored in sufficient time .
• Iron supplementation improves learning, memory, and cognitive test performance in adolescents who have low levels of iron. Iron supplementation also improves the performance of athletes with anemia and iron deficiency.

The gastrointestinal tract may be the cause, even in the absence of signs of gastrointestinal bleeding^[16]. The prevalence of gastrointestinal lesions among asymptomatic patients with iron deficiency were^[16]:

• Occult blood positive: 67%
• Occult blood negative: 41%

Gastrointestinal evaluation is underused^[17][18][19].

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