Iron deficiency

Severe iron deficiency in adult men and women is almost always caused by gastrointestinal bleeding.

One of the most common nutritional problems of humanity.

Iron deficiency can be described as absolute, when iron stores are too depleted to support red blood cell production or functional, when iron stores cannot be mobilized quickly enough to be used for RBC production despite being adequate in supply.

Absolute iron deficiency is defined as iron stores which are depleted as evidenced by a serum ferritin level of less than 100 ng/mL or transferin saturation that is less than 20%.

Approximately 3 billion people around the world have iron deficiency, and countless causes exist.

Associated with serious health problems including abnormal mental and motor development in infancy, impaired work capacity, increased risk of premature delivery and increased maternal and infant mortality when associated with severe anemia.

The prevalence of low iron levels including ferritin and transferrin saturation is seen among a variety of conditions including: chronic kidney disease, inflammatory bowel disease, chronic heart failure, abnormal uterine bleeding.

Nearly half of the patients with colorectal cancer are found to have iron deficiency anemia.

In patients with cancer iron deficiency causes immunologic dysfunction and genomic instability, ultimately changing the microenvironment, disturbing multicellular signaling pathways, and helping tumor angiogenesis.

Iron deficiency, among patients with malignancies.

Affects one in five women of childbearing age, and half for pregnant women due to increase demand on iron stores. 


Low levels of iron during pregnancy and early childhood is associated with mental and behavioral delays in children. 


Its development as a consequence of interaction of risk factors: increased host requirements, limited supply, and increased blood loss.

Perinatal iron deficiency associated with delayed neurocognitive development and psychiatric illness.

Even following iron repletion in infancy, cognitive abnormalities can persist at aged 10 years.

Increased requirements are a result of increased physiologic need and is designated physiological or nutritional.

Low body Iron stores are associated with low performance in cognitive executive function in undergraduate women.

Pathological iron deficiency is most often the result of gastrointestinal disease with abnormal blood loss or malabsorption.

Well known to cause thrombocytosis and rarely thrombocytopenia.

Manifestations relate to anemia of iron deficiency and to tissue deficiency of iron.

Associated with fatigue, decreased exercise capacity, neurocognitive alterations, pica, and restless leg syndrome.

Manifestations include: negative effects on work capacity, endurance, low birth weight, preterm delivery, effects motor and mental development in infants, children and teens.

Manifestations of anemia and lack of tissue iron often overlap.

Causes of iron deficiency include: Inadequate dietary intake-single food diets in infants, dieting, malnutrition, diets with inhibitors of iron asorption. Increaed iron requirements-growth spurts, menstruation, pregnancy, erythropoietin treatment.

There is inadequate iron delivered to the fetus if the mother is severely iron deficient, and infants who were born iron deficient have a significant increase in cognitive and behavioral abnormalities.

Increased iron losses-menorrhagia, gastrointestinal bleeding, genitourinary bleeding, hemosiderinuria die to intravascular hemolysis, parasitic infections, exercise related and blood donation, decreased iron absorption-celiac disease, autoimmune atrophic gastritis, helicobacter pylori gastritis, hereditary and chronic inflammation.

In many cases multiple causative factors interact to produce iron deficiency.

If infants who do not receive iron fortified nutrition are at high risk of developing iron deficiency anemia.

Growth spurt in adolescence results in increased iron requirement related to increase in lean body mass, expanded blood volume and onset of menstruation in females.

Growth spurt blood volume increase adds to the daily iron requirements for iron by additional amounts of 0.18 mg per day in males and 0.14 mg in females.

Increased lean body mass in adolescence associated with requirements of additional 0.33 mg of iron per day in females and 0.55 mg per day in males.

Menstruation requires an additional daily iron requirement of 0.56 mg per day, with a range of 0.17-1.08 mg per day.

In pregnant patients in the third trimester who is hemoglobin is less than 10 g/dL in the second trimester should receive IV iron to ensure enough iron gets to the fetus.

Diagnostic efforts to identify pathologies depends on the likelihood of encountering such pathology: patients with low-risk disease such as the majority of fertile women, detailed anatomical studies are rarely necessary.

Hepcidin is a peptide hormone that plays in important role in the pathophysiology of iron deficiency anemia as it is regulated by circulating and stored iron to manage further iron absorption and storage.

In men and postmenopausal women the risk of underlying gastrointestinal disease is high and gastrointestinal workup is mandatory.

Endoscopic and radiographic testing to identify the source of gastrointestinal blood loss is not successful in a substantial number of patients even with capsule endoscopy.

Iron deficiency, with or without anemia, decreases aerobic performance and is accompanied by fatigue and exercise intolerance (Haas JD).

Chronic iron deficiency may impair exercise capacity by altering myocytes (Brownlie YY). ab

Patients with heart failure may be prone to iron deficiency secondary to depletion of iron stores or defective iron absorption and decreased availability of iron recycled by the reticuloendothelial system (Opasich C, Nanas JN).

Adding iron to patients with congestive heart failure and iron deficiency may help improve function, even in the absence of anemia.

Oral iron is the initial preferred treatment, but failure to respond to such therapy occurs in a significant proportion of patients regardless of risk category.

Approximately 70% of people who receive oral iron therapy report significant G.I. perturbation which markedly decreases adherence.

Administering oral iron every other day is associated with increased absorption compared with daily or twice daily dosing.

Refractory iron deficiency is defined his failure to respond to treatment at a dose of at least 100 mg of elemental iron per day after 4-6 weeks of therapy.

Refractory iron deficiency to oral iron can be related to celiac disease without other manifestations of malabsorption syndrome.

Helicobacter pylori may be related to refractory iron deficiency anemia to oral iron therapy and a favorable response to its eradication.

Autoimmune atrophic gastritis, is associated with chronic idiopathic iron deficiency and is responsible for refractory iron deficiency anemia in over 20% of patients with no evidence of gastrointestinal blood loss.

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).

FERRIC-HF (Ferric Iron Sucrose in Heart Failure) trial of 35 patients with iron deficiency and CHF improved global assessment score and peak oxygen uptake increased significantly in patients with anemia (Okonko DO).

Ferinject Assessment in Patients with Iron Deficiency and Chronic Heart Failure (FAIR-HF)used intravenous ferric carboxymaltose and found that in such patients, with or without anemia, symptoms are improved, functional capacity increased and quality of life improved (SD Anker).

Iron repletion improves cognition, and exercise performance (Davies KJ).

Prevalence of iron deficiency ranges from 5-21% and may be related to malabsorption, long-term aspirin, and uremic gastritis (Anand IS).

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