Iron-deficiency anemia
also see Anemia, General Approach

Iron in the body:

• 65% in hemoglobin (in the red blood cells)
• 30% stored as ferritin in the liver, bone marrow, and spleen.
• 4% in myoglobin (in skeletal muscle)
• A small percentage is in transport, as part of transferrin, traveling between various parts of the body via the blood stream.

Labs

• iron deficiency usually does not cause a microcytic anemia until the hematocrit drops below 30%. 
• Ferritin is useful for diagnosing iron deficiency. Since ferritin is an acute phase reactant, some say it should not be used in the setting of inflammation; others say that in chronic inflammation a ferritin < 50 is highly suggestive of iron deficiency. 
• Mentzer Index
• RDW (reflecting anisocytosis) is high.
• Serum iron, transferrin and TIBC
  • A serum iron test actually measures the amount of iron in transferrin.
  • Each transferrin molecule can carry 2 iron atoms, and normally, about 30% of the available "spaces" for iron are filled. By artificially filling up all the available spaces, doctors can measure the total iron binding capacity, or TIBC, of your blood.  Think of transferrin as a gang of motorcycles. TIBC relates to the number of empty seats in the motorcycle gang. TIBC is usually higher-than-normal when the body's iron stores are low; there are empty motorcycles, because there are fewer potential passengers in the neighbourhood.
  • Normal Values: iron: 60-170 mcg/dl, TIBC: 240-450 mcg/dl, transferrin saturation: 20-50%
  • Higher-than-normal TIBC may indicate: iron deficiency anemia, pregnancy (late)
  • Lower-than-normal TIBC may indicate: cirrhosis, hemolytic anemia, hypoproteinemia, pernicious anemia, sickle cell anemia, inflammation, malnutrition, liver disease

Iron deficiency: signs and symptoms: decreased work capacity, growth retardation, increased susceptibility to infection, irritability, stomatitis, glossitis, cheilitis, disaccharidase deficiency, increased lead absorption, craving for ice (pagophagia), lower IQ scores/decreased scholastic performance

Iron-Deficiency anemia associated with excessive milk intake

There are 5 reasons that increased milk ingestion causes iron deficiency:

1. When children ingest large amounts of milk, they do so at the expense of other iron-rich foods.  Therefore, iron intake is inadequate.
2. Milk irritates the GI lining, leading to small microhemorrhages. Therefore, GI blood loss.
3. These factors decrease iron absorption:
   • Calcium
   • fat in milk
   • milk neutralizes stomach acid. Increased pH inhibits Fe absorption to some degree.

Treatment consists of limiting milk ingestion to 16-20 oz of milk/day and supplementing with Fe 6 mg/kg/day.  Recheck hemoglobin in 1 month. If it's pure iron deficiency anemia, the hemoglobin should be back up to normal, and then continue the Fe therapy for 4-6 more months.  If the hemoglobin is still low, you need to check a full CBC, looking for other causes of a microcytic anemia, such as thalassemia.

Therapy

• Ferrous iron 4-6 mg/kg /day div bid/tid. Also see Iron Toxicity
• Give on empty stomach, with Vit-C containing juice to increase absorption (lower pH aids absorption)
• Transfuse only if cardiovascular compromise (rare)
• Parental iron dextran only for severe non-compliance, malabsorption, or if ongoing loss exceeds absorption capacity
• Iron Containing Foods: meats, fish, poultry. Also raisins, dried fruit, sweet potatoes, lima beans, chili beans, green peas, peanut butter, and enriched foods

Follow-up

• Retic count should double in 1-2 weeks
• Hb should rise 1 g/dl in 2-4 weeks
• Check CBC and retic count at 2 weeks to assess response
• continue iron for 3 mos to replete body stores
   

Neonatal iron deficiency is very uncommon because iron transport across the placenta is programmed to support the fetus, even in the face of maternal iron deficiency. As neonatal erythropoiesis declines markedly in the first 6 to 8 weeks after birth, iron from red blood cell breakdown is salvaged by the reticuloendothelial system, augmenting neonatal iron stores. As the infant emerges from the physiologic nadir and active erythropoiesis resumes, adequate iron stores must be present to support this process. In term infants, iron stores rarely are depleted before 4 months of age, and iron deficiency anemia is unlikely to occur if iron-fortified cereal or other solid foods are introduced by 6 months of age. In preterm infants, total body iron is less at birth than in term infants, and neonatal iron stores are depleted more rapidly. Iron deficiency can, therefore, develop by 2 to 3 months of age in preterm infants who are either breastfed or bottle-fed with a formula that is not iron-supplemented. It is generally recommended that preterm infants begin iron supplementation at 1 month of age, either as iron-fortified formula or as iron supplementation in breastfed infants. (PREP 2004)