The most prevalent form of anemia, that affects one in eight individuals worldwide.
Occurs in two main forms: absolute or functional.
Absolute iron deficiency results when total body iron stores are low or exhausted and functional iron deficiency is a disorder in which total body iron stores are normal or increased, but the available iron supply to the bone marrow is inadequate.
Both forms of iron deficiency can coexist.
Functional iron deficiency is present in many acute and chronic inflammatory states.
Iron is in the central component of hemoglobin in red blood cells and myoglobin in muscles, containing around 60% of the total body iron.
Iron is necessary for various cellular mechanisms, including enzymatic processes, DNA synthesis, and mitochondrial energy production.
Specific signs include color of the skin, conjunctivae and nail beds.
Other presenting signs and symptoms result from hypoxic functioning such as fatigue, dyspnea on exertion, vertigo, syncope headache, tachycardia, flow murmurs, shortness of breath at rest, angina and hemodynamic instability.
Clinical features depend on the severity of the process, age, comorbidities, speed of onset, and chronicity.
In many cases patients are asymptomatic and diagnose incidentally after laboratory evaluation.
Hepcidin is the major regulator of iron homeostasis and has a key role in the pathogenesis of functional iron deficiency.
In the presence of iron deficiency anemia, hepcidin is sometimes below detectable levels.
Hepcidin is increased in the presence of systemic inflammation or infection.
Affects epithelial cells with rapid turnover, causing dryness and roughness of skin, dry and damaged hair follicles, moderate alopecia, and spoon shaped fingernails.
Loss of tongue papillae occurs in patients with moderate disease and is a good gauge of length of deficiency.
Affects approximately one third of the worlds population.
Half the cases of worldwide anemia are due to iron deficiency.
Prevalence of iron deficiency in the US ranges from 4 1/2 to 18%, but the burden of iron deficiency anemia is about 2.9%.
Children ages 0-5 years, women of childbearing age, and pregnant women are particularly at risk.
A low serum f2242itin is diagnostic of iron depletion.
Microcytic anemia with increased RBC distribution (RDW) favors the diagnosis of iron deficiency anemia over anemia of chronic disease.
Most common cause of microcytic anemia.
More than 600 million people worldwide affected.
Cigar-shaped RBCs and elliptocytes characteristically present on blood smear.
Most common in women of childbearing age.
About one fourth of patients with iron deficiency anemia have restless leg syndrome and experience significant sleep related morbidity.
More common in developing countries.
The administration of iron to children with iron deficiency anemia can enhance motor and cognitive development.
Associated with pica, with ice eating (pagophagia) the most common, while clay and dirt eating also occur.
In severe cases atrophic glossitis may occur.
Associated with restless leg syndrome.
Oral absorption of non-heme iron requires stochastic acid.
Oral iron associated with gastric cramping, metallic taste, worsening constipation and poor adherence.
A meta-analysis of trials revealed gastrointestinal perturbation in more than 70% of patients on oral iron (Tolkien).
Gastritis, gastric bypass procedures and proton pump inhibitors decrease iron absorption.
Associated with celiac disease.
The total iron-binding capacity (TIBC) is increased.
The body contains 3-5 g of iron.
20-25 mg of iron is needed daily for production of red blood cells and cellular metabolism.
Dietary intake is limited 1-2 mg per day and other sources are needed for homeostasis including recycling of aging erythrocytes in macrophages, exchanges of iron in iron containing enzymes, and iron stores.
About 1-2 mg of iron is lost daily from the skin desquamation, menstrual bleeding, sweating, and urinary excretion.
Dietary iron is available in two forms: heme and nonheme iron.
Oral iron supplementation is the first line of treatment for iron deficiency anemia: many do not receive repletion or may not tolerate the G.I. side effects.
Oral iron therapy is associated with poor adherence and compliance, malabsorption with food, concomitant medications for chronic inflammatory conditions that may prevent iron absorption and repletion.
Intravenous iron in patients with congestive heart failure and iron deficiency anemia improved the Minnesota Living with Heart Failure score, decreased level of CRP, BNP, and increased left ventricular ejection fraction and the distance on a 6 minute walk-test (Toblli JE).
IV iron administration has practical advantages over oral iron supplementation.
Absorption and utilization of IV iron is complete, while absorption of oral iron is fractional at best, and at worst compromised by chelation of iron salts by intraluminal di-and trivalent cations, including calcium, by medications, which block gastric acid formation, and by of the medications, including quinolones and tetracyclines.
Intravenous iron administration avoids the adverse gastrointestinal symptoms associated with oral iron.
IV iron administration assures compliance, whereas noncompliance with oral iron may be as high as 32% within two months after the initiation of therapy.
Iron refractory iron deficiency anemia (IRIDA) is a genetic process with inappropriately high production of hepcidin, limiting iron absorption and utilization.