Download understanding iron deficiency and anemia

Nutrition 411
Understanding Iron Deficiency and Anemia
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Functions of Iron
Although regarded as a trace element (the human
body requires only small amounts), iron is considered
an essential element because there are serious consequences when it is deficient. Iron has numerous functions in the body; it serves as a cofactor for dozens of
enzymes involved in diverse bodily processes such as ATP
production, DNA synthesis, and amino acid metabolism.
Most importantly, it functions as a component of hemecontaining proteins, such as hemoglobin and myoglobin.
Iron is required for the synthesis of the heme, which occurs within the erythropoietic cells in the bone marrow.
Iron is delivered to these cells by the iron-binding transport protein transferrin. Because there are approximately
25 trillion red blood cells in the body, and each red blood
cell contains millions of hemoglobin molecules, each
with four heme groups apiece, the synthesis of heme accounts for the largest use of iron in the body. Hemoglobin
binds oxygen within red blood cells for transport from
the lungs to body tissues. The atom of iron at the center of the heme molecules in hemoglobin binds to oxygen loosely for easy transfer to bodily tissues. Myoglobin
has a structure similar to hemoglobin — it consists of
an iron-containing heme group — but it is found in the
cytosol of muscle cells instead of in red blood cells. Its
function is to facilitate the diffusion of oxygen from the
hemoglobin in red blood cells into muscle cells, where it
then is used for aerobic metabolism. 1
occurs as a result of either acute blood loss from injury
or from chronic blood loss, such as seen in gastrointestinal bleeding. This leads to a substantial reduction in the
number of red blood cells and impaired oxygen delivery. Hemolytic anemia refers to the destruction of red blood
cells, which can occur as a result of genetic abnormalities
in red blood cell membranes or from repeated damage to
blood capillaries, sometimes seen in long-distance runners.
Deficiencies in nutrients other than iron can also cause
anemia by affecting the size or composition of red blood
cells. Deficiencies in vitamin B12 or folic acid, both of
which function in DNA synthesis and cell division, can
cause megaloblastic macrocytic anemia, in which normally
anucleated red blood cells differentiate incorrectly within
the bone marrow and develop into abnormally large, nucleated red blood cells.1 These deformed red blood cells
then function poorly and diminish the blood’s oxygen-carrying capacity. Iron-deficiency anemia results in microcytic
and hypochromic red blood cells, because iron gives red
blood cells their red color.3 Iron-deficiency anemia is the
most common nutritional anemia and affects many different groups; groups most at risk are children under the
age of 2, menstruating women, pregnant women, and frail
elderly persons, particularly those with chronic wounds.3
Iron-deficiency anemia has many causes, including inadequate iron intake in the diet (vegetarians, vegans), poor
absorption of iron in the gastrointestinal tract (celiac disease, drug interference), and increased need for iron in the
body (infancy, pregnancy). Clinical signs and symptoms
of anemia are listed in Table 1. It is important to note that
in mild cases of anemia, no symptoms may be present.
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atients with wounds frequently have low levels of
hemoglobin and hematocrit, and clinicians often
automatically think “iron deficiency.” Although in many
cases that diagnosis may be correct, identifying a specific
type of anemia takes a bit more investigation, including
a nutrition-focused physical examination and additional
biochemical data. This article reviews the basics about
iron deficiency and anemia.
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Nancy Collins, PhD, RD, LD/N, FAPWCA; and Allison Schnitzer, dietetics student
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Anemia: Types, Causes, and Stages
Anemia is defined as a deficiency in the size or number of red blood cells or in the amount of hemoglobin
they contain, the consequence of which is an inadequate
supply of oxygen to body tissues. 2 Not all forms of anemia result from an iron deficiency. Hemorrhagic anemia
Assessing Iron Status
Iron-deficiency anemia develops in progressive biochemical stages (see Table 2), with a drop in serum iron
levels occurring late in the progression. Additionally, serum iron levels change significantly throughout the day,
even in healthy individuals; therefore, assessing only serum iron levels is not an accurate way to determine iron
status. Hematocrit (packed red blood cell volume) and
hemoglobin are usually used together to evaluate iron
status, but this method is not sufficient for diagnosing
iron-deficiency anemia because low values are seen in all
types of anemia, not just iron-deficiency anemia.
Nancy Collins, PhD, RD, LD/N, FAPWCA, is founder and executive director of Nutrition411.com and Wounds411.com. For the past 20 years, she has served
as a consultant to healthcare institutions and as a medico-legal expert to law firms involved in healthcare litigation. Allison Schnitzer is a dietetics student at the
University of Nevada, Las Vegas and will soon be entering her internship.This article was not subject to the Ostomy Wound Management peer-review process.
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Table 2. Stages of iron deficiency2
• Fatigue
Stage I: Early negative iron balance
• Lethargy
• Decreased iron stores
• Cheilosis (dry scaling and fissuring of the lips)
• Decreased plasma ferritin (<25 mcg/L)
• Glossitis (inflammation of the tongue)
Stage II: Iron depletion
• Pallor
• Further decrease in iron stores
• Pale sclera
• Decreased plasma ferritin (20 mcg/L)
• Spoon-shaped fingernails
• Increased transferrin (>360 mcg/100mL)
• Clubbing of joints in the digits
Stage III: Iron-deficient erythropoiesis
• Cold extremities
• Depleted iron stores
• Muscle aches
• Decreased plasma ferritin (10 mcg/L)
• Difficulty concentrating
• Increased transferrin (>390 mcg/100mL)
• Sleepiness
• Decreased serum iron (<60 mcg/100mL)
• Irritability
• Decreased transferrin saturation percentage (<15%)
• General malaise
Stage IV: Iron-deficiency anemia
• Pica (unusual food cravings)
• Depleted iron stores
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Table 1. Clinical signs and symptoms of anemia5
• Decreased appetite
• Decreased plasma ferritin (<10 mcg/L)
• Headache – frontal
• Increased transferrin (>410 mcg/100mL)
• Gastrointestinal distress
(nausea, vomiting, diarrhea, cramping)
• Decreased serum iron (<40 mcg/100mL)
• Decreased transferrin saturation percentage (<15%)
• Microcytic, hypochromic erythrocytes
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• Reproductive dysfunction (amenorrhea, loss of libido)
• Cardiovascular dysfunction
(palpitation, tachycardia, dyspnea, angina)
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• Paresthesias (tingling or numbness in the extremities)
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Ferritin is the storage protein that sequesters iron in
the liver, spleen, and bone marrow. As iron supply increases, so does the amount of ferritin. A small amount
escapes into the bloodstream, and this amount can be
measured and used to estimate the amount of stored
iron. Ultimately, plasma ferritin is the most sensitive indicator of iron deficiency, because plasma ferritin levels
drop early in negative iron balance.2
Another biochemical marker of iron status is transferrin, a protein that transports iron to the bone marrow for
hemoglobin production. When iron stores are low, transferrin synthesis increases in an attempt to capture more
iron. Total iron-binding capacity also increases for this
same reason. Conversely, transferrin saturation percentage decreases with limited available iron. High transferrin
and total iron-binding capacity levels and low transferrin
saturation percentages are seen in iron-deficiency anemia.
Another factor to consider in diagnosing iron-deficiency anemia is the size of red blood cells, because they
are microcytic in iron-deficiency anemia. Mean corpuscular volume (MCV) is the biochemical marker used to
determine the average size of red blood cells; it is lowered in iron-deficiency anemia. Also lowered in irondeficiency anemia are mean corpuscular hemoglobin
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(MCH, the average weight of hemoglobin per red blood
cell) and mean corpuscular hemoglobin concentration
(MHCH, the average concentration of hemoglobin in the
red blood cells).2 Because clinical symptoms of iron-deficiency anemia do not usually present until later stages of
development, it is important to use biochemical markers
such as serum ferritin to identify and correct deficiencies
before they cause serious symptoms.
Treatment for Iron-Deficiency Anemia
Recommendations for iron are provided in the Dietary Reference Intakes (DRIs) developed by the Institute
of Medicine of the National Academy of Sciences. 4 Table
3 outlines the recommendations for various age groups.
The first step in the treatment of iron-deficiency anemia is to identify and correct its cause. A common cause
of iron-deficiency anemia is the lack of iron-rich foods in
the diet. Iron in food is found in one of two forms: heme
iron and nonheme iron. Heme iron in food is derived
directly from the hemoglobin and myoglobin of animals;
therefore, it is found only in animal products. Good
sources of heme iron include red meat, liver, egg yolks,
oysters, clams, and the dark meat of chicken. 5 Because
it is a soluble compound, heme iron is readily absorbed
across the brush border of the small intestine.1 Nonheme
iron is commonly found in its oxidized, or ferric (Fe3+)
form in food. Stomach acid reduces some of the ferric
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Table 3. Recommended dietary allowances for iron
for infants (7 to 12 months), children, and adults4
Table 4. Drug recommendations/interactions with
iron supplements5
Age
• Iron supplements should be taken 2 hours before or
after other medications
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N/A
N/A
1 to 3
years
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7
N/A
N/A
4 to 8
years
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10
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N/A
9 to 13
years
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8
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N/A
14 to 18
years
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15
27
10
19 to 50
years
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18
27
9
51+ years
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N/A
N/A
• Iron supplements can inhibit the effectiveness of
thyroid medications, antibiotics (tetracycline,
penicillamine, ciprofloxacin), some antidepressants,
and the anti-Parkinson’s drugs methyldopa, levodopa,
and carbidopa
• Antacids can reduce iron absorption
Practice Points
Proper diagnosis and timely correction of iron-deficiency anemia is important for all patients with chronic
wounds. The diagnosis of iron-deficiency anemia requires both biochemical data and a nutrition-focused
physical examination to look for clinical symptoms. Biochemical values should be looked at as a whole to determine the extent of the anemia. Serum ferritin is the first
biochemical value to decrease in negative iron balance.
Note that when anemia is mild, there may be no overt
physical symptoms. In addition, not all cases of anemia
are caused by lack of iron in the diet. Clinicians should
assess for deficiencies in folic acid or B12, as well as for
chronic bleeding or absorption issues. Ascorbic acid and
heme iron enhance the absorption of nonheme iron.
Food sources of nonheme iron should be consumed with
foods rich in vitamin C or with meat products in order
to increase their biological value. In practical terms, this
might mean serving a glass of orange juice with dinner.
Many medications have interactions with iron supplements, so it is important to educate the patient to take
iron supplements 2 hours before or after other medications. Iron supplements often can cause gastrointestinal
distress, so patients should try several brands and forms
(eg, pills, liquid) to find the one that agrees with them.
Often, patients with chronic wounds have other nutritional challenges as well such as unintended weight loss,
increased blood glucose levels, or a host of other concerns. Keying into nutrition and consulting a registered
dietitian (RD) when necessary is essential for healing. n
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iron to ferrous iron (Fe2+), but the ferric iron absorbed
frequently complexes into ferric hydroxide, an insoluble
compound that aggregates and precipitates, making the
iron less available in the body. 1 Certain dietary factors
enhance the absorption of nonheme iron. Sugars, especially fructose and sorbitol, certain acids, such as ascorbic and citric acid, and meat products containing heme
iron all aid in the absorption of nonheme iron. Good
sources of nonheme iron, such as spinach, kidney beans,
dried fruits, and enriched cereals, should be consumed
with foods rich in vitamin C or with meat products in
order to increase their biological value.5 Unfortunately,
several substances inhibit the absorption of nonheme
iron. Polyphenols such as those found in tea and coffee;
oxalic acid found in spinach, chard, chocolate, and berries; phytic acid found in whole grains and legumes; and
divalent cations, such as calcium found in dairy foods,
all complex with nonheme iron and make it less absorbable. Persons who follow strict vegan diets often are at
risk for iron-deficiency anemia because of the low bioavailability of iron from plant foods. Once a person is
diagnosed with iron-deficiency anemia, iron supplementation usually is the prescribed course of action. Ferrous
salts (Feosol, Media Consumer Healthcare, Marietta, GA;
Fer-In-Sol, Mead Johnson, Glenview, IL; mol-iron) or
tablets (Feostat, Forest Pharmaceuticals, St. Louis, MO;
Fergon, Bayer Consumer Care Products, Morristown,
NJ) improve absorption with fewer side effects than ferrous sulfate pills.5 Several drug interactions inhibit iron
absorption or render medication ineffective when taken
with an iron supplement (see Table 4). It usually takes 4
to 30 days to see improvements after initiation of iron
therapy, and iron stores are usually replaced after 1 to 3
months of treatment.5
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7 to 12
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Males
Females Pregnancy Lactation
(mg/day) (mg/day) (mg/day) (mg/day)
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References
1. Gropper S, Smith J. Advanced Nutrition and Human Metabolism, 6th
ed. Belmont, CA: Cengage Learning;2013.
2. Mahan LK, Escott-Stump S, Raymond J. Krause’s Food & the Nutrition Care Process, 13 ed. St. Louis, MO: WB Saunders Co;2012.
3. Nelms M, Sucher KP, Lacey K, Roth SL. Nutrition Therapy and Pathophysiology, 2nd ed. Belmont, CA: Brooks/Cole Cengage Learning;2011.
4. Institute of Medicine. Food and Nutrition Board. Dietary Reference
Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper,
Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium and
Zinc. Washington, DC: National Academy Press;2001.
5. Escott-Stump S. Nutrition and Diagnosis-Related Care. Baltimore,
MD: Lippincott Williams & Wilkins;2012.
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