Iron deficiency is a common worldwide cause of anemia affecting persons of all ages. The anemia results from dietary deficiency, loss of iron through bleeding, or increased demands. Because iron is a component of haem, a deficiency lead to decreased hemoglobin synthesis and consequent impairment of oxygen delivery.
Body iron is used repeatedly. When red cells become senescent and are broken down, their iron is released and reused in the production of new red cells. Despite this efficiency, small amounts of iron are lost in the feces and need to be replaced by dietary uptake.
Iron balance is maintained by the absorption of 0.5 to 1.5 mg. daily to replace the 1mg lost in the feces. The average Western diet supplies about 20 mg. The absorbed iron is more than sufficient to supply the needs of most individuals, but may be barely adequate in toddlers, adolescents, and women of child bearing age.
The usual reason for iron deficiency in adults in the Western world is chronic blood loss because iron cannot be recycled to the pool. In men and postmenopausal women, blood loss may occur from gastrointestinal bleeding because of peptic ulcer, intestinal polyps, hemorrhoids, or cancer. Excessive aspirin intake may cause undetected gastrointestinal bleeding. In women, menstruation may account for an average of 1.5 mg of iron lost per day, causing a deficiency. Although cessation of menstruation removes a major source of iron loss in the pregnant woman, iron requirements increase at this time, and deficiency is common. The expansion of the mother’s blood volume requires approximately 500 mg of additional iron, and the growing fetus requires approximately 360 mg during pregnancy. In the postnatal period, lactation requires approximately 1 mg of iron daily.
A child’s growth places extra demands on the body. Blood volume increase, with a greater need for iron. Iron requirements are proportionally higher in infancy (3to 24months) that at any other age, although they are also increased in childhood and adolescence. In infancy, the two main causes of iron deficiency anemia are low iron levels at birth because of maternal deficiency and a diet consisting mainly of cow’s milk, which is low in absorbable iron. Adolescents are also susceptible to iron deficiency because of high requirements due to growth spurts, dietary deficiencies, and menstrual loss.
Iron deficiency anemia is characterized by low hemoglobin and hematocrit, decreased iron stores, and low serum iron and ferritin levels. The red cells are decreased in number and are microcytic and hypochromic. Poikilocytosis (irregular shape) and anisocytosis (irregular size) are also present. Laboratory values indicate reduced. MCHC and MCV. Membrane changes may predispose to hemolysis, causing further loss of red cells.
The manifestations of iron deficiency anemia are related to impaired oxygen transport and lack of hemoglobin. Depending on the severity of the anemia, pallor, easy fatigability, dyspnea, and tachycardia may occur. Epithelial atrophy is common and results in waxy pallor, brittle hair and nails, sometimes a spoon shaped deformity of the fingernails, smooth tongue, sores in the corners of the mouth, and sometimes dysphagia and decreased acid secretion.
A poorly understood symptom occasionally seen is pica, the bizarre, compulsive eating of ice, dirt, or other abnormal substances. Iron deficiency in infants may also result in long term manifestation such as poor cognitive, motor, and emotional functions that may be related to effects on brain development or neurotransmitter function.
Prevention of iron deficiency is a primary concern in infants and children. Avoidance of cow’s milk, iron supplementation at 4 to 6 months of age in breast fed infants, and use of iron fortified formulas and cereals are recommended for infants younger that 1 year of age. In the second year, a diet rich in iron containing foods and use of iron fortified vitamins will help prevent iron deficiency. The treatment of iron deficiency anemia in children and adults is directed towards controlling chronic blood loss, increasing dietary intake of iron, and administering supplemental iron. Ferrous sulfate, which is usual oral replacement therapy, replenishes iron stores in several months. Parental iron therapy may be used when oral forms are not tolerated or are ineffective. Caution is required because of the possibility of severe hypersensitivity reactions.
Individuals at increased Risk of Iron Deficiency
Infants and Children between the Ages of 6 Months and 4 Years: – A full term infant’s iron stores are usually sufficient to last for 6 months. High iron requirements are due to the rapid growth rates sustained during this period.
Adolescents: – Early adolescence is another period of rapid growth. In females, the blood loss that occurs with menstruation adds to the increased iron requirement of adolescence.
Pregnant Women: – Increased iron utilization by the developing fetus and placenta as well as blood volume expansion significantly increase the iron requirement during pregnancy.
Individuals with Chronic Blood Loss: – Chronic bleeding or acute blood loss may result in iron deficiency. One milliliter of blood with a hemoglobin concentration of 150g/L contains 0.5 mg of iron. Thus, chronic loss of very small amounts of blood may result in iron deficiency. A common cause of chronic blood loss and iron deficiency in developing countries is intestinal parasitic infection. Individuals who donate blood frequently, especially menstruating women, may need to increase their iron intake to prevent deficiency because each 500 ml of blood donated contains between 200 and 250 mg of iron.
Individuals with Helicobacter pylori infection: – H. pylori infection is associated with iron deficiency anemia, especially in children, even in the absence of gastrointestinal bleeding.
Vegetarians:- Because iron from plant sources is less efficiency absorbed than that form animal sources, the U.S. Food and Nutrition Board (FNB) has estimated that the bio-availability of iron from a vegetarian diet is only 10%, and it is 18% from a mixed diet. Therefore, the recommended dietary allowance (RDA) for iron from a completely vegetarian diet should be adjusted as follow: 14 mg/d for adult men and postmenopausal women, 33 mg/d for premenopausal women, and 26 mg/d adolescent girls.
Individuals, Who Engage in Regular, Intense Exercise: – Daily iron losses have been found to be greater in athletes involved in intense endurance training. This may be due to increased microscopic bleeding from the gastrointestinal tract or increased fragility and hemolysis of red blood cells. The FNB estimates that the average requirement for iron may be 30% higher for those who engage in regular intense exercise.
Causes of iron deficiency anemia
- Gastrointestinal bleeding
- Angiodysplasia of the colon
- Hereditary, hemorrhagic, telangiectasia syndrome (Osler-Weber-Rendu syndrome)
- Peptic ulcer
- Non-steroidal, anti-inflammatory drugs
- Oral anticoagulation
- Hiatal hernia
- Meckel diverticulum
- Intestinal polyps
- Inflammatory bowel disease
- Hookworm: Necator americanus, ancylostoma duodenale
- Frequent, blood donations
- Erythrocyturia: bladder neoplasm
- Paroxysmal, nocturnal Hemoglobinuria
- Erythrocyte fragmental in prosthetic heart valves
- Factitious anemia
- Intravenous and intra arterial drug abuse
- Nosocomial blood loss due to frequent venisection
- Chronic, atrophic gastritis
- Gastric resection and bypass
- Intestinal bypass operations
- Celiac disease (non-tropical sprue)
- Tropical sprue
Increased iron requirements
- Pregnancy and lactation
Symptoms of Iron Deficiency
Most of the symptoms of iron deficiency are a result of the associated anemia and may include fatigue, rapid heart rate, palpitations, and rapid breathing on exertion. Iron deficiency impairs athletic performance and physical work capacity in several ways. In iron deficiency anemia, the reduced hemoglobin content of red blood cells results in decreased oxygen delivery to active tissues. Reduced myoglobin levels in muscle cells limit the amount of oxygen that can be delivered to mitochondria for oxidative metabolism. Iron depletion also reduces the oxidative capacity of muscle by reducing the mitochondrial content of cytochromes and other iron dependent enzymes required for electron transport and ATP synthesis. Lactic and production is also increased in iron deficiency.
The ability to maintain a normal body temperature on exposure to cold is also impaired in iron deficient individuals. Severe iron deficiency anemia may result in brittle and spoon shaped nails, sores at the corners of the mouth, taste bud atrophy, and sore tongue.
In some cases, advanced iron deficiency anemia may cause difficulty in swallowing due to the formation of webs of tissue in the throat and esophagus. The development of esophageal webs, also known as Plummer-Vinson syndrome, may require a genetic pre-disposition in addition to iron deficiency. Pica, a behavioral disturbance characterized by the consumption of nonfood items, may be a symptom and a cause of iron deficiency.
Laboratory Tests to Evaluate Iron Metabolism in Iron Deficiency Anemia
Various laboratory tests that measure iron stores, iron transport, and iron metabolism can be used as diagnostic tests in patients with suspected iron deficiency anemia. These include measurements of serum ferritin, serum iron binding capacity.
A very small amount of ferritin (about 100 micrograms per liter) is normally present in blood serum, and this amount is proportional to the total amount of ferritin stored in the body. Consequently, measurement of serum ferritin can be used to estimate total body iron stores. One can also measure the amount of iron being transported by transferring and can also determine the maximum amount of iron that can be carried when all of the iron binding sites on transferring are fully saturated with iron. When iron stores are normal, the concentration of iron in the serum is about 100 micrograms per 100 mL.