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ANEMIA

Edited by
Liniyanti D.Oswari, MD., MSc.
Anemia affects more than 30 percent of the world's population, and it is one of the most
important worldwide health problems. It has a significant prevalence in both developing
and industrialized nations. Causes of anemia include nutritional deficiencies,
particularly of iron, vitamin B12, and folate (folic acid); excess blood loss from
menstruation or chronic illness and infection; ingestion of toxic substances, such as lead,
ethanol, and other compounds; and genetic abnormalities such as thalassemia and
sideroblastosis.
Anemia is caused by a deficiency in the intake and absorption elements required to make
red blood cells. The condition is defined as one in which the blood is deficient in red
blood cells, in hemoglobin, or in total volume. This results in blood that is incapable of
meeting the oxygen needs of the body's tissues. Anemia is characterized by changes in
the size and color of red blood cells. Red blood cells, or erythrocytes, are primarily
responsible for oxygen transport from the lungs to the body's many cells. Hemoglobin is
an oxygen-carrying protein in the red blood cell that incorporates iron into its structure.
Therefore, iron is an essential building block of blood erythrocytes. When red blood cells
are larger than normal, the anemia is termed macrocytic, and when they are smaller than
normal, it is called microcytic. Normal red cell color is termed normochromic, and if the
red cells appear pale, the anemia is called hypochromic. When extensive lab testing is not
available for diagnosis, the use of a portable colorimeter can be used to detect anemia.

Iron-Deficiency Anemia
Anemia in the developing world is most commonly caused by an iron deficiency, which
affects up to 50 percent of the population in some countries. Iron deficiency not only
impairs the production of red cells in the blood, but also affects general cell growth and
proliferation in tissues like the nervous system and the gastrointestinal tract. Red cells
in a patient with iron-deficiency anemia are both microcytic and hypochromic.
Iron deficiency affects young children, adolescents, and women of reproductive age
three periods of rapid growth during which the body's iron needs are higher than normal.
In children, iron requirements are highest between the ages of six and eighteen months,
and can be ten times the requirement of a normal adult. Iron is commonly absorbed from
both human milk and cow's milk, and, if consumed in good quantities, these sources can
meet the body's iron needs. A deficiency can result from inadequate intake, or it can occur
if milk remains the sole source of a child's nutrition after the age of four months, when
iron needs exceed that provided by milk alone. Research in Chile has shown that 40
percent of children whose main source of nutrition was breast milk developed irondeficiency anemia. Such children can appear tired and inattentive, and they can suffer
from delayed motor development. Some children can even develop mild to moderate
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mental retardation as a result of iron-deficiency anemia. Recent research has shown that
iron-deficiency anemia can also contribute to emotional development problems, with
malnourished children acting more irritable and fussy.

TYPES AND CAUSES OF ANEMIA


Type
Lab values
Causes
Macrocytic,
normochromic

MCV: > 100fl Vitamin B12 deficiency, folate deficiency, vitamin C


MCHC: 34
deficiency, chemotherapy (megaloblastic marrow);
aplastic anemia, hypothyroidism (normoblastic
marrow)

Microcytic,
hypochromic

MCV: < 80
Iron deficiency, thalassemia, sideroblastic anemia,
MCHC: < 30 chronic lead poisoning, anemia of chronic illness

Normocytic,
normochromic

MCV: 8099fl Iron deficiency (early), chronic disease


MCHC: 34 + /
-2

MCV: mean corpuscular volume


MCHS: mean corpuscular hemoglobin concentration
fl: femtoliter (one quadrillionth of a liter)
Pregnant women can have up to double the requirement of iron for a normal adult, with
the majority of the mother's iron being transferred to her growing fetus. Adult diets in
most of the developing world tend to be iron-poor, and a low dietary intake can result in
iron deficiency. Deficiency can also occur as a result of poor iron absorption due to
gastrointestinal pathology, blood loss due to normal menstruation, blood loss from
parasitic infections such as hookworm and malaria, and blood loss from chronic
diarrheaall of which are common in developing countries.

Other Causes
The two other primary causes of nutritional anemia are deficiencies in vitamin B12 and
folic acid, both of which are necessary for the production of DNA, RNA, and protein.
Without these necessary factors, red blood cells can develop abnormally, or even die

prematurely in the bone marrow where they are made. This leads to what is known as
megaloblastic anemia.
Folate deficiency is most often caused by poor intestinal absorption or low intake of
folate-rich foods, such as human milk, cow's milk, fruits, green vegetables, and certain
meats. It is also caused by congenital defects in intestinal absorption. Just as with iron,
folic acid requirements are highest during periods of rapid growth, particularly infancy
and pregnancy. Folate-deficient children present with common symptoms of anemia, as
well as chronic diarrhea. Folate deficiency can also occur with kwashiorkor or
marasmus. If it occurs during pregnancy, folate deficiency can lead to neural tube
defects, spontaneous abortions, and prematurity.
Vitamin B12, derived from a substance called cobalamin, is mainly found in meats and
other animal productshumans cannot synthesize this vitamin on their own. A good
amount of its absorption depends on the presence of a substance called intrinsic factor
(see sidebar). It does not normally occur with kwashiorkor or marasmus. Both folate and
vitamin B12 deficiencies have also been linked to cardiovascular disease, mood
disorders, and increased frequency of chromosomal breaks (which may contribute to the
development of cancer).

Pernicious Anemia
Pernicious anemia is a common cause of cobalamin/vitamin B12 deficiency. It is primarily
a disease of the elderly and caused by an abnormality in the immune system where the
body creates antibodies to intrinsic factor (a substance that facilitates absorption of
vitamin B12) or to the cells in the stomach that secrete it. The lack of intrinsic factor B12
leads to vitamin B12 deficiency. It can also be caused by physiologic or anatomic
disturbances of the stomach that might prevent intrinsic factor secretion. In children, an
atypical and rare form of pernicious anemia can be inherited. It is an autosomal recessive
disorder that results in an inability to secrete intrinsic factor, and it presents with
anorexia, weakness, a painful red tongue, and neurologic abnormalities.

Treatment
Each of the important causes of nutritional anemia can be eradicated through prevention
and treatment. Many countries have begun this process by instituting food
supplementation programs in which grains and cereals are fortified with iron, folate, or
vitamin B12. Given adequate resources, these deficiencies can also be ameliorated with
direct oral supplements of absorbable iron, vitamin B12, and folic acid. Injectable forms of
iron are also available. It has been found that the supplementation of vitamin A to at-risk
populations improves anemia more efficiently than iron supplementation alone.
Treatment plans must also focus on the causes of anemia and therefore must include
sanitation, treatment of infections such as malaria and HIV, and, most important,
treatment of intestinal parasites. Much work is needed to address general malnutrition

not only concerning these deficiencies, but also other commonly occurring ones (e.g.,
vitamin A, zinc, copper, calcium). Programs dedicated to decreasing the rates of
infection and illness in developing countriesthrough health education, immunization,
sanitation, and appropriate treatmentwill also contribute to a lower incidence and
prevalence of worldwide anemia.

Bibliography
Behrman, Robert E.; Kliegman, Robert M.; and Jenson, Hal B., eds. (2000). Nelson
Textbook of Pediatrics, 16th edition. Philadelphia, PA: W. B. Saunders.
Hoffbrand, A. V., and Herbert, V. (1999). "Nutritional Anemias." Seminars in
Hematology 36(4).
Isselbacher, Kurt J. (1994). Harrison's Textbook of Internal Medicine, 13th edition. New
York: McGraw-Hill.
Pollitt, E. (2000). "Developmental Sequela from Early Nutritional Deficiencies:
Conclusive and Probability Judgments." Journal of Nutrition 130.
Ramakrishnan, U., ed. (2001). Nutritional Anemias. Boca Raton, FL: CRC Press.
Rhoades, R. A., and Tanner, G. A. (1995). Medical Physiology. Boston: Little Brown.
Yip, R., and Ramakrishnan, U. (2002). "Experiences and Challenges in Developing
Countries." Journal of Nutrition 132.

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