Anemia

For other uses, see Anemia (disambiguation). common in females than males[8] among children, dur-
ing pregnancy and in the elderly.[4] Anemia increases
costs of medical care and lowers a person’s productiv-
Anemia or anaemia (/əˈniːmiə/; also spelled anæmia) is [5]
usually defined as a decrease in amount of red blood cells ity through a decreased ability to work. The name is
derived from Ancient Greek: ἀναιμία anaimia, mean-
(RBCs) or the amount of hemoglobin in the blood.[1][2]
It can also be defined as a lowered ability of the blood ing “lack[9]of blood”, from ἀν- an-, “not” + αἷμα haima,
“blood”.
to carry oxygen.[3] When anemia comes on slowly the
symptoms are often vague and may include: feeling tired,
weakness, shortness of breath or a poor ability to exercise.
Anemia that comes on quickly often has greater symp- 1 Signs and symptoms
toms which may include: confusion, feeling like one is
going to pass out, and an increased desire to drink flu-
ids. There needs to be significant anemia before a person
becomes noticeably pale. There may be additional symp-
toms depending on the underlying cause.[4]
There are three main types of anemia, that due to blood
loss, that due to decreased red blood cell production, and
that due to increased red blood cell breakdown. Causes
of blood loss include trauma and gastrointestinal bleeding
among others. Causes of decreased production include
iron deficiency, a lack of vitamin B12, thalassemia and
a number of neoplasms of the bone marrow among oth-
ers. Causes of increased breakdown include a number
of genetic conditions such as sickle cell anemia, infec-
tions like malaria and some autoimmune diseases among
others. It can also be classified based on the size of red
blood cells and amount of hemoglobin in each cell. If the
cells are small it is microcytic anemia, if they are large
it is macrocytic anemia and if they are normal sized it
is normocytic anemia. Diagnosis in men is based on a Main symptoms that may appear in anemia[10]
hemoglobin of less than 130 to 140 g/L (13 to 14 g/dL)
while in women it must be less 120 to 130 g/L (12 to 13 Anemia goes undetected in many people, and symp-
g/dL).[4][5] Further testing is then required to determine toms can be minor or vague. The signs and symptoms
the cause.[4] can be related to the underlying cause or the anemia it-
self. Most commonly, people with anemia report feel-
Certain groups of individuals, such as pregnant women, ings of weakness, or fatigue, general malaise, and some-
benefit from the use of iron pills for prevention.[4][6] times poor concentration. They may also report dyspnea
Dietary supplementation, without determining the spe- (shortness of breath) on exertion. In very severe ane-
cific cause, is not recommended. The use of blood mia, the body may compensate for the lack of oxygen-
transfusions is typically based on a persons signs and carrying capability of the blood by increasing cardiac out-
symptoms.[4] In those without symptoms they are not put. The patient may have symptoms related to this, such
recommended unless hemoglobin levels are less than 60 as palpitations, angina (if pre-existing heart disease is
to 80 g/L (6 to 8 g/dL).[4][7] These recommendations present), intermittent claudication of the legs, and symp-
may also apply to some people with acute bleeding.[4] toms of heart failure. On examination, the signs exhibited
Erythropoiesis-stimulating medications are only recom- may include pallor (pale skin, lining mucosa, conjunctiva
mended in those with severe anemia.[7] and nail beds), but this is not a reliable sign. There may
Anemia is the most common disorder of the blood with be signs of specific causes of anemia, e.g., koilonychia
it affecting about a quarter of people globally.[4] Iron- (in iron deficiency), jaundice (when anemia results from
deficiency anemia affects nearly 1 billion.[8] It is more abnormal break down of red blood cells — in hemolytic
anemia), bone deformities (found in thalassemia major)

1
2 2
or leg ulcers (seen in sickle-cell disease). In severe ane-
mia, there may be signs of a hyperdynamic circulation:
tachycardia (a fast heart rate), bounding pulse, flow mur-
murs, and cardiac ventricular hypertrophy (enlargement).
There may be signs of heart failure. Pica, the consump-
tion of non-food items such as ice, but also paper, wax,
or grass, and even hair or dirt, may be a symptom of iron
deficiency, although it occurs often in those who have
normal levels of hemoglobin. Chronic anemia may result
in behavioral disturbances in children as a direct result
of impaired neurological development in infants, and re-
duced scholastic performance in children of school age.
Restless legs syndrome is more common in those with
iron-deficiency anemia
2 Causes
Broadly, causes of anemia may be classified as impaired
red blood cell (RBC) production, increased RBC destruc-
tion (hemolytic anemias), blood loss and fluid overload
(hypervolemia). Several of these may interplay to cause
anemia eventually. Indeed, the most common cause of
anemia is blood loss, but this usually does not cause any
lasting symptoms unless a relatively impaired RBC pro-
duction develops, in turn most commonly by iron defi-
ciency.[11] (See Iron deficiency anemia)
2.1 Impaired production
• Disturbance of proliferation and differentiation of
stem cells
--- Pure red cell aplasia[12]
[12]
--- Aplastic anemia affects all kinds of blood
cells. Fanconi anemia is a hereditary disorder
or defect featuring aplastic anemia and various
other abnormalities.
[12]
--- Anemia of renal failure by insufficient
erythropoietin production
--- Anemia of endocrine disorders
• Disturbance of proliferation and maturation of
erythroblasts
[12]
--- Pernicious anemia is a form of
megaloblastic anemia due to vitamin B12
deficiency dependent on impaired absorption
of vitamin B12 . Lack of dietary B12 causes
non-pernicious megaloblastic anemia
--- Anemia of folic acid deficiency,[12] as with vi-
tamin B12 , causes megaloblastic anemia
--- Anemia of prematurity, by diminished ery-
thropoietin response to declining hematocrit
levels, combined with blood loss from labo-
ratory testing, generally occurs in premature
infants at two to six weeks of age.
CAUSES
--- Iron deficiency anemia, resulting in deficient
heme synthesis[12]
--- Thalassemias, causing deficient globin
synthesis[12]
--- Congenital dyserythropoietic anemias, causing
ineffective erythropoiesis
--- Anemia of renal failure[12] (also causing stem
cell dysfunction)
• Other mechanisms of impaired RBC production
--- Myelophthisic anemia[12] or myelophthisis is a
severe type of anemia resulting from the re-
placement of bone marrow by other materials,
such as malignant tumors or granulomas.
--- Myelodysplastic syndrome[12]
--- anemia of chronic inflammation[12]
2.2 Increased destruction
Further information: Hemolytic anemia
Anemias of increased red blood cell destruction are gen-
erally classified as hemolytic anemias. These are gener-
ally featuring jaundice and elevated lactate dehydroge-
nase levels.
• Intrinsic (intracorpuscular) abnormalities[12] cause
premature destruction. All of these, except
paroxysmal nocturnal hemoglobinuria, are heredi-
tary genetic disorders.[13]
--- Hereditary spherocytosis[12] is a hereditary de-
fect that results in defects in the RBC cell
membrane, causing the erythrocytes to be se-
questered and destroyed by the spleen.
--- Hereditary elliptocytosis[12] is another defect
in membrane skeleton proteins.
--- Abetalipoproteinemia,[12] causing defects in
membrane lipids
--- Enzyme deficiencies
∗ Pyruvate kinase and hexokinase
deficiencies,[12] causing defect glycolysis
∗ Glucose-6-phosphate dehydrogenase
deficiency and glutathione synthetase
deficiency,[12] causing increased oxidative
stress
--- Hemoglobinopathies
∗ Sickle cell anemia[12]
∗ Hemoglobinopathies causing unstable
hemoglobins[12]
--- Paroxysmal nocturnal hemoglobinuria[12]
• Extrinsic (extracorpuscular) abnormalities
 3

--- Antibody-mediated • General causes of hypervolemia include excessive

∗ Warm autoimmune hemolytic ane- sodium or fluid intake, sodium or water retention
mia is caused by autoimmune attack and fluid shift into the intravascular space.[19]
against red blood cells, primarily by • Anemia of pregnancy is induced by blood volume
IgG. It is the most common of the expansion experienced in pregnancy.
autoimmune hemolytic diseases.[14]
It can be idiopathic, that is, without
any known cause, drug-associated or
secondary to another disease such as 3 Diagnosis
systemic lupus erythematosus, or a
malignancy, such as chronic lymphocytic
leukemia.[15][15]
∗ Cold agglutinin hemolytic anemia is pri-
marily mediated by IgM. It can be
idiopathic[16] or result from an underlying
condition.
∗ Rh disease,[12] one of the causes of
hemolytic disease of the newborn
∗ Transfusion reaction to blood transfu-
sions[12]
--- Mechanical trauma to red cells
∗ Microangiopathic hemolytic anemias,
including thrombotic thrombocytopenic
purpura and disseminated intravascular Peripheral blood smear microscopy of a patient with iron-
coagulation[12] deficiency anemia
∗ Infections, including malaria[12]
∗ Heart surgery Anemia is typically diagnosed on a complete blood count.
∗ Haemodialysis Apart from reporting the number of red blood cells and
the hemoglobin level, the automatic counters also mea-
sure the size of the red blood cells by flow cytometry,
2.3 Blood loss which is an important tool in distinguishing between the
causes of anemia. Examination of a stained blood smear
• Anemia of prematurity from frequent blood sam- using a microscope can also be helpful, and it is some-
pling for laboratory testing, combined with insuffi- times a necessity in regions of the world where automated
cient RBC production analysis is less accessible. In modern counters, four pa-
rameters (RBC count, hemoglobin concentration, MCV
• Trauma[12] or surgery, causing acute blood loss and RDW) are measured, allowing others (hematocrit,
MCH and MCHC) to be calculated, and compared to val-
• Gastrointestinal tract lesions,[12] causing either acute ues adjusted for age and sex. Some counters estimate
bleeds (e.g. variceal lesions, peptic ulcers or chronic hematocrit from direct measurements.
blood loss (e.g. angiodysplasia)
Reticulocyte counts, and the “kinetic” approach to ane-
• Gynecologic disturbances, also generally causing mia, have become more common than in the past in
[12]

chronic blood loss the large medical centers of the United States and some
other wealthy nations, in part because some automatic
• From menstruation, mostly among young women or counters now have the capacity to include reticulocyte
older women who have fibroids counts. A reticulocyte count is a quantitative measure of
the bone marrow's production of new red blood cells. The
• Infection by intestinal nematodes feeding on blood, reticulocyte production index is a calculation of the ratio
such as hookworms[17] and the whipworm Trichuris between the level of anemia and the extent to which the
trichiura.[18] reticulocyte count has risen in response. If the degree of
anemia is significant, even a “normal” reticulocyte count
actually may reflect an inadequate response. If an au-
2.4 Fluid overload tomated count is not available, a reticulocyte count can
be done manually following special staining of the blood
Fluid overload (hypervolemia) causes decreased film. In manual examination, activity of the bone marrow
hemoglobin concentration and apparent anemia: can also be gauged qualitatively by subtle changes in the
4 3 DIAGNOSIS
numbers and the morphology of young RBCs by exami-
nation under a microscope. Newly formed RBCs are usu-
ally slightly larger than older RBCs and show polychro-
masia. Even where the source of blood loss is obvious,
evaluation of erythropoiesis can help assess whether the
bone marrow will be able to compensate for the loss, and
at what rate. When the cause is not obvious, clinicians use
other tests, such as: ESR, ferritin, serum iron, transferrin,
RBC folate level, serum vitamin B12 , hemoglobin elec-
trophoresis, renal function tests (e.g. serum creatinine)
although the tests will depend on the clinical hypothesis
that is being investigated. When the diagnosis remains
difficult, a bone marrow examination allows direct ex-
amination of the precursors to red cells, although is rarely
used as is painful, invasive and is hence reserved for cases
where severe pathology needs to be determined or ex-
cluded.
3.1 Red blood cell size
In the morphological approach, anemia is classified by
the size of red blood cells; this is either done automati-
cally or on microscopic examination of a peripheral blood
smear. The size is reflected in the mean corpuscular vol-
ume (MCV). If the cells are smaller than normal (un-
der 80 fl), the anemia is said to be microcytic; if they
are normal size (80–100 fl), normocytic; and if they are
larger than normal (over 100 fl), the anemia is classified
as macrocytic. This scheme quickly exposes some of the
most common causes of anemia; for instance, a micro-
cytic anemia is often the result of iron deficiency. In clin-
ical workup, the MCV will be one of the first pieces of
information available, so even among clinicians who con-
sider the “kinetic” approach more useful philosophically,
morphology will remain an important element of classifi-
cation and diagnosis. Limitations of MCV include cases
where the underlying cause is due to a combination of fac-
tors - such as iron deficiency (a cause of microcytosis) and
vitamin B12 deficiency (a cause of macrocytosis) where
the net result can be normocytic cells.
3.2 Production vs. destruction or loss
The “kinetic” approach to anemia yields arguably the
most clinically relevant classification of anemia. This
classification depends on evaluation of several hemato-
logical parameters, particularly the blood reticulocyte
(precursor of mature RBCs) count. This then yields the
classification of defects by decreased RBC production
versus increased RBC destruction and/or loss. Clinical
signs of loss or destruction include abnormal peripheral
blood smear with signs of hemolysis; elevated LDH sug-
gesting cell destruction; or clinical signs of bleeding, such
as guaiac-positive stool, radiographic findings, or frank
bleeding. The following is a simplified schematic of this
approach:
Anemia
Reticulocyte production index shows inadequate produc-
tion response to anemia.
Reticulocyte production index shows appropriate re-
sponse to anemia = ongoing hemolysis or blood loss
without RBC production problem.
No clinical findings consistent with hemolysis or blood
loss: pure disorder of production.
Clinical findings and abnormal MCV: hemolysis or loss
and chronic disorder of production*.
Clinical findings and normal MCV= acute hemolysis or
loss without adequate time for bone marrow production
to compensate**.
Macrocytic anemia (MCV>100)
Normocytic anemia (80<MCV<100)
Microcytic anemia (MCV<80)
* For instance, sickle cell anemia with superimposed iron
deficiency; chronic gastric bleeding with B12 and folate
deficiency; and other instances of anemia with more than
one cause.
** Confirm by repeating reticulocyte count: ongoing com-
bination of low reticulocyte production index, normal
MCV and hemolysis or loss may be seen in bone marrow
failure or anemia of chronic disease, with superimposed
or related hemolysis or blood loss. Here is a schematic
representation of how to consider anemia with MCV as
the starting point:
Other characteristics visible on the peripheral smear may
provide valuable clues about a more specific diagnosis; for
example, abnormal white blood cells may point to a cause
in the bone marrow.
3.2.1 Microcytic
Main article: Microcytic anemia
Microcytic anemia is primarily a result of hemoglobin
synthesis failure/insufficiency, which could be caused by
several etiologies:
• Heme synthesis defect
--- Iron deficiency anemia (microcytosis is not al-
ways present)
--- Anemia of chronic disease (more commonly
presenting as normocytic anemia)
• Globin synthesis defect
--- Alpha-, and beta-thalassemia
--- HbE syndrome
--- HbC syndrome
--- Various other unstable hemoglobin diseases
• Sideroblastic defect
3.2 Production vs. destruction or loss
--- Hereditary sideroblastic anemia
--- Acquired sideroblastic anemia, including lead
toxicity
--- Reversible sideroblastic anemia
Iron deficiency anemia is the most common type of ane-
mia overall and it has many causes. RBCs often appear
hypochromic (paler than usual) and microcytic (smaller
than usual) when viewed with a microscope.
• Iron deficiency anemia is due to insufficient di-
etary intake or absorption of iron to meet the body’s
needs. Infants, toddlers, and pregnant women have
higher than average needs. Increased iron intake
is also needed to offset blood losses due to diges-
tive tract issues, frequent blood donations, or heavy
menstrual periods.[21] Iron is an essential part of
hemoglobin, and low iron levels result in decreased
incorporation of hemoglobin into red blood cells.
In the United States, 12% of all women of child-
bearing age have iron deficiency, compared with
only 2% of adult men. The incidence is as high as
20% among African American and Mexican Amer-
ican women.[22] Studies have shown iron deficiency
without anemia causes poor school performance and
lower IQ in teenage girls, although this may be due to
socioeconomic factors.[23][24] Iron deficiency is the
most prevalent deficiency state on a worldwide ba-
sis. It is sometimes the cause of abnormal fissuring
of the angular (corner) sections of the lips (angular
stomatitis).
• In the United States, the most common cause of iron
deficiency is bleeding or blood loss, usually from
the gastrointestinal tract. Fecal occult blood test-
ing, upper endoscopy and lower endoscopy should
be performed to identify bleeding lesions. In older
men and women, the chances are higher that bleed-
ing from the gastrointestinal tract could be due to
colon polyps or colorectal cancer.
• Worldwide, the most common cause of iron defi-
ciency anemia is parasitic infestation (hookworms,
amebiasis, schistosomiasis and whipworms).[25]
The Mentzer index (mean cell volume divided by the
RBC count) predicts whether microcytic anaemia may be
due to iron deficiency or thallasemia, although it requires
confirmation.
3.2.2 Macrocytic
Main article: Macrocytic anemia
• Megaloblastic anemia, the most common cause of
macrocytic anemia, is due to a deficiency of either
5
vitamin B12 , folic acid, or both. Deficiency in folate
and/or vitamin B12 can be due either to inadequate
intake or insufficient absorption. Folate deficiency
normally does not produce neurological symptoms,
while B12 deficiency does.
--- Pernicious anemia is caused by a lack of
intrinsic factor, which is required to absorb vi-
tamin B12 from food. A lack of intrinsic fac-
tor may arise from an autoimmune condition
targeting the parietal cells (atrophic gastritis)
that produce intrinsic factor or against intrin-
sic factor itself. These lead to poor absorption
of vitamin B12 .
--- Macrocytic anemia can also be caused by re-
moval of the functional portion of the stomach,
such as during gastric bypass surgery, lead-
ing to reduced vitamin B12 /folate absorption.
Therefore, one must always be aware of ane-
mia following this procedure.
• Hypothyroidism
• Alcoholism commonly causes a macrocytosis, al-
though not specifically anemia. Other types of liver
disease can also cause macrocytosis.
• Drugs such as Methotrexate, zidovudine, and other
substances may inhibit DNA replication such as
heavy metals (e.g. Lead)
Macrocytic anemia can be further divided into “mega-
loblastic anemia” or “nonmegaloblastic macrocytic ane-
mia”. The cause of megaloblastic anemia is primarily a
failure of DNA synthesis with preserved RNA synthe-
sis, which results in restricted cell division of the pro-
genitor cells. The megaloblastic anemias often present
with neutrophil hypersegmentation (six to 10 lobes). The
nonmegaloblastic macrocytic anemias have different eti-
ologies (i.e. unimpaired DNA globin synthesis,) which
occur, for example, in alcoholism. In addition to the
nonspecific symptoms of anemia, specific features of vi-
tamin B12 deficiency include peripheral neuropathy and
subacute combined degeneration of the cord with result-
ing balance difficulties from posterior column spinal cord
pathology.[26] Other features may include a smooth, red
tongue and glossitis. The treatment for vitamin B12 -
deficient anemia was first devised by William Murphy,
who bled dogs to make them anemic, and then fed them
various substances to see what (if anything) would make
them healthy again. He discovered that ingesting large
amounts of liver seemed to cure the disease. George
Minot and George Whipple then set about to isolate the
curative substance chemically and ultimately were able to
isolate the vitamin B12 from the liver. All three shared
the 1934 Nobel Prize in Medicine.[27]
6 4 TREATMENTS

3.2.3 Normocytic 3.4 Refractory anemia

Main article: Normocytic anemia
Normocytic anemia occurs when the overall hemoglobin
levels are decreased, but the red blood cell size (mean
corpuscular volume) remains normal. Causes include:
Refractory anemia, an anemia which does not respond to
treatment,[29] is often seen secondary to myelodysplastic
syndromes.[30] Iron deficiency anemia may also be refrac-
tory as a clinical manifestation of gastrointestinal prob-
lems which disrupt iron absorption or cause occult bleed-
ing. [31]

• Acute blood loss

4 Treatments
• Anemia of chronic disease
Treatments for anemia depend on cause and severity. Vi-
• Aplastic anemia (bone marrow failure) tamin supplements given orally (folic acid or vitamin B12 )
or intramuscularly (vitamin B12 ) will replace specific de-
• Hemolytic anemia ficiencies.

3.2.4 Dimorphic 4.1 Oral iron

Nutritional iron deficiency is common in developing na-
A dimorphic appearance on a peripheral blood smear oc-
tions. An estimated two-thirds of children and of women
curs when there are two simultaneous populations of red
of childbearing age in most developing nations are esti-
blood cells, typically of different size and hemoglobin
mated to suffer from iron deficiency; one-third of them
content (this last feature affecting the color of the red
have the more severe form of the disorder, anemia.[32]
blood cell on a stained peripheral blood smear). For ex-
Iron deficiency from nutritional causes is rare in men
ample, a person recently transfused for iron deficiency
and postmenopausal women. The diagnosis of iron de-
would have small, pale, iron deficient red blood cells
ficiency mandates a search for potential sources of loss,
(RBCs) and the donor RBCs of normal size and color.
such as gastrointestinal bleeding from ulcers or colon can-
Similarly, a person transfused for severe folate or vita-
cer. Mild to moderate iron-deficiency anemia is treated
min B12 deficiency would have two cell populations, but,
by oral iron supplementation with ferrous sulfate, ferrous
in this case, the patient’s RBCs would be larger and paler
fumarate, or ferrous gluconate. When taking iron sup-
than the donor’s RBCs. A person with sideroblastic ane-
plements, stomach upset and/or darkening of the feces
mia (a defect in heme synthesis, commonly caused by al-
are commonly experienced. The stomach upset can be
coholism, but also drugs/toxins, nutritional deficiencies,
alleviated by taking the iron with food; however, this de-
a few acquired and rare congenital diseases) can have
creases the amount of iron absorbed. Vitamin C aids in
a dimorphic smear from the sideroblastic anemia alone.
the body’s ability to absorb iron, so taking oral iron sup-
Evidence for multiple causes appears with an elevated
plements with orange juice is of benefit.
RBC distribution width (RDW), indicating a wider-than-
normal range of red cell sizes, also seen in common nu- In anemias of chronic disease, associated with
tritional anemia. chemotherapy, or associated with renal disease,
some clinicians prescribe recombinant erythropoietin
or epoetin alfa, to stimulate RBC production, although
3.2.5 Heinz body anemia since there is also concurrent iron deficiency and inflam-
mation present, parenteral iron is advised to be taken
[33]
Heinz bodies form in the cytoplasm of RBCs and appear concurrently.
as small dark dots under the microscope. Heinz body
anemia has many causes, and some forms can be drug-
4.2 Injectable iron
induced. It is triggered in cats by eating onions[28] or
acetaminophen (paracetamol). It can be triggered in dogs
In cases where oral iron has either proven ineffective,
by ingesting onions or zinc, and in horses by ingesting dry
would be too slow (for example, pre-operatively) or where
red maple leaves.
absorption is impeded (for example in cases of inflamma-
tion), parenteral iron can be used. The body can absorb
up to 6 mg iron daily from the gastrointestinal tract. In
3.3 Hyperanemia many cases the patient has a deficit of over 1,000 mg of
iron which would require several months to replace. This
Hyperanemia is a severe form of anemia, in which the can be given concurrently with erythropoietin to ensure
hematocrit is below 10%. sufficient iron for increased rates of erythropoiesis.

4.3 Blood transfusions
Blood transfusions in those without symptoms is not rec-
ommended until the hemoglobin is below 60 to 80 g/L
(6 to 8 g/dL).[4] In those with coronary artery disease
who are not actively bleeding transfusions are only rec-
ommended when the hemoglobin is below 70 to 80g/L
(7 to 8 g/dL).[7] Transfusing earlier does not improve
survival.[34]
Transfusions otherwise should only be undertaken in
cases of cardiovascular instability.[35]
4.4 Erythropoiesis-stimulating agent
The motive for the administration of an erythropoiesis-
stimulating agent (ESA) is to maintain hemoglobin at the
lowest level that both minimizes transfusions and meets
the individual persons needs.[36] They should not be used
for mild or moderate anemia.[34] They are not recom-
mended in people with chronic kidney disease unless
hemoglobin levels are less than 10 g/dL or they have
symptoms of anemia. Their use should be along with
parenteral iron.[36][37]
4.5 Hyperbaric oxygen
Treatment of exceptional blood loss (anemia) is recog-
nized as an indication for hyperbaric oxygen (HBO) by
the Undersea and Hyperbaric Medical Society.[38][39] The
use of HBO is indicated when oxygen delivery to tissue
is not sufficient in patients who cannot be given blood
transfusions for medical or religious reasons. HBO may
be used for medical reasons when threat of blood product
incompatibility or concern for transmissible disease are
factors.[38] The beliefs of some religions (ex: Jehovah’s
Witnesses) may require they use the HBO method.[38] A
2005 review of the use of HBO in severe anemia found
all publications reported positive results.[40]
5 Epidemiology
A moderate degree of iron-deficiency anemia affected
approximately 610 million people worldwide or 8.8% of [11] National Heart Lung and Blood Institute > What Causes
the population.[8] It is slightly more common in female
(9.9%) than males (7.8%).[8] Mild iron deficiency anemia [12] Table 12-1 in: Mitchell, Richard Sheppard; Kumar,
affects another 375 million.[8]
6 History
Evidence of anemia goes back more than 4000 years.[41]
7
7 References
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[2] Stedman’s medical dictionary (28th ed. ed.). Philadelphia:
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9780781733908.
[3] Hematology : clinical principles and applications (3. ed.
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9781416030065. |first1= missing |last1= in Authors list
(help)
[4] Janz, TG; Johnson, RL; Rubenstein, SD (Nov 2013).
“Anemia in the emergency department: evaluation and
treatment.”. Emergency medicine practice 15 (11): 1–15;
quiz 15–6. PMID 24716235.
[5] Smith RE, Jr (Mar 2010). “The clinical and economic
burden of anemia.”. The American journal of managed
care. 16 Suppl Issues: S59–66. PMID 20297873.
[6] Bhutta, ZA; Das, JK; Rizvi, A; Gaffey, MF; Walker, N;
Horton, S; Webb, P; Lartey, A; Black, RE; Lancet Nu-
trition Interventions Review, Group; Maternal and Child
Nutrition Study, Group (Aug 3, 2013). “Evidence-based
interventions for improvement of maternal and child nu-
trition: what can be done and at what cost? extquot-
edbl. Lancet 382 (9890): 452–77. doi:10.1016/S0140-
6736(13)60996-4. PMID 23746776.
[7] Qaseem, A; Humphrey, LL; Fitterman, N; Starkey, M;
Shekelle, P; Clinical Guidelines Committee of the Amer-
ican College of, Physicians (Dec 3, 2013). “Treat-
ment of anemia in patients with heart disease: a clinical
practice guideline from the American College of Physi-
cians.”. Annals of internal medicine 159 (11): 770–
9. doi:10.7326/0003-4819-159-11-201312030-00009.
PMID 24297193.
[8] Vos, T; Flaxman, AD; Naghavi, M; Lozano, R; Michaud,
C; Ezzati, M; Shibuya, K; Salomon, JA et al. (Dec
15, 2012). “Years lived with disability (YLDs) for
1160 sequelae of 289 diseases and injuries 1990-2010:
a systematic analysis for the Global Burden of Dis-
ease Study 2010”. Lancet 380 (9859): 2163–96.
doi:10.1016/S0140-6736(12)61729-2. PMID 23245607.
[9] “anaemia”. Dictionary.com. Retrieved 7 July 2014.
[10] eMedicineHealth > anemia article Author: Saimak T.
Nabili, MD, MPH. Editor: Melissa Conrad Stöppler, MD.
Last Editorial Review: 12/9/2008. Retrieved on 4 April
2009
Anemia? Retrieved on June 9, 2010
Vinay; Abbas, Abul K.; Fausto, Nelson. Robbins Basic
Pathology. Philadelphia: Saunders. ISBN 1-4160-2973-
7. 8th edition.
[13] Kumar, Vinay; Abbas, Abul K.; Fausto, Nelson; &
Mitchell, Richard N. (2007). Robbins Basic Pathology
(8th ed.). Saunders Elsevier. p. 432 ISBN 978-1-4160-
2973-1
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 9

8 External links
• National Anemia Action Council (USA)

• Anemia - Lab Tests Online

10 9 TEXT AND IMAGE SOURCES, CONTRIBUTORS, AND LICENSES

9 Text and image sources, contributors, and licenses

9.1 Text
• Anemia Source: http://en.wikipedia.org/wiki/Anemia?oldid=629488928 Contributors: AxelBoldt, Kpjas, Tarquin, Koyaanis Qatsi,
Alex.tan, Andre Engels, Christian List, Imran, Rsabbatini, Jaknouse, Someone else, Mgmei, Ixfd64, Egil, Ahoerstemeier, Ronz, Snoyes,
Statkit1, Bjb, Kimiko, Tristanb, Jiang, Jengod, Tpbradbury, Taxman, Raul654, Cvaneg, Jni, Chuunen Baka, Robbot, Fredrik, Romanm,
Chris Roy, Postdlf, Puckly, Auric, Sunray, Hadal, Wikibot, Calvinchong, Diberri, GreatWhiteNortherner, Dina, Fabiform, Gwalla, Nmg20,
Nunh-huh, Tom harrison, Everyking, Jfdwolff, Pne, Utcursch, Knutux, Antandrus, Jossi, Bodnotbod, JeffreyN, Generica, Poccil, Rich
Farmbrough, Guanabot, Bender235, ESkog, Wee Jimmy, PatrikR, Bobo192, Comtebenoit, Yonghokim, Davidruben, Arcadian, Bobbis,
Alansohn, Wouterstomp, Axl, Ynhockey, Sp00n17, Idont Havaname, Amorymeltzer, Kyouketsusha, Benji2, Angr, Camw, Kiltman67,
MONGO, Trevor Andersen, JRHorse, Palica, RuM, Mandarax, Jclemens, Enzo Aquarius, Rjwilmsi, Koavf, Kinu, Wikibofh, TK-P, Pin-
chasC, SpNeo, FlaBot, Latka, Margosbot, Nihiltres, Cherubino, Gurch, Choess, Stevenfruitsmaak, Preslethe, King of Hearts, Chobot,
DVdm, WriterHound, Jasonauk, Uriah923, YurikBot, Brandmeister (old), RussBot, Joewright, Pigman, Chaser, Casey56, Stephenb, Fri-
day, Dysmorodrepanis, Cleared as filed, Daniel Bonniot de Ruisselet, Nephron, Moe Epsilon, Supten, Sliggy, BOT-Superzerocool, Kander,
ColdFusion650, Dddstone, Yudiweb, Nick123, Closedmouth, Abune, SV Resolution, Smith2267, Kubra, Kungfuadam, Jonathan.s.kt,
Miniyazz, DVD R W, SmackBot, Xnyxx, Mangoe, CSZero, Jfurr1981, Eskimbot, Gilliam, Ohnoitsjamie, Skizzik, Chris the speller, Blue-
bot, MK8, James Fryer, DHN-bot, Can't sleep, clown will eat me, Snowmanradio, Yamitoyume, LuisEBenavente, ARA, Addshore, E.
Sn0 =31337=, Decltype, DMacks, Balaji Ravichandran, Davidone, Kkailas, Zackwhittaker, Spiritia, SashatoBot, Polihale, Zahid Abdass-
abur, Kuru, AmiDaniel, JackLumber, Solon.KR, Gobonobo, Joelmills, ScottRaw, Fuzzbox, Martian.knight, SeveredSpirit, Danilot, Hu12,
DabMachine, Ginkgo100, Iridescent, Shoeofdeath, Nubzor, Dlohcierekim, Jh12, Harold f, Suougibma, JForget, Will314159, Wavy, Ale
jrb, Scohoust, Green caterpillar, WeggeBot, Neelix, Cydebot, Mato, VashiDonsk, Gogo Dodo, Anthonyhcole, Hopping, Redsox00002,
B, Quibik, CDrecche, Epbr123, N5iln, Gamer007, Marek69, Mandy Kaur, Alphius, Nick Number, Mentifisto, Flosseveryday, AntiVan-
dalBot, Seaphoto, Opelio, Axxaer, Spencer, Arthur Albano, Storkk, Deflective, MER-C, Deadk82, LittleOldMe, VoABot II, AtticusX,
MastCell, Sarahj2107, EdwardLockhart, Jo Mengele, Tommy Bergin, Still relentless, Moss S, Twsx, Caesarjbsquitti, Wikkipedia, Wael
El Kabbany, WhatamIdoing, Chinesesurname, Sgr927, DrAlvi, Allstarecho, Sushmav, DerHexer, Restepc, Wiki wiki1, Yobol, Martin-
Bot, Moggie2002, Infrangible, Kateshortforbob, Mycroft7, CommonsDelinker, Larschan, Jeffhall318, J.delanoy, Pharaoh of the Wizards,
Peter Chastain, Boghog, Eliz81, Choihei, Jkvandeusen, McSly, Mikael Häggström, AntiSpamBot, Belovedfreak, Cadwaladr, Bigdumbdi-
nosaur, Juliancolton, Eshywiki, Jtdaugir, TBAmes, Idioma-bot, Ravensun, Gfirman en, VolkovBot, Lass Lethe, Gene Hobbs, Quentonamos,
Philip Trueman, TXiKiBoT, Seanconway21, Anonymous Dissident, Chris Fookes, Cereis, GlobeGores, Gilvala, LeaveSleaves, AussieJake,
Dr.michael.benjamin, Madhero88, Hallbrianh, Andy Dingley, Papte, Nmani77, Adam.J.W.C., Synthebot, Falcon8765, Kemfaye, Jmh649,
Caps tiki, EmxBot, LB48Steve03, Shadow4ARE, SieBot, Coffee, 4wajzkd02, Tiddly Tom, Graham Beards, WereSpielChequers, Lu-
boogers25, VVVBot, Gerakibot, Rodrigotorres, PhD Dre, Truddle, Linzhoo2u, Smsarmad, Arda Xi, Flyer22, Radon210, Dacheatcode,
Oxymoron83, Yrsamama, Steven Zhang, Lightmouse, Fleester, Techman224, SimonTrew, Fratrep, Mygerardromance, Dimboukas, Rob-
WBartel, Denisarona, Drgarden, POVpushee, Aechase1, NorthStarGirl, ClueBot, ParlerVousWiki, GorillaWarfare, The Thing That Should
Not Be, Matdrodes, IceUnshattered, Supertouch, Sassf, CrazyGlu, CounterVandalismBot, Sintesk7, PMDrive1061, Excirial, Alexbot, Pix-
elBot, Eeekster, Winston365, Invocatus, SO-intO-yOuxX, Cenarium, Peter.C, Cakloss, Saebjorn, La Pianista, Cr299, Thingg, SoxBot
III, Queerbubbles, Tapanhp, Spitfire, BodhisattvaBot, Tony K10, Avoided, SchwarzeMelancholie, Addbot, Twaz, DOI bot, Fyrael, Lan-
don1980, Ocdnctx, Taquittee, Novalia, Fieldday-sunday, Okunderground, CanadianLinuxUser, Download, LAAFan, Jomunro, LinkFA-
Bot, Scienceislife, Tide rolls, Slgcat, Angrysockhop, Ben Ben, Legobot, Kendall35, Luckas-bot, Yobot, Raclemens, Kartano, Ptbotgourou,
Craigwwoods, Freikorp, Gobbleswoggler, Scientificone, Synchronism, AnomieBOT, KDS4444, Lycheeberries, AdjustShift, Dinesh smita,
Dogdocdvm, Bluerasberry, The High Fin Sperm Whale, Citation bot, Mamemimomundem, Windweilder, Neurolysis, ArthurBot, Reyps,
Xqbot, Capricorn42, Hoshin12, Gigemag76, Zerofenrir, Meewam, BritishWatcher, Polemyx, Inferno, Lord of Penguins, Touque, Grou-
choBot, DVMresearcher, ProtectionTaggingBot, RibotBOT, Lovepinkhore, GhalyBot, Erik9, Some standardized rigour, Thehelpfulbot,
FrescoBot, 27 Juni, Bgtuc84, RoshanMcG, BenzolBot, Citation bot 1, Machn, HRoestBot, Pzrmd, Calmer Waters, SpaceFlight89, Flo-
jesy, Elygra, Booksrule9, Trappist the monk, Kalaiarasy, Ndkartik, Dmlevy 99, Vrenator, Diannaa, Suffusion of Yellow, Mean as custard,
RjwilmsiBot, Aidan Kehoe, Alph Bot, Ripchip Bot, Doc.mari, Notyoyoma, Alison22, DASHBot, WikitanvirBot, Immunize, Majkine-
tor, Nuujinn, Syncategoremata, RA0808, Tommy2010, TuHan-Bot, Wikipelli, K6ka, John Cline, Shuipzv3, MithrandirAgain, Maypi-
geon of Liberty, Anir1uph, Ganesh Paudel, Joelloyd7, Alpha Quadrant (alt), Habeeb Anju, Donner60, Cforrester101, Orange Suede Sofa,
ChuispastonBot, 12637man, TYelliot, DASHBotAV, YuriSuassuna, ClueBot NG, Vldscore, The Master of Mayhem, Twillisjr, 123Hedge-
hog456, Marechal Ney, Helpful Pixie Bot, Trsalmon, AHIMS INDIA, Curb Chain, Johnnymadness, BG19bot, Troutbagel, Dimketr, Da-
vidiad, Zyxwv99, Causeandedit, Rm1271, Brycechipmunk, MrBill3, Geekchick77, Drparthnsy, Zujua, Smettems, HumanNaturOriginal,
Redrecks, BattyBot, Biosthmors, Riley Huntley, Mograi jamal, JYBot, Dexbot, Uofhealth, Windows.dll, Rory 20 uk, Mogism, BDE1982,
Frosty, Yopogono, WiHkibew, Hall4Life, Epicgenius, Furious Style, Bayushie, Arripay, Nikki Louladdl, Monkbot, BethNaught, Pratha
naik, DeborahDBartlett, Dnepro86, MarcDanilidou, Arctickinkajou, Piesquared93, DonnieJDube, Djsejpal, Rachelmk77, Tymon.r and
Anonymous: 769

9.2 Images
• File:Iron_deficiency_anemia.jpg Source: http://upload.wikimedia.org/wikipedia/commons/f/fc/Iron_deficiency_anemia.jpg License:
CC-BY-SA-2.0 Contributors: http://www.flickr.com/photos/euthman/2274260085/ Original artist: E. Uthman, MD
• File:Symptoms_of_anemia.png Source: http://upload.wikimedia.org/wikipedia/commons/9/91/Symptoms_of_anemia.png License:
Public domain Contributors: eMedicineHealth > anemia article Author: Saimak T. Nabili, MD, MPH. Editor: Melissa Conrad Stöppler,
MD. Last Editorial Review: 12/9/2008. Retrieved on 4 April, 2009
Original artist: Mikael Häggström.

9.3 Content license

• Creative Commons Attribution-Share Alike 3.0