Iron-deficiency anemia is a common, easily treated condition that occurs if you don't have enough iron

in your body. Low iron levels usually are due to blood loss, poor diet, or an inability to absorb enough
iron from food.

Overview

Iron-deficiency anemia is a common type of anemia. The term "anemia" usually refers to a condition
in which your blood has a lower than normal number of red blood cells. Red blood cells carry oxygen
and remove carbon dioxide (a waste product) from your body.

Anemia also can occur if your red blood cells don't contain enough hemoglobin (HEE-muh-glow-bin).
Hemoglobin is an iron-rich protein that carries oxygen from the lungs to the rest of the body.

Iron-deficiency anemia usually develops over time if your body doesn't have enough iron to build
healthy red blood cells. Without enough iron, your body starts using the iron it has stored. Soon, the
stored iron gets used up.

After the stored iron is gone, your body makes fewer red blood cells. The red blood cells it does make
have less hemoglobin than normal.

Iron-deficiency anemia can cause fatigue (tiredness), shortness of breath, chest pain, and other
symptoms. Severe iron-deficiency anemia can lead to heart problems, infections, problems with
growth and development in children, and other complications.

Infants and young children and women are the two groups at highest risk for iron-deficiency anemia.

Outlook

Doctors usually can successfully treat iron-deficiency anemia. Treatment will depend on the cause and
severity of the condition. Treatments may include dietary changes, medicines, and surgery.

Severe iron-deficiency anemia may require treatment in a hospital, blood transfusions, iron injections,
or intravenous iron therapy.

What Causes Iron-Deficiency Anemia?

Not having enough iron in your body causes iron-deficiency anemia. Lack of iron usually is due to
blood loss, poor diet, or an inability to absorb enough iron from food.

Blood Loss

When you lose blood, you lose iron. If you don't have enough iron stored in your body to make up for
the lost iron, you'll develop iron-deficiency anemia.

In women, long or heavy menstrual periods or bleeding fibroids in the uterus may cause low iron
levels. Blood loss that occurs during childbirth is another cause of low iron levels in women.

Internal bleeding (bleeding inside the body) also may lead to iron-deficiency anemia. This type of
blood loss isn't always obvious, and it may occur slowly. Some causes of internal bleeding are:

 A bleeding ulcer, colon polyp, or colon cancer

 Regular use of aspirin or other pain medicines, such as nonsteroidal anti-inflammatory drugs (for
example, ibuprofen and naproxen)
 Urinary tract bleeding

Blood loss from severe injuries, surgery, or frequent blood drawings also can cause iron-deficiency
anemia.

Poor Diet

The best sources of iron are meat, poultry, fish, and iron-fortified foods (foods that have iron added).
If you don't eat these foods regularly, or if you don't take an iron supplement, you're more likely to
develop iron-deficiency anemia.

Vegetarian diets can provide enough iron if you eat the right foods. For example, good nonmeat
sources of iron include iron-fortified breads and cereals, beans, tofu, dried fruits, and spinach and
other dark green leafy vegetables.

During some stages of life, such as pregnancy and childhood, it may be hard to get enough iron in
your diet. This is because your need for iron increases during these times of growth and development.

Inability To Absorb Enough Iron

Even if you have enough iron in your diet, your body may not be able to absorb it. This can happen if
you have intestinal surgery (such as gastric bypass) or a disease of the intestine (such as Crohn's
disease or celiac disease).

Prescription medicines that reduce acid in the stomach also can interfere with iron absorption.

Who Is at Risk for Iron-Deficiency Anemia?

Infants and Young Children

Infants and young children need a lot of iron to grow and develop. The iron that full-term infants have
stored in their bodies is used up in the first 4 to 6 months of life.

Premature and low-birth-weight babies (weighing less than 5.5 pounds) are at even greater risk for
iron-deficiency anemia. These babies don't have as much iron stored in their bodies as larger, full-
term infants.

Iron-fortified baby food or iron supplements, when used properly, can help prevent iron-deficiency
anemia in infants and young children. Talk with your child's doctor about your child's diet.

Young children who drink a lot of cow's milk may be at risk for iron-deficiency anemia. Milk is low in
iron, and too much milk may take the place of iron-rich foods in the diet. Too much milk also may
prevent children's bodies from absorbing iron from other foods.

Children who have lead in their blood also may be at risk for iron-deficiency anemia. Lead can
interfere with the body's ability to make hemoglobin. Lead may get into the body from breathing in
lead dust, eating lead in paint or soil, or drinking water that contains lead.

Teens
 Teens are at risk for iron-deficiency anemia if they're underweight or have chronic (ongoing) illnesses.
Teenage girls who have heavy periods also are at increased risk for the condition.

Women

Women of childbearing age are at higher risk for iron-deficiency anemia because of blood loss during
their monthly periods. About 1 in 5 women of childbearing age has iron-deficiency anemia.

Pregnant women also are at higher risk for the condition because they need twice as much iron as
usual. The extra iron is needed for increased blood volume and for the fetus' growth.

About half of all pregnant women develop iron-deficiency anemia. The condition can increase a
pregnant woman's risk for a premature or low-birth-weight baby.

Adults Who Have Internal Bleeding

Adults who have internal bleeding, such as intestinal bleeding, can develop iron-deficiency anemia due
to blood loss. Certain conditions, such as colon cancer and bleeding ulcers, can cause blood loss.
Some medicines, such as aspirin, also can cause internal bleeding.

Other At-Risk Groups

People who get kidney dialysis treatment may develop iron-deficiency anemia. This is because blood is
lost during dialysis. Also, the kidneys are no longer able to make enough of a hormone that the body
needs to produce red blood cells.

People who have gastric bypass surgery also may develop iron-deficiency anemia. This type of surgery
can prevent the body from absorbing enough iron.

Certain eating patterns or habits may put you at higher risk for iron-deficiency anemia. This can
happen if you:

 Follow a diet that excludes meat and fish, which are the best sources of iron. However, vegetarian
diets can provide enough iron if you eat the right foods. For example, good nonmeat sources of iron
include iron-fortified breads and cereals, beans, tofu, dried fruits, and spinach and other dark green
leafy vegetables.
 Eat poorly because of money, social, health, or other problems.
 Follow a very low-fat diet over a long time. Some higher fat foods, like meat, are the best sources of
iron.
 Follow a high-fiber diet. Large amounts of fiber can slow the absorption of iron.

What Are the Signs and Symptoms of Iron-Deficiency

Anemia?
The signs and symptoms of iron-deficiency anemia depend on its severity. Mild to moderate iron-
deficiency anemia may have no signs or symptoms.

When signs and symptoms do occur, they can range from mild to severe. Many of the signs and
symptoms of iron-deficiency anemia apply to all types of anemia.

Signs and Symptoms of Anemia

The most common symptom of all types of anemia is fatigue (tiredness). Fatigue occurs because your
body doesn't have enough red blood cells to carry oxygen to its many parts.

Also, the red blood cells your body makes have less hemoglobin than normal. Hemoglobin is an iron-
rich protein in red blood cells. It helps red blood cells carry oxygen from the lungs to the rest of the
body.

Anemia also can cause shortness of breath, dizziness, headache, coldness in your hands and feet, pale
skin, chest pain, weakness, and fatigue (tiredness).

If you don't have enough hemoglobin-carrying red blood cells, your heart has to work harder to move
oxygen-rich blood through your body. This can lead to irregular heartbeats called arrhythmias (ah-
RITH-me-ahs), a heart murmur, an enlarged heart, or evenheart failure.

In infants and young children, signs of anemia include poor appetite, slowed growth and development,
and behavioral problems.

Signs and Symptoms of Iron Deficiency

Signs and symptoms of iron deficiency may include brittle nails, swelling or soreness of the tongue,
cracks in the sides of the mouth, an enlarged spleen, and frequent infections.

People who have iron-deficiency anemia may have an unusual craving for nonfood items, such as ice,
dirt, paint, or starch. This craving is called pica (PI-ka or PE-ka).

Some people who have iron-deficiency anemia develop restless legs syndrome (RLS). RLS is a
disorder that causes a strong urge to move the legs. This urge to move often occurs with strange and
unpleasant feelings in the legs. People who have RLS often have a hard time sleeping.

Iron-deficiency anemia can put children at greater risk for lead poisoning and infections.

Some signs and symptoms of iron-deficiency anemia are related to the condition's causes. For
example, a sign of intestinal bleeding is bright red blood in the stools or black, tarry-looking stools.

Very heavy menstrual bleeding, long periods, or other vaginal bleeding may suggest that a woman is
at risk for iron-deficiency anemia.

How Is Iron-Deficiency Anemia Diagnosed?

Your doctor will diagnose iron-deficiency anemia based on your medical history, a physical exam, and
the results from tests and procedures.

Once your doctor knows the cause and severity of the condition, he or she can create a treatment plan
for you.

Mild to moderate iron-deficiency anemia may have no signs or symptoms. Thus, you may not know
you have it unless your doctor discovers it from a screening test or while checking for other problems.

Specialists Involved

Primary care doctors often diagnose and treat iron-deficiency anemia. These doctors include
pediatricians, family doctors, gynecologists/obstetricians, and internal medicine specialists.
 A hematologist (a blood disease specialist), a gastroenterologist (a digestive system specialist), and
other specialists also may help treat iron-deficiency anemia.

Medical History

Your doctor will ask about your signs and symptoms and any past problems you've had with anemia or
low iron. He or she also may ask about your diet and whether you're taking any medicines.

If you're a woman, your doctor may ask whether you might be pregnant.

Physical Exam

Your doctor will do a physical exam to look for signs of iron-deficiency anemia. He or she may:

 Look at your skin, gums, and nail beds to see whether they're pale
 Listen to your heart for rapid or irregular heartbeats
 Listen to your lungs for rapid or uneven breathing
 Feel your abdomen to check the size of your liver and spleen
 Do a pelvic and rectal exam to check for internal bleeding

Diagnostic Tests and Procedures

Many tests and procedures are used to diagnose iron-deficiency anemia. They can help confirm a
diagnosis, look for a cause, and find out how severe the condition is.

Complete Blood Count

Often, the first test used to diagnose anemia is a complete blood count (CBC). The CBC measures
many parts of your blood.

This test checks your hemoglobin and hematocrit (hee-MAT-oh-crit) levels. Hemoglobin is an iron-rich
protein in red blood cells that carries oxygen to the body. Hematocrit is a measure of how much space
red blood cells take up in your blood. A low level of hemoglobin or hematocrit is a sign of anemia.

The normal range of these levels varies in certain racial and ethnic populations. Your doctor can
explain your test results to you.

The CBC also checks the number of red blood cells, white blood cells, and platelets in your blood.
Abnormal results may be a sign of infection, a blood disorder, or another condition.

Finally, the CBC looks at mean corpuscular (kor-PUS-kyu-lar) volume (MCV). MCV is a measure of the
average size of your red blood cells. The results may be a clue as to the cause of your anemia. In
iron-deficiency anemia, for example, red blood cells usually are smaller than normal.

Other Blood Tests

If the CBC results confirm you have anemia, you may need other blood tests to find out what's
causing the condition, how severe it is, and the best way to treat it.

Reticulocyte count. This test measures the number of reticulocytes (re-TIK-u-lo-sites) in your blood.
Reticulocytes are young, immature red blood cells. Over time, reticulocytes become mature red blood
cells that carry oxygen throughout your body.
 A reticulocyte count shows whether your bone marrow is making red blood cells at the correct rate.

Peripheral smear. For this test, a sample of your blood is examined under a microscope. If you have
iron-deficiency anemia, your red blood cells will look smaller and paler than normal.

Tests to measure iron levels. These tests can show how much iron has been used from your body's
stored iron. Tests to measure iron levels include:

 Serum iron. This test measures the amount of iron in your blood. The level of iron in your blood may
be normal even if the total amount of iron in your body is low. For this reason, other iron tests also
are done.
 Serum ferritin. Ferritin is a protein that helps store iron in your body. A measure of this protein helps
your doctor find out how much of your body's stored iron has been used.
 Transferrin level, or total iron-binding capacity. Transferrin is a protein that carries iron in your blood.
Total iron-binding capacity measures how much of the transferrin in your blood isn't carrying iron. If
you have iron-deficiency anemia, you'll have a high level of transferrin that has no iron.

Other tests. Your doctor also may recommend tests to check your hormone levels, especially your
thyroid hormone. You also may have a blood test for a chemical called erythrocyte protoporphyrin.
This chemical is a building block for hemoglobin.

Children also may be tested for the level of lead in their blood. Lead can make it hard for the body to
produce hemoglobin.

Tests and Procedures for Gastrointestinal Blood Loss

To check whether internal bleeding is causing your iron-deficiency anemia, your doctor may suggest a
fecal occult blood test. This test looks for blood in the stools and can detect bleeding in the intestines.

If the test finds blood, you may have other tests and procedures to find the exact spot of the bleeding.
These tests and procedures may look for bleeding in the stomach, upper intestines, colon, or pelvic
organs.

How Is Iron-Deficiency Anemia Treated?

Treatment for iron-deficiency anemia will depend on its cause and severity. Treatments may include
dietary changes and supplements, medicines, and surgery.

Severe iron-deficiency anemia may require a blood transfusion, iron injections, or intravenous (IV)
iron therapy. Treatment may need to be done in a hospital.

The goals of treating iron-deficiency anemia are to treat its underlying cause and restore normal levels
of red blood cells, hemoglobin, and iron.

Dietary Changes and Supplements

Iron

You may need iron supplements to build up your iron levels as quickly as possible. Iron supplements
can correct low iron levels within months. Supplements come in pill form or in drops for children.
 Large amounts of iron can be harmful, so take iron supplements only as your doctor prescribes. Keep
iron supplements out of reach from children. This will prevent them from taking an overdose of iron.

Iron supplements can cause side effects, such as dark stools, stomach irritation, and heartburn. Iron
also can cause constipation, so your doctor may suggest that you use a stool softener.

Your doctor may advise you to eat more foods that are rich in iron. The best source of iron is red
meat, especially beef and liver. Chicken, turkey, pork, fish, and shellfish also are good sources of iron.

The body tends to absorb iron from meat better than iron from nonmeat foods. However, some
nonmeat foods also can help you raise your iron levels. Examples of nonmeat foods that are good
sources of iron include:

 Iron-fortified breads and cereals

 Peas; lentils; white, red, and baked beans; soybeans; and chickpeas
 Tofu
 Dried fruits, such as prunes, raisins, and apricots
 Spinach and other dark green leafy vegetables
 Prune juice

The Nutrition Facts labels on packaged foods will show how much iron the items contain. The amount
is given as a percentage of the total amount of iron you need every day.

Vitamin C

Vitamin C helps the body absorb iron. Good sources of vitamin C are vegetables and fruits, especially
citrus fruits. Citrus fruits include oranges, grapefruits, tangerines, and similar fruits. Fresh and frozen
fruits, vegetables, and juices usually have more vitamin C than canned ones.

If you're taking medicines, ask your doctor or pharmacist whether you can eat grapefruit or drink
grapefruit juice. Grapefruit can affect the strength of a few medicines and how well they work.

Other fruits rich in vitamin C include kiwi fruit, strawberries, and cantaloupes.

Vegetables rich in vitamin C include broccoli, peppers, Brussels sprouts, tomatoes, cabbage, potatoes,
and leafy green vegetables like turnip greens and spinach.

Treatment To Stop Bleeding

If blood loss is causing iron-deficiency anemia, treatment will depend on the cause of the bleeding. For
example, if you have a bleeding ulcer, your doctor may prescribe antibiotics and other medicines to
treat the ulcer.

If a polyp or cancerous tumor in your intestine is causing bleeding, you may need surgery to remove
the growth.

If you have heavy menstrual flow, your doctor may prescribe birth control pills to help reduce your
monthly blood flow. In some cases, surgery may be advised.

Treatments for Severe Iron-Deficiency Anemia

Blood Transfusion

If your iron-deficiency anemia is severe, you may get a transfusion of red blood cells. A blood
transfusion is a safe, common procedure in which blood is given to you through an IV line in one of
your blood vessels. A transfusion requires careful matching of donated blood with the recipient's
blood.

A transfusion of red blood cells will treat your anemia right away. The red blood cells also give a
source of iron that your body can reuse. However, a blood transfusion is only a short-term treatment.
Your doctor will need to find and treat the cause of your anemia.

Blood transfusions are usually reserved for people whose anemia puts them at a higher risk for heart
problems or other severe health issues.

For more information, go to the Health Topics Blood Transfusion article.

Iron Therapy

If you have severe anemia, your doctor may recommend iron therapy. For this treatment, iron is
injected into a muscle or an IV line in one of your blood vessels.

IV iron therapy presents some safety concerns. It must be done in a hospital or clinic by experienced
staff. Iron therapy usually is given to people who need iron long-term but can't take iron supplements
by mouth. This therapy also is given to people who need immediate treatment for iron-deficiency
anemia.

How Can Iron-Deficiency Anemia Be Prevented?

Eating a well-balanced diet that includes iron-rich foods may help you prevent iron-deficiency anemia.

Taking iron supplements also may lower your risk for the condition if you're not able to get enough
iron from food. Large amounts of iron can be harmful, so take iron supplements only as your doctor
prescribes.

For more information about diet and supplements, go to "How Is Iron-Deficiency Anemia Treated?"

Infants and young children and women are the two groups at highest risk for iron-deficiency anemia.
Special measures can help prevent the condition in these groups.

Infants and Young Children

A baby's diet can affect his or her risk for iron-deficiency anemia. For example, cow's milk is low in
iron. For this and other reasons, cow's milk isn't recommended for babies in their first year. After the
first year, you may need to limit the amount of cow's milk your baby drinks.

Also, babies need more iron as they grow and begin to eat solid foods. Talk with your child's doctor
about a healthy diet and food choices that will help your child get enough iron.

Your child's doctor may recommend iron drops. However, giving a child too much iron can be harmful.
Follow the doctor's instructions and keep iron supplements and vitamins away from children. Asking
for child-proof packages for supplements can help prevent overdosing in children.
 Because recent research supports concerns that iron deficiency during infancy and childhood can have
long-lasting, negative effects on brain health, the American Academy of Pediatrics recommends
testing all infants for anemia at 1 year of age.

Women and Girls

Women of childbearing age may be tested for iron-deficiency anemia, especially if they have:

 A history of iron-deficiency anemia

 Heavy blood loss during their monthly periods
 Other risk factors for iron-deficiency anemia

The Centers for Disease Control and Prevention (CDC) has developed guidelines for who should be
screened for iron deficiency, and how often:

 Girls aged 12 to 18 and women of childbearing age who are not pregnant: Every 5 to 10 years.
 Women who have risk factors for iron deficiency: Once a year.
 Pregnant women: At the first prenatal visit.

For pregnant women, medical care during pregnancy usually includes screening for anemia. Also, your
doctor may prescribe iron supplements or advise you to eat more iron-rich foods. This not only will
help you avoid iron-deficiency anemia, but also may lower your risk of having a low-birth-weight baby.

Living With Iron-Deficiency Anemia

If you have iron-deficiency anemia, get ongoing care to make sure your iron levels are improving. At
your checkups, your doctor may change your medicines or supplements. He or she also may suggest
ways to improve your diet.

Take iron supplements only with your doctor's approval, and only as he or she prescribes. It's possible
to have too much iron in your body (a condition called iron overload). Too much iron in your body can
damage your organs.

You may have fatigue (tiredness) and other symptoms of iron-deficiency anemia until your iron levels
return to normal, which can take months. Tell your doctor if you have any new symptoms or if your
symptoms get worse.

Clinical Trials
The National Heart, Lung, and Blood Institute (NHLBI) is strongly committed to supporting research
aimed at preventing and treating heart, lung, and blood diseases and conditions and sleep disorders.

Researchers have learned a lot about anemia and other blood diseases and conditions over the years.
That knowledge has led to advances in medical care.

Many questions remain about blood diseases and conditions, including iron-deficiency anemia. The
NHLBI continues to support research aimed at learning more about these illnesses.

For example, NHLBI-supported research on iron-deficiency anemia includes studies that explore:
 Ways to prevent iron deficiency among infants, such as giving iron supplements at various stages of
development
 The causes of unexplained anemia in older people
 The lifespan of red blood cells in both younger and older adults and their role in anemia

Much of this research depends on the willingness of volunteers to take part in clinical trials.

Clinical trials test new ways to prevent, diagnose, or treat various diseases and conditions. For
example, new treatments for a disease or condition (such as medicines, medical devices, surgeries, or
procedures) are tested in volunteers who have the illness. Testing shows whether a treatment is safe
and effective in humans before it is made available for widespread use.

By taking part in a clinical trial, you can gain access to new treatments before they're widely available.
You also will have the support of a team of health care providers, who will likely monitor your health
closely. Even if you don't directly benefit from the results of a clinical trial, the information gathered
can help others and add to scientific knowledge.

If you volunteer for a clinical trial, the research will be explained to you in detail. You'll learn about
treatments and tests you may receive, and the benefits and risks they may pose. You'll also be given
a chance to ask questions about the research. This process is called informed consent.

If you agree to take part in the trial, you'll be asked to sign an informed consent form. This form is not
a contract. You have the right to withdraw from a study at any time, for any reason. Also, you have
the right to learn about new risks or findings that emerge during the trial.

For more information about clinical trials related to iron-deficiency anemia, talk with your doctor. You
also can visit the following Web sites to learn more about clinical research and to search for clinical
trials:

 http://clinicalresearch.nih.gov
 www.clinicaltrials.gov
 www.nhlbi.nih.gov/studies/index.htm
 www.researchmatch.org(link is external)

For more information about clinical trials for children, visit the NHLBI's Children and Clinical
Studies Web page.

What Is Anemia?
Anemia (uh-NEE-me-uh) is a condition in which your blood has a lower than normal number of red
blood cells.

Anemia also can occur if your red blood cells don't contain enough hemoglobin (HEE-muh-glow-bin).
Hemoglobin is an iron-rich protein that gives blood its red color. This protein helps red blood cells
carry oxygen from the lungs to the rest of the body.

If you have anemia, your body doesn't get enough oxygen-rich blood. As a result, you may feel tired
or weak. You also may have other symptoms, such as shortness of breath, dizziness, or headaches.

Severe or long-lasting anemia can damage your heart, brain, and other organs in your body. Very
severe anemia may even cause death.

Overview
 Blood is made up of many parts, including red blood cells, white blood cells, platelets (PLATE-lets),
and plasma (the fluid portion of blood).

Red blood cells are disc-shaped and look like doughnuts without holes in the center. They carry
oxygen and remove carbon dioxide (a waste product) from your body. These cells are made in the
bone marrow—a sponge-like tissue inside the bones.

White blood cells and platelets (PLATE-lets) also are made in the bone marrow. White blood cells help
fight infection. Platelets stick together to seal small cuts or breaks on the blood vessel walls and stop
bleeding. With some types of anemia, you may have low numbers of all three types of blood cells.

Anemia has three main causes: blood loss, lack of red blood cell production, or high rates of red blood
cell destruction. These causes might be the result of diseases, conditions, or other factors.

Outlook

Many types of anemia can be mild, short term, and easily treated. You can even prevent some types
with a healthy diet. Other types can be treated with dietary supplements.

However, certain types of anemia can be severe, long lasting, and even life threatening if not
diagnosed and treated.

If you have signs or symptoms of anemia, see your doctor to find out whether you have the condition.
Treatment will depend on the cause of the anemia and how severe it is.

Types of anaemia and their symptoms

A person with anaemia doesn’t have enough haemoglobin in theirblood or has fewer red blood cells than
normal.
Symptoms of anaemia will vary depending on the type and cause, but include:

 Fatigue and loss of energy

 Unusually rapid heartbeat, particularly with exercise
 Shortness of breath and headache, particularly with exercise
 Difficulty concentrating
 Dizziness
 Pale skin
 Leg cramps
 Insomnia

Other symptoms are associated with specific forms of anaemia.

Anaemia caused by iron deficiency:

 Hunger or craving for strange substances such as paper, ice, or dirt (a condition called pica)
 Upward curvature of the nails, referred to as koilonychia
 Soreness of the mouth with cracks at the corners
 A smooth or sore tongue

With iron deficiency anaemia your doctor may recommend iron supplements that contain the ferrous form
of iron, which your body can absorb easily. Always consult with your doctor before taking
iron supplements. Excess iron intake can be harmful. Symptoms of iron overload
include fatigue, vomiting, diarrhoea, headaches, irritability and joint problems.
 Anaemia caused by vitamin B12 deficiency:

 A tingling, "pins and needles" sensation in the hands or feet

 Loss of sense of touch
 An unsteady, wobbly gait and difficulty walking
 Clumsiness and stiffness of the arms and legs
 Dementia

For vitamin B12 and folate deficiency anaemia, the treatment depends on the cause of the deficiency. If
your body stores are depleted of vitamin B12, your doctor is most likely to prescribe vitamin B12
injections. If the vitamin B12 levels are borderline low then your doctor may try oral tablets in a high dose
first to see your response. There is a good chance that many of the symptoms associated with this type of
deficiency will improve very quickly once the body is provided with the needed B12.
Anaemia caused by chronic lead poisoning:

 A blue-black line on the gums referred to as a lead line

 Abdominal pain
 Constipation
 Vomiting
 Seizures in severe cases, especially in children

Lead poisoning is treated by discontinuing exposure to lead and administering amedicine that binds and
draws lead out of the body. Where the household is suspected as the source of lead poisoning, calling
the local environmental health department is essential. Old lead water piping used to be a problem in
older houses.
Anaemia caused by chronic red blood cell destruction (haemolysis):

 Jaundice (yellow skin and eyes)

 Brown or red urine
 Leg ulcers
 Failure to thrive in infancy
 Symptoms of gallstones

Anaemia caused by sudden red blood cell destruction (haemolysis):

 Abdominal pain
 Brown or red urine
 Jaundice (yellow skin and eyes)
 Small bruises under the skin
 Seizures
 Symptoms of kidney failure

Anaemia caused by increased red blood cell destruction

The treatment of haemolytic anaemia may be tailored to the underlying cause. It is important to consider
altering or stopping any medication or agent that is causing the condition. Adding folate supplements is
often needed as levels drop. Some patients may require blood transfusion or iron replacement therapy
but it is a complex decision as to whether either is given.
 Types of anaemia and their symptoms
(continued)

Sickle cell anaemia:

 Fatigue
 Susceptibility to infection
 Delayed growth and development in children
 Episodes of severe pain, especially in the joints, abdomen and limbs

Sickle cell anaemia treatment. The drug hydroxycarbamide is sometimes recommended if a person has
recurring sickle cell crisis episodes. It appears to stimulate the formation of an alternate form of
haemoglobin that isn't susceptible to the sickling. This medicine may help to limit the number of episodes
and the severity.
When to seek medical advice

Seek medical advice if notice any of these possible signs or symptoms of anaemia, or if you suffer any of
the following:

 Persistent fatigue, breathlessness, rapid heart rate, pale skin, or any other symptoms of anaemia
 Very heavy menstrual periods
 Symptoms of an ulcer, gastritis, haemorrhoids, or colorectal cancer
 Concern about environmental exposure to lead
 A hereditary anaemia runs in your family and you would like genetic counselling before having a child

Further reading:

 Anaemia slideshow: Symptoms, causes, and treatments

 Slideshow: Answers to your top period questions
 Normal menstrual cycle and periods
 Vitamin B12 deficiency
 Iron deficiency anaemia: Symptoms, causes, treatments & diagnosis
 Thalassaemia
 Dietary iron and iron supplements
 See all Anaemia topics

Complications

Most cases of anemia are mild, including those that occur as a result of chronic disease. Nevertheless, even mild
anemia can reduce oxygen transport in the blood, causing fatigue and a diminished physical capacity. Moderate-to-
severe iron-deficiency anemia is known to reduce endurance. Some studies indicate that even iron
deficiency withoutanemia can produce a subtle but still lower capacity for exercise.

Because a reduction in red blood cells decreases the ability to absorb oxygen from the lungs, serious problems can
occur in prolonged and severe anemia that is not treated. Anemia can lead to secondary organ dysfunction or damage,
including heart arrhythmia and heart failure.

Certain inherited forms of anemia, including thalassemia major, pernicious anemia, and sickle-cell anemia, can be life
threatening. Thalassemia major and sickle-cell anemia affect children and are particularly devastating.
EFFECTS OF ANEMIA IN PREGNANT WOMEN

Pregnant women with significant anemia may have an increased risk for poor pregnancy outcomes, particularly if
they are anemic in the first trimester.
COMPLICATIONS FROM ANEMIA IN CHILDREN AND ADOLESCENTS

In children, severe anemia can impair growth and motor and mental development. Children may exhibit a shortened
attention span and decreased alertness. Children with severe iron-deficiency anemia may also have an increased risk
for stroke.
EFFECTS OF ANEMIA IN THE ELDERLY

Anemia is common in older people and can have significantly more severe complications than anemia in younger
adults. Effects of anemia in the elderly include decreased strength and increased risk for falls. Anemia may have
adverse effects on the heart and increase the severity of cardiac conditions, including reducing survival rates from
heart failure and heart attacks. Even mild anemia may possibly lead to cognitive impairment or worsen existing
dementia.
EFFECTS OF VITAMIN B12 DEFICIENCIES AND PERNICIOUS ANEMIA

In addition to anemia, vitamin B12 deficiency can cause neurologic damage, which can be irreversible if it continues
for long periods without treatment.
ANEMIA IN PATIENTS WITH CANCER

Anemia is particularly serious in cancer patients. In people with many common cancers, the presence of anemia is
associated with a shorter survival time.
ANEMIA IN PATIENTS WITH KIDNEY DISEASE

Anemia is associated with higher mortality rates and possibly heart disease in patients with kidney disease.
ANEMIA IN PATIENTS WITH HEART FAILURE

The combination of anemia and heart failure can increase the risk of hospitalization or death by 30 - 60%. Patients
with heart failure whose hemoglobin levels decline do worse than patients with stable levels.
EFFECTS OF EXCESS IRON

Blood transfusions. Patients with certain types of anemia require frequent blood transfusions. These transfusions can
cause iron overload.

Complications list for Anemia:

The list of complications that have been mentioned in various sources for Anemia includes:

 High-output heart failure

 Angina
 Heart damage
 Heart failure
 Heart attack
See also the symptoms of Anemia andAnemia: Introduction.
Complications and sequelae of Anemia from the Diseases Database include:

 Skin discoloration
 Cardiac failure, high output
 Hypertension, systemic
 Copper levels raised (serum or plasma)
 Breathlessness
 Flow murmur
 Roth spots
 Hypopigmentation
 Chest pain
 Menorrhagia
 Headache

About prognosis:
The 'prognosis' of Anemia usually refers to the likely outcome of Anemia. The prognosis of
Anemia may include the duration of Anemia, chances of complications of Anemia, probable
outcomes, prospects for recovery, recovery period for Anemia, survival rates, death rates, and
other outcome possibilities in the overall prognosis of Anemia. Naturally, such forecast issues
are by their nature unpredictable.

Prognosis of Anemia Discussion

If iron-deficiency anemia is treated by stopping the source of the blood loss, the anemia should resolve
once the iron stores are repleted, and should not reoccur unless another site of bleeding arises.
Pernicious anemia, caused by B12 deficiency, generally must be treated life-long with B12 injections,
and will reoccur if the B12 treatment is stopped. Inherited anemias, such as thalassemia, are lifelong
conditions as well. (Source: excerpt from Anemia: NWHIC)
Death Statistics for Anemia

The following are statistics from various sources about deaths related to Anemia:

 4,627 people died from anemia each year in the US 2001 (Deaths: Final Data for 2001, NCHS,
CDC)
 1.6 people per 100,000 died from anemia each year in the US 2001 (Deaths: Final Data for 2001,
NCHS, CDC)

Anemia: Introduction

Anemia is a general term for the most common blood disorder in the U.S. Anemia occurs when there
are too few red blood cells in the blood. Anemia is a symptom of a wide variety of mild to serious
diseases, disorders and conditions. Anemia can result fromnutritional
deficiencies, trauma, hemorrhage,transfusion reaction, malabsorption, chronic diseases, inherited
diseases, autoimmune diseases, malignancy, and treatments formalignancy, such as chemotherapy
and radiation therapy.
Anemia can occur when the body does not produce enough red blood cells, such as invitamin B12
deficiency. Anemia can also occur when the body destroys old red blood cells faster than it produces
now ones, such as in hemolytic anemia and sickle cell disease. Anemia can also occur when there is a
deficiency of hemoglobin in the red blood cells, such as in iron deficiency anemia andthalassemia. Any
disease, disorder or condition that causes heavy bleeding (hemorrhage) can also cause anemia. These
can include postpartum hemorrhage,postoperative hemorrhage, gastrointestinal bleeding, peptic
ulcer, colorectal cancer,ulcerative colitis, ruptured aneurysm, andtrauma that causes hemorrhage.
The most important element of red blood cells is called hemoglobin. Hemoglobin is a protein that carries
vital oxygen from the lungs through the bloodstream to the cells, tissues and organs of the body. Many
symptoms of anemia are due to a decreased amount of hemoglobin in the blood. These symptoms can
includedizziness, shortness of breath, weakness, palpitations,fatigue,
and fainting. Hypotension and pallor or pale skin are also common symptoms.
There are also many other symptoms that can accompany the symptoms of anemia, depending on the
disease, disorder or condition that is causing anemia. Complications of anemia can be serious, even
life-threatening. Underlying diseases, disorders or conditions of anemia can also cause complications.
For more details about symptoms and complications, see symptoms of anemia.
Diagnosing anemia and its underlying cause begins with taking a thorough personal and family medical
history, including symptoms, and completing a physical examination.

Anemia can be generally diagnosed with a blood test called a complete blood count (CBC). A complete
blood count can determine the number, size, and color of the red blood cells and the amount of
hemoglobin they hold.

Making a diagnosis also includes performing a variety of other tests to help to diagnose the underlying
disease, condition or disorder causing anemia. This may include a blood test that measures ferritin, a
test for vitamin B12 deficiency and tests to determine if a person has sickle cell trait or thalassemia trait.

A digital rectal examination and testing for fecal occult blood are also generally performed. A digital
rectal examination involves inserting a finger into the rectum to feel for any abnormalities and obtain a
sample of stool to test for the presence of blood, which may not be visible to the naked eye. If blood is
present in stool, the cause of anemia may be a disease or condition that causes bleeding in the
gastrointestinal tract, a common cause of anemia.

In this case, making a diagnosis of the underlying cause of anemia includes performing special imaging
tests to see a picture of the inside of the gastrointestinal tract. These may consist of some combination
of tests, such as a barium X-ray, CT scan, MRI, and a variety of tests using video imaging technology,
such as sigmoidoscopy or colonoscopy.

Sigmoidoscopy or colonoscopy involves passing a small flexible tube fitted with a camera through the
anus into the colon to look for abnormal areas and sites of bleeding. The upper areas of the
gastrointestinal tract, such as the esophagus and stomach, can be examined in a similar way through
the mouth and esophagus in an endoscopy procedure.

A diagnosis of anemia and its cause can easily be delayed or missed because symptoms can be similar
to symptoms of other conditions. In addition, tiny amounts of bleeding from the gastrointestinal tract may
not be noticeable for long periods of time. For information on misdiagnosis, refer to misdiagnosis of
anemia.
Treatment of anemia involves diagnosing and treating the underlying disease, disorder or condition that
is causing it. Some conditions can be easily and successfully treated and cured, while others may
require more intensive treatment and may not have an optimal prognosis. Treatment may or may not
include blood transfusion. For more information on treatment, refer to treatment of anemia. ...more »
Anemia: Anemia refers to a low red blood cell count. Hallmark symptoms
include fatigue and pallor(pale skin). Mild forms of anemia may go undiagnosed. Anemia is also a
common complication of pregnancy and it is important to diagnose it in pregnancy, because of the high
risk to the mother of maternal bleeding in childbirth. There are various types of anemia and causes of
anemia. ...more »

Anemia: Symptoms

Symptoms of anemia can vary greatly from person to person, depending on the severity of anemia and
the underlying cause. Symptoms can be mild to severe and can include symptoms of complications,
such ashypotension and shock.
In anemia, there are a low number of red blood cells in the blood. Red blood cells contain the protein
hemoglobin, which is vital to carrying ...more symptoms »

Anemia: Treatments

Treatment plans for anemia are individualized depending on the underlying cause, the severity, the
presence of coexisting diseases, the age of the patient, and other factors. Treatment involves a
multifaceted plan that addresses the underlying cause, such as sickle cell disease or Vitamin B12
deficiency.
For example, iron deficiency anemia and ...more treatments »

Anemia: Misdiagnosis

Diagnosing anemia and its underlying cause may be delayed or missed because in some cases anemia
develops gradually and the symptoms may not be severe enough for a person to seek medical care. In
addition, some people may believe that some symptoms of anemia, such asconfusion, dizziness,
and falls, are a normal part of aging. Mild symptoms may also be attributed ...more misdiagnosis »

Symptoms of Anemia
Click to Check
  Weakness
 Fatigue
 Tiredness
 Mild early symptoms
 Shortness of breath after exercise
 more symptoms...»
See full list of 26 symptoms of Anemia

Treatments for Anemia

 Iron supplements
 High-iron diet
 Healthy diet
 Intravenous iron - mainly for those on kidney dialysis
 Vitamin B12 supplements
 more treatments...»
See full list of 12 treatments for Anemia

Home Diagnostic Testing

Home medical testing related to Anemia:

 Fatigue: Related Home Tests:

o Home Anemia Tests
o Home Thyroid Gland Function Tests
o Home Adrenal Gland Function Tests
 more...»

Wrongly Diagnosed with Anemia?

 Misdiagnosis of Anemia
 Failure to diagnose Anemia
 Hidden causes of Anemia (possibly wrongly diagnosed)
 Undiagnosed: Anemia

Anemia: Related Patient Stories

 Does anyone know what iron & blood levels should be?
 Low FSH Levels/PCOS
 Living low on energy
  1 year old - undiagnosed fast breather/low oxygen levels
 Low WBC - Drs have no clue
 constant shimmering in peripheral vision
 Can Being An Anemic Cause Miscarriages???
 low to no tsh with opposite symptoms
 Low Everything... Dr not sure what to do
 hemoglobin
 Microcyte anaemia
 weird blood work - high HDL & low B12
 13-months old, low temp - 93.4
 I my tsh level too low?
 B12 dropping very rapidly, NOT pericious anaemia
 slight loss of peripheral vision
 anemic symtoms
 are these numbers low. could it be hypoglycemia??
 Low Bp, Cmp Results
 Low MPV levels

Anemia: Deaths

Read more about Deaths and Anemia.

Alternative Treatments for Anemia

Alternative treatments or home remedies that have been listed in various sources as possibly beneficial
for Anemia may include:

 Clams
 Iron-containing food
 Vitamin C to boost dietary iron absorption
 Poultry
 more treatments »

Types of Anemia
 Iron deficiency anemia - the most common cause.
 Sickle Cell Anemia
 Autoimmune Hemolytic Anemia
 Pernicious anemia
 Thalassemia
  more types...»

See full list of 11 Types of Anemia

Curable Types of Anemia

Possibly curable types of Anemia include:

 Nutritional anemia
 Renal diseases related anemia
 Anemia related to chronic diseases
 Hepatitis related anemia
 Vitamin B12 deficiency anemia
 Folate deficiency anemia
 Iron deficiency anemia
 more types...»

Rare Types of Anemia:

Rare types of Anemia include:

 Herditary xerocytosis
 Congenital dyserythropoietic anemia
 Rh null disease
 Infectious mononucleosis related anemia
 Drugs related anemia
 Aplastic anemia
 more types...»

Anemia: Complications

Review possible medical complications related to Anemia:

 High-output heart failure

 Angina
 Heart damage
 Heart failure
  Heart attack
 more complications...»

Causes of Anemia
 Poor diet - lack of iron
o Vegetarian diet
o Vegan diet
o Excessive dieting
o Neglect
 more causes...»
See full list of 743 causes of Anemia
More information about causes of Anemia:

 Medications, drugs, or substances causing Anemia (466 listings)

 Drug interactions causing Anemia (241 listings)
 Underlying causes of Anemia
 Anemia as a complication caused by other conditions
 Anemia as a symptom
 Medical news summaries relating to Causes of Anemia

Disease Topics Related To Anemia

Research the causes of these diseases that are similar to, or related to, Anemia:

 Decreased production of RBCs

 Heme iron
 Decrease in red blood cell
 Decrease in RBC mass
 Hereditary spherocytosis
 Glucose-6-phosphate dehydrogenase deficiency
 G-6-PD deficiency
 more related diseases...»

Anemia: Undiagnosed Conditions

Commonly undiagnosed diseases in related medical categories:

  Women's Reproductive Health: diseases that are commonly undiagnosed:
o Overactive Bladder Syndrome -- Undiagnosed
o PCOS -- Undiagnosed
o Chlamydia -- Undiagnosed
o Pelvic Inflammatory Disease -- Undiagnosed
o Cervical Cancer -- Undiagnosed
o Breast Cancer -- Undiagnosed
o Ovarian Cancer -- Undiagnosed
o Von Willebrand Disease -- Undiagnosed
o more ...»
 more undiagnosed conditions...»

Misdiagnosis and Anemia

Unnecessary hysterectomies due to undiagnosed bleeding disorder in women: The bleeding

disorder called Von Willebrand's disease is quite...read more »
Anemia undiagnosed in pregnancy: The onset of anemia (low red blood cells) in pregnancy is
sometimes overlooked, despite it being a well-known complication of pregnancy. The problem may be
that the main symptom, i.e. fatigue, is also a...read more »
ADHD diagnosis overlooked hidden nutritional disorder: The book "A Dose of Sanity" reports on a
case of a boy diagnosed with ADHD and receiving...read more »
Cluster of diseases with difficult diagnosis issues: There is a well-known list of medical conditions
that are all somewhat difficult to diagnose, and all can present in a variety of different severities....read
more »
Rare type of breast cancer without a lump: There is a less common form of breast
cancer calledinflammatory breast cancer. Its symptoms can be an inflammation of the breast tissue,
such as with a breast rash...read more »
Pituitary conditions often undiagnosed cause of symptoms: There are a variety of symptoms that
can be caused by a pituitary disorder (see symptoms of...read more »
Vitamin B12 deficiency under-diagnosed: The condition of Vitamin B12 deficiency is a possible
misdiagnosis of various conditions, such as multiple sclerosis (see symptoms of multiple sclerosis). See
...read more »
Epidemiology of anemia in older adults.
Author information
Abstract
Anemia is a common, multifactorial condition among older adults. The World Health Organization
(WHO) definition of anemia (hemoglobin concentration <12 g/dL in women and <13 g/dL in men) is
most often used in epidemiologic studies of older adults. More than 10% of community-dwelling
adults age 65 years and older has WHO-defined anemia. After age 50 years, prevalence of anemia
increases with advancing age and exceeds 20% in those 85 years and older. In nursing homes,
anemia is present in 48% to 63% of residents. Incidence of anemia in older adults is not well
characterized. Among older adults with anemia, approximately one third have evidence of iron,
folate, and/or vitamin B(12) deficiency, another third have renal insufficiency and/or chronic
inflammation, and the remaining third have anemia that is unexplained. Several studies demonstrate
that anemia is associated with poorer survival in older adults. This review details the distribution and
consequences of anemia in older adults and identifies future epidemiologic research needs.

Epidemiology of anemia in the elderly: information on

diagnostic evaluation.
Balducci L1.

Author information
Abstract
A rise in the aging population has been predicted, and, as a result, it is expected that the incidence
of age-related health conditions will also increase. Although common in the elderly, anemia is often
mild and asymptomatic and rarely requires hospitalization. However, untreated anemia can be
detrimental, because it is associated with increased mortality, poor health, fatigue, and functional
dependence and can lead to cardiovascular and neurological complications. Several factors have
been suggested to cause anemia in this population, for example, blood loss or chronic disease. In
some cases, the cause is unknown. It has been suggested that this is a result of the presence of
comorbid conditions that can mask the symptoms of anemia. Therefore, appropriate diagnosis and
management strategies of anemia in the elderly need to be identified, particularly because anemia
may indicate the presence of other serious diseases.

References

1. Alleyne M, Horne MK, Miller JL. Individualized treatment for iron-deficiency anemia in adults. Am J Med.
2008 Nov;121(11):943-8.
2. American College of Obstetricians and Gynecologists. ACOG Practice Bulletin No. 95: anemia in
pregnancy. Obstet Gynecol. 2008 Jul;112(1):201-7.

3. Antony AC. Megaloblastic anemias. In: Goldman L, Ausiello D, eds. Cecil Medicine. 23rd ed. Philadelphia,
Pa: Saunders Elsevier; 2007:chap 170.

4. Bennett CL, Silver SM, Djulbegovic B, Samaras AT, Blau CA, Gleason KJ, et al. Venous thromboembolism
and mortality associated with recombinant erythropoietin and darbepoetin administration for the treatment
of cancer-associated anemia. JAMA. 2008 Feb 27;299(8):914-24.

5. Brotanek JM, Gosz J, Weitzman M, Flores G. Iron deficiency in early childhood in the United States: risk
factors and racial/ethnic disparities.Pediatrics. 2007 Sep;120(3):568-75.

6. Ginder GD. Microcytic and hypochromic anemias. In: Goldman L, Ausiello D, eds. Cecil Medicine. 23rd ed.
Philadelphia, Pa: Saunders Elsevier; 2007:chap 163.

7. Groenveld HF, Januzzi JL, Damman K, van Wijngaarden J, Hillege HL, van Veldhuisen DJ, et al. Anemia
and mortality in heart failure patients a systematic review and meta-analysis. J Am Coll Cardiol.2008 Sep
2;52(10):818-27.

8. Killip S, Bennett JM, Chambers MD. Iron deficiency anemia. Am Fam Physician. 2007 Mar 1;75(5):671-8.

9. KDOQI. KDOQI Clinical Practice Guideline and Clinical Practice Recommendations for anemia in chronic
kidney disease: 2007 update of hemoglobin target. Am J Kidney Dis. 2007 Sep;50(3):471-530.

10. Maguire JL, deVeber G, Parkin PC. Association between iron-deficiency anemia and stroke in young
children. Pediatrics. 2007 Nov;120(5):1053-7.

11. MartÃ-Carvajal AJ, Solà I. Treatment for anemia in people with AIDS.Cochrane Database Syst Rev. 2007
Jan 24;(1):CD004776.

12. Notebaert E, Chauny JM, Albert M. Short-term benefits and risks of intravenous iron: a systematic review
and meta-analysis. Transfusion. 2007 Oct;47(10):1905-18.

13. Reveiz L, Gyte GM, Cuervo LG. Treatments for iron-deficiency anaemia in pregnancy. Cochrane Database
Syst Rev. 2007 Apr 18;(2):CD003094.

14. Rizzo JD, Somerfield MR, Hagerty KL, et al. Use of epoetin and darbepoetin in patients with cancer: 2007
American Society of Clinical Oncology/American Society of Hematology Clinical Practice Guideline
Update. J Clin Oncol. 2007 Dec 21 [Epub ahead of print]

15. Rodgers GM 3rd, Becker PS, Bennett CL, Cella D, Chanan-Khan A, Chesney C, et al. Cancer- and
chemotherapy-induced anemia. J Natl Compr Canc Netw. 2008 Jul;6(6):536-64.

16. Zuckerman KS. Approach to the anemias. In: Goldman L, Ausiello D, eds.Cecil Medicine. 23rd ed.
Philadelphia, Pa: Saunders Elsevier; 2007:chap 162.
Conclusion
The Hemoglobin protein is composed of relatively few Amino Acids; however
there are many locations at which mutations lead to varying degrees of sickle cell
anemia. Four such mutations listed above are substitutions at codons 11, 15, 23 and
43. The mutations result in the change in the shape of the red blood cells, jaundice
and abnormal oxygen affinity. This tragic disease is usually recognized soon after
birth, but if treated correctly can allow the patient to live a relatively normal life.
There are many side affects to Sickle cell anemia, as shown on the illustration to the
right, however most of the side affects are able to be controlled with medication.
There are several treatments for sickle cell anemia ranging from medication to more
intrusive treatments such as bone marrow transfusion. Though these treatments are
affective in keeping the disease at bay, it doesn't completely cure the patient. Studies
have shown that only "50% of patients with sickle cell anemia live into their forties."
"Teens with sickle cell disease may need to put some limits on their lives, but with the
help of doctors, friends, and family, they can manage the condition and live their lives
to the fullest."

Iron Supplementation
The appropriate treatment of anemia due to blood loss is correction of the underlying condition and oral
administration of ferrous sulfate until the anemia is corrected and for several months afterward to ensure that
body stores are replete with iron. Relatively few indications exist for the use of parenteral iron therapy, and
blood transfusions should be reserved for the treatment of shock or hypoxia.

Although the traditional dosage of ferrous sulfate is 325 mg (65 mg of elemental iron) orally three times a day,
lower doses (eg, 15-20 mg of elemental iron daily) may be as effective and cause fewer side effects. To
promote absorption, patients should avoid tea and coffee and may take vitamin C (500 units) with the iron pill
once daily. If ferrous sulfate has unacceptable side effects, ferrous gluconate, 325 mg daily (35 mg of
elemental iron) is a possible alternative for patients who cannot tolerate ferrous sulfate.[14]

A study in Iran demonstrated that once-weekly, low-dose iron supplementation can be effective in improving
iron status and in treating iron deficiency anemia.[15]Mozaffari-Khosravi et al randomly selected and assigned
193 adolescent girls aged 14-16 years to receive either 150 mg ferrous sulfate once weekly for 16 weeks or no
iron supplementation. Before and after intervention, the percentage of anemia, iron deficiency anemia, and iron
deficiency were measured in both groups of girls.

Although the parameters measured before the intervention were not significantly different, at the end of 16
weeks, the group that received the ferrous sulfate had significant improvement in the same parameters. [15] In
addition, all cases of iron deficiency anemia were resolved in the group receiving the low-dose iron
supplementation.

Adults with iron deficiency anemia who cannot tolerate oral iron or who have an unsatisfactory response to it
can be treated with ferric carboxymaltose injection (Injectafer). The agent is given in two intravenous infusions
one week apart.
 Nutritional Therapy and Dietary Considerations
Nutritional therapy is used to treat deficiencies of iron, vitamin B-12, and folic acid. Pyridoxine may be useful in
the treatment of certain patients with sideroblastic anemia, even though this is not a deficiency disorder. A strict
vegetarian diet requires iron and vitamin B-12 supplementation.

Iron deficiency anemia is prevalent in geographic locations where little meat is in the diet. Many of these
locations have sufficient dietary inorganic iron to equal the iron content in persons residing in countries in which
meat is eaten. However, heme iron is more efficiently absorbed than inorganic food iron. Folic acid deficiency
occurs among people who consume few leafy vegetables. Coexistence of iron and folic acid deficiency is
common in developing nations.

Management of Aplastic Disorders

Treatment of aplastic disorders includes removal of the offending agent whenever it can be identified,
supportive therapy for the anemia and thrombocytopenia, and prompt treatment of infection. Avoid transfusion
in patients with a potential bone marrow donor, because transfusion worsens the probability of cure from
transplantation.

As part of supportive therapy, British Committee for Standards in Haematology guidelines recommend
immunosuppression with antithymocyte globulin and cyclosporine as first-line therapy in the following adult
patients[16] :

 Patients with severe or very severe aplastic anemia who lack a matched sibling donor (MSD)
 Patients with severe or very severe aplastic anemia aged >35-50 years
The British guidelines recommend up-front hematopoietic stem cell transplant (HSCT) for young and adult
patients who have an MSD. Similarly, Italian guidelines for treatment of aplasti anemia in children recommend
HSCT from an MSD as the treatment of choice, with immunosuppressive therapy or unrelated-donor HSCT as
options if an MSD is not available.[17]

Splenectomy may provide sufficient improvement for patients with hypoplastic, but not totally aplastic, marrow
so that transfusion is not necessary and platelet and granulocyte counts increase to less dangerous levels.

Ambulatory Management of Common

Forms of Anemia
DAVID R. LITTLE, M.D., M.S., Wright State University School of Medicine, Dayton, Ohio
Am Fam Physician. 1999 Mar 15;59(6):1598-1604.

Anemia is a prevalent condition with a variety of underlying causes. Once the etiology has
been established, many forms of anemia can be easily managed by the family physician. Iron
deficiency, the most common form of anemia, may be treated orally or, rarely, parenterally.
Vitamin B12 deficiency has traditionally been treated with intramuscular injections, although
oral and intranasal preparations are also available. The treatment of folate deficiency is
straightforward, relying on oral supplements. Folic acid supplementation is also
recommended for women of child-bearing age to reduce their risk of neural tube defects.
Current research focuses on folate's role in reducing the risk of premature cardiovascular
disease.
Anemia is a common clinical syndrome frequently diagnosed and managed by the family physician.
The prevalence of anemia in the United States has been reported to be about 29 to 30 cases per
1,000 females of all ages and six cases per 1,000 males under the age of 45, rising to a peak of 18.5
cases per 1,000 men over age 75.1

Anemia is defined as a reduction below normal in the total red blood cell volume (hematocrit) or in
the concentration of blood hemoglobin.2 The normal values for hematocrit and hemoglobin vary with
age and sex (Table 1).2 Proper management of the patient with anemia requires a precise etiologic
diagnosis. Published algorithms can assist the physician in determining the cause of the
anemia.3 Deficiencies of iron, vitamin B12 and folic acid are among the most common causes. These
forms of anemia can be readily managed in an ambulatory setting.

Iron
Iron deficiency is the most common cause of anemia worldwide.2 In children, the deficiency is
typically caused by diet.4 In adults, the cause should be considered to be a result of chronic blood
loss until a definitive diagnosis is established. Once the underlying cause of iron deficiency has been
determined, iron replacement therapy can be initiated. Iron is available in oral and parenteral forms.

Oral iron preparations are available in both ferrous and ferric states. Ferrous salts are absorbed
much more readily and are generally preferred.5 Commonly available oral preparations (Table
2)include ferrous sulfate, ferrous gluconate and ferrous fumarate (Hemocyte). All three forms are
well absorbed but differ in elemental iron content. Ferrous sulfate is the least expensive and most
commonly used oral iron supplement.

For iron replacement therapy, most authorities recommend a dosage equivalent to 150 to 200 mg of
elemental iron per day.5,6 However, recent investigations have suggested that elemental iron in
dosages as low as 60 mg once or twice weekly is beneficial in selected populations.7,8 Further
research is needed to determine the optimal dosing schedule for iron replacement therapy.

A standard daily dosage of 325 mg of ferrous sulfate, in three divided doses, will provide the
necessary elemental iron for patients receiving replacement therapy. Hematocrit levels should show
improvement within one to two months of initiation of therapy; however, the serum ferritin level is a
more accurate measure of total body iron stores. Adequate iron replacement has typically occurred
when the serum ferritin level reaches 50 μg per L (8.9 μmol per L).9–11Depending on the cause and
severity of the anemia, and on whether there is continuing blood loss, replacement of low iron stores
usually requires four to six months of iron supplementation. Yet one recent study showed a benefit
from replacement therapy persisting for two years.12 In patients with continuing iron requirements, a
daily dosage of 325 mg of ferrous sulfate may be necessary for maintenance therapy. This is, of
course, dependent on the amount of iron in the patient's diet.

Side effects from oral iron replacement therapy are common in most patients. They are mostly
gastrointestinal in origin and include nausea, constipation, diarrhea and abdominal pain. To minimize
side effects, iron supplements should be taken with food; however, this may decrease iron
absorption by as much as 40 to 66 percent.5 Changing to a different iron salt or to a controlled-
release preparation13 may also reduce side effects. Nevertheless, 10 to 20 percent of patients
discontinue iron supplementation because of side effects.

For optimum delivery, oral iron supplements must dissolve rapidly in the stomach so that the iron
can be absorbed in the duodenum and upper jejunum. Enteric-coated preparations are ineffective
since they do not dissolve in the stomach.13 Drug interactions may also occur in patients receiving
oral iron supplementation, resulting in reduced iron absorption or interference with other
medications (Table 3)

A variety of products that contain combinations of iron, vitamin B12, folate and other nutrients are
available. Use of these products is strongly discouraged, except in patients with nutritional anemias
related to very poor diets or malnutrition.14 Even in these patients, use of more specific replacement
therapies is preferable. Vitamin C (ascorbic acid) has been shown to enhance iron absorption, which
has led to the creation of combination products that include iron and vitamin C. In practice, however,
the additional amount of iron absorbed with this combination product is rarely clinically useful and
does not justify the higher cost.14 Another recent study15 has shown zinc deficiency to be a
contributing factor to iron deficiency anemia in female endurance runners, although further study will
be needed to fully explain the clinical significance of this relationship.

Use of iron preparations (or any hematinic agents) for empiric therapy in patients with
undifferentiated symptoms is inappropriate. In many instances, this practice may be detrimental to
the patient. For example, iron administration will aggravate the condition of patients with
undiagnosed hemochromatosis.16 The use of folic acid in patients with undiagnosed vitamin
B12deficiency will produce transient hematologic improvements but will mask the clinical symptoms of
vitamin B12 deficiency, allowing neurologic deterioration to continue.17

When treating patients with documented iron deficiency anemia who do not respond to oral
replacement therapy, the physician should try to identify the cause of the resistance to iron. Potential
causes include continuing blood loss, ineffective intake and ineffective absorption (Table
4).18 Continuing blood loss may be overt (e.g., menstruation, hemorrhoids) or occult (e.g.,
gastrointestinal malignancies, intestinal parasites, side effects of nonsteroidal anti-inflammatory
drugs). These sources of blood loss should be assessed in the initial evaluation of the patient with
iron deficiency anemia.

Ineffective iron intake may be the result of poor compliance, often related to the frequent
gastrointestinal side effects of oral iron. Iron uptake and absorption may be impaired by the
concomitant use of medications that reduce stomach acid content, including antacids, H2-receptor
blockers and proton pump inhibitors.9 Caffeinated beverages, particularly tea, will also reduce iron
absorption.6,19 Drugs that interact significantly with oral iron supplements are listed in Table 3.

Ineffective absorption of iron may also be the result of malabsorption states, such as those in
patients with celiac disease, Crohn's disease or pernicious anemia with achlorhydria. Gastric surgery
may also result in iron malabsorption. To determine whether iron malabsorption is present, serum
iron levels should be measured two and four hours after the patient is given 325 mg of oral ferrous
sulfate. Failure of the iron level to rise by at least 115 μg per dL (20.6 μmol per L) over the
pretreatment value indicates poor iron absorption.6

If the patient does not respond adequately to oral iron supplementation, parenteral treatment with
iron dextran (Infed) should be considered. Specific indications for treatment with parenteral iron
include the patient's inability to tolerate oral iron supplements, noncompliance with medication,
malabsorption of iron after acid reduction surgery or continued blood loss.19 The severity of anemia
or the desire to correct it quickly do not justify the use of parenteral iron therapy. Regardless of the
route of delivery, the red blood cell requires the same length of time to utilize the supplemental iron.20

Unpredictable absorption and local complications of intramuscular administration make the

intravenous route preferable for parenteral iron treatment. Parenteral iron dextran may be
administered as a single dose. The total dosage required to replenish body stores is determined by
body weight and hemoglobin deficit. The dosage may be calculated using the following

formula5:

Injectable iron dextran, containing 50 mg of iron per mL, is supplied in a 2-mL single-dose vial and is
available to the pharmacist for an average wholesale price of $37.00.21 Adverse reactions may occur
with the used of injectable iron dextran. Immediate reactions include headache, dyspnea, flushing,
nausea and vomiting, fever, hypotension, seizures, urticaria, anaphylaxis and chest, abdominal or
back pain. A small test dose (0.5 mL) should be given to the patient first to determine whether an
anaphylactic reaction will occur.22 If the patient tolerates the test dose, the full-dosage infusion may
then be given at a rate of 50 mg per minute, up to a total daily dosage of 100 mg.

Vitamin B12
Since body stores of vitamin B12 are adequate for up to five years, deficiency is generally the result of
the body's prolonged failure to absorb it. Pernicious anemia, Crohn's disease and other intestinal
disorders are the most frequent causes of vitamin B12 deficiency. Intramuscular, oral or intranasal
preparations are available for B12 replacement (Table 5). The traditional approach to treatment
consists of intramuscular injections of cyanocobalamin. In patients with severe vitamin B12 deficiency,
daily injections of 1,000 μg of cyanocobalamin are recommended for five days, followed by weekly
injections for four weeks.23 Cyanocobalamin injections are well tolerated and rarely produce side
effects. Hematologic improvement should begin within five to seven days, and the deficiency should
resolve after three to four weeks of treatment. However, six months of therapy or longer will be
required for signs of improvement in the neurologic manifestations of vitamin B12 deficiency.
Complete or partial resolution of neurologic symptoms occurs in as many as 80 percent of
patients.24 Neurologic improvement is less likely to occur in patients with severe or longstanding
deficiency, and in patients whose accompanying anemia is less severe.

Most causes of vitamin B12 deficiency, such as pernicious anemia and postsurgical malabsorption
states, are chronic. As a result, patients usually require lifetime maintenance therapy consisting of
1,000 μg injections of cyanocobalamin every one to three months25 (Table 6). To determine whether
maintenance therapy is adequate, serum cobalamin levels should be measured. The physician may
want to consider serial measurement of cobalamin levels, since the neurologic symptoms of vitamin
B12 deficiency do not consistently correlate with the severity of the anemia.24,26 However, elevated
serum homocysteine or urinary methylmalonic acid levels may be more sensitive indicators
of27 vitamin B12 deficiency27.

Oral and intranasal preparations of vitamin B12 are also available. These routes of administration
were not previously considered practical.28 However, patients with pernicious anemia will absorb 1 to
2 percent of orally ingested cobalamin without the need for intrinsic factor.23 Treating these patients
with high oral dosages of vitamin B12, such as 1,000 to 2,000 μg daily, may be an alternative to
parenteral therapy. Combination products containing vitamin B12 and intrinsic factor are available but
are not readily absorbed. These preparations frequently induce allergic sensitization, and their use is
not recommended.14

An intranasal gel containing cyanocobalamin (Nascobol) has recently been labeled for maintenance
therapy of patients in hematologic remission after intramuscular vitamin B12 therapy for a variety of
deficiency states. Administration of this product once weekly provides a 500-μg dose of
cyanocobalamin. The patient's hematologic parameters must be within normal limits at initiation of
therapy and should be monitored very closely throughout treatment. Preliminary reports suggest that
intranasal cyanocobalamin may also be effective as replacement therapy in patients with vitamin
B12 deficiency, although further study is needed to confirm its long-term effectiveness.29

Folate
Folate deficiency is characterized by megaloblastic anemia and low serum folate levels. Effective
management of folate deficiency requires understanding its cause. Most patients with folate
deficiency have inadequate intake, increased folate requirements, or both. Drug therapy with folate
antagonists such as methotrexate (Rheumatrex), pyrimethamine (Daraprim), trimethoprim
(Proloprim) or triamterene (Dyrenium) may also lead to folate deficiency. Treatment of folate
deficiency is straightforward. In the absence of a folate malabsorption state, a once-daily dosage of
1 mg of folic acid given orally will replenish body stores in about three weeks30 (Table 5).

Folate supplementation is also recommended for women of child-bearing age to reduce the
incidence of fetal neural tube defects. Current recommendations include initiating folic acid
supplementation at a dosage of 0.4 mg daily before conception. Most prenatal vitamins contain this
amount of folic acid. Women who have previously given birth to a child with a neural tube defect
should take 4 to 5 mg of folic acid daily.31 It is believed that higher dosages do not provide any
additional protection against neural tube defects.32

Research is currently underway to determine whether folic acid supplementation may reduce the risk
of premature atherosclerotic cardiovascular disease.33 Elevated serum homocysteine levels are
associated with an increased risk for myocardial infarction,34 stroke35 and, possibly, deep venous
thrombosis.36 It remains unclear whether an elevated serum homocysteine level is directly involved in
the pathogenesis of these events or merely a marker for potential cardiovascular disease. If an
elevated homocysteine level is found to be associated with the atherosclerotic process, folic acid
supplementation could reduce these levels, thereby reducing the risk of adverse cardiovascular
events.37

The opportunity to decrease the incidence of neural tube defects and the theoretic possibility of
reducing the risk of cardiovascular disease has led some nutrition authorities to recommend routine
folic acid fortification of bread and other food products.31 However, because the use of folic acid
supplementation partially corrects the hematologic abnormalities of vitamin B12deficiency but not the
associated neurologic deterioration,10 other experts have recommended that all foods fortified with
folic acid also include vitamin B12 supplementation38.

The Author
show all author info

DAVID R. LITTLE, M.D., M.S., is assistant professor in the Department of Family Medicine and
associate director in the Division of Research at Wright State University School of Medicine, Dayton,
Ohio. He received a medical degree from Northeastern Ohio Universities College of Medicine,
Rootstown, and completed a fellowship in academic family medicine at the Ohio State University
College of Medicine, Columbus, where he obtain a master's degree in allied health education....

REFERENCES
show all references

1. Current estimates from the National Health Interview Survey, 1994. Hyattsville, Md.: Dept of
Health and Human Services, Public Health Service, Centers for Disease Control, National Center for
Health Statistics, 1995; DHHS publication no. 95-1521....
Each year, members of two different medical faculties develop articles for “Practical Therapeutics.”
This article is one in a series coordinated by the Department of Family Medicine at Wright State
University School of Medicine, Dayton, Ohio. Guest editors of the series are Cynthia G. Olsen, M.D.,
and Gordon S. Walbroehl, M.D.

Anemia: Types list

The list of types of Anemia mentioned in various sources includes:

 Iron deficiency anemia - the most common cause.

 Sickle Cell Anemia
 Autoimmune Hemolytic Anemia
 Pernicious anemia
 Thalassemia
 Categories of anemias:
 o Microcytic hypochromic anemia - about 90% of cases
o Megaloblastic hyperchromic anemia - about 7% of cases; immature megaloblast cells wrongly
enter the blood.
o Aplastic anemia - bone marrow not producing enough red blood cells.
o Hemolytic anemia - caused by early destruction of red blood cells in the blood.
o Sideroblastic anemia

Curable Types of Anemia:

 Nutritional anemia
 Renal diseases related anemia
 Anemia related to chronic diseases
 Hepatitis related anemia
 Vitamin B12 deficiency anemia
 Folate deficiency anemia
 Iron deficiency anemia
 Pregnancy related anemia

Rare Types of Anemia:

 Herditary xerocytosis
 Congenital dyserythropoietic anemia
 Rh null disease
 Infectious mononucleosis related anemia
 Drugs related anemia
 Aplastic anemia
 Microcytic anemia
 Macrocytic anemia
 Normocytic anemia
 Haemolytic anemia
 Poikilocytic anemia
 Spherocytic anemia
 Drepanocytic anemia
 Normochromic anemia
 Hyperchromic anemia
 Hypochromic anemia
 Macrocytic-normochromic anemia
 Microcytic-hypochromic anemia
 Normocytic-normochromic anemia
 Iron-deficiency anemia
 Pernicious anemia
 Folate-deficiency anemia
 Thalassemia
 Sideroblastic anemia
 Posthemorrhagic anemia
 Sickle cell anemia
 Chronic anemia
 Achrestic anemia
 Autoimmune haemolytic anemia
 Cooley's anemia
 Drug-induced immune haemolytic anemia
 Erythroblastic anemia
 Hypoplastic anemia
 Diamond-Blackfan anemia
 Pearson's anemia
 Transient anemia
 Fanconi's anemia - Complementation group N
 Lederer's anemia
 Myelpathic anemia
 Nutritional anemia
 Spur-cell anemia
 Von Jaksh's anemia
 Sideroblatic anemia
 Sideropenic anemia
 Alpha thalassemia - silent carrier
 Beta thalassemia
 Alpha thalassemia trait
 Alpha thalassemia minor
 Hemoglobin H disease
 Alpha thalassemia major
 Beta Thalassemia minor
 Beta Thalassemia intermedia
 Beta Thalassemia major
 Acute Acquired Hemolytic Anemia
 Warm Autoimmune Hemolytic Anemia
 Cold Autoimmune Hemolytic Anemia
 Primary Cold Autoimmune Hemolytic Anemia
 Secondary Cold Autoimmune Hemolytic Anemia
 Secondary Autoimmune Hemolytic Anemia
 Primary Autoimmune Hemolytic Anemia
  X-linked Sideroblastic anemia
 Sideroblastic anemia, pyridoxine-responsive, autosomal recessive
 Pyridoxine-responsive anemia
 Nutritional Sideroblastic anemia
 Pyridoxine deficiency-induced Sideroblastic anemia
 Copper deficiency-induced Sideroblastic anemia
 Cycloserine-induced Sideroblastic anemia
 Chloramphenicol-induced Sideroblastic anemia
 Ethanol-induced Sideroblastic anemia
 Isoniazid-induced Sideroblastic anemia
 Drug-induced Sideroblastic anemia
 Toxin-induced Sideroblastic anemia
 Diamond-Blackfan anemia 1
 Diamond-Blackfan anemia 2
 Diamond-Blackfan anemia 3
 Diamond-Blackfan anemia 4
 Diamond-Blackfan anemia 5
 Diamond-Blackfan anemia 6
 Diamond-Blackfan anemia 7
 Diamond-Blackfan anemia 8
 Microcytic Hyperchromic Anemia
 Macrocytic Hyperchromic Anemia
 Megalocytic-Normochromic anemia
 Microcytic-Normochromic anemia
 Sulphonamide -induced Immune Hemolytic Anemia
 Doxepine-induced Immune Hemolytic Anemia
 Quinidine-induced Immune Hemolytic Anemia
 Penicillin-induced Immune Hemolytic Anemia
 Methyldopa-induced Immune Hemolytic Anemia
 Cephalosporin-induced Immune Hemolytic Anemia
 Drug-induced Immune Hemolytic Anemia
 Non-hereditary spherocytic anemia
 Inherited spherocytic anemia
 Congenital Spherocytic Anemia

Types discussion:

There are several kinds of anemia produced by a variety of underlying causes, but the most common
and most severe type of anemia, iron-deficiency anemia (IDA). Just as the name implies, this form of
anemia is due to insufficient iron. In the United States, 20% of all women of childbearing age have iron-
deficiency anemia, compared with only 2% of adult men. The principal cause of iron-deficiency anemia
in premenopausal women is blood lost during menses. (Source: excerpt from Anemia: NWHIC)

Anemia: Rare Types

Related Anemia Info

Related Pages
1. Anemia: Introduction
2. Types of Anemia
3. Curable Types
4. Rare Types
5. Types Discussion
6. Complications
7. Doctors & Specialists
8. Prognosis
9. Treatments
10. Alternative Treatments
11. Misdiagnosis
12. Deaths
Rare types of medical conditions and diseases in related medical categories:

 Women's Reproductive Health -- rare types of diseases:

o Overactive Bladder Syndrome -- Rare Types
o PCOS -- Rare Types
o Chlamydia -- Rare Types
o Pelvic Inflammatory Disease -- Rare Types
o Cervical Cancer -- Rare Types
o Breast Cancer -- Rare Types
o Ovarian Cancer -- Rare Types
o Von Willebrand Disease -- Rare Types

"Addison's anaemia" redirects here. For the disease affecting the adrenal glands, see Addison's
disease.

Pernicious anemia

Biermer's anemia,[1] Addison's anemia,[2] Addison–

 Biermer anemia[3]

Normal red blood cells

Classification and external resources

Specialty Hematology

ICD-10 D51.0

ICD-9-CM 281.0

DiseasesDB 9870

MedlinePlus 000569

eMedicine med/1799

MeSH D000752
 [edit on Wikidata]

Pernicious anemia, also known as vitamin B12 deficiency anemia,[4] is a disease in which there
are not enough red blood cells due to a lack of vitamin B12.[5] The most common initial symptom is
feeling tired. Other symptoms may include shortness of breath, pale skin, chest pain, numbness in
the hands and feet, poor balance, a smooth, red tongue, poor reflexes, and confusion.[6] If treatment
is not provided, some of these problems may become permanent.[5]
Although pernicious anemia technically refers to cases resulting from not enough intrinsic factor, it is
often used to describe all cases of anemia due to not enough vitamin B12.[5] Lack of intrinsic factor is
most commonly due to an autoimmune attack on the cells that make it in the stomach. It can also
occur following the surgical removal of part of the stomach or from an inherited disorder. Other
causes of low vitamin B12 include a poor diet, celiac disease, and a tapeworm infection.[7] When
suspected, diagnosis is made by blood and, occasionally, bone marrow tests. Blood tests may
show fewer but larger red blood cells, low numbers of young red blood cells, low levels of vitamin
B12, and antibodies to intrinsic factor.[8]
Pernicious anemia due to lack of intrinsic factor is not preventable. Vitamin B12 deficiency due to
other causes may be prevented with a balanced diet or with supplements.[9] Pernicious anemia can
be easily treated with either injections or pills of vitamin B12. If the symptoms are severe, injections
are typically recommended initially. For those who have trouble swallowing pills, a nasal spray is
available.[10] Often treatment is lifelong.[11]
Pernicious anemia due to autoimmune problems occurs in about 1 per 1000 people. Among those
over the age of 60 about 2% have the condition.[1] It more commonly affects people of northern
European descent.[2] Women are more commonly affected than men.[12] With proper treatment most
people live normal lives.[5] Due to a higher risk of stomach cancer, those with pernicious anemia
should be checked regularly for this.[11] The first clear description was by Thomas Addison in
1849.[13][14] The term "pernicious" means "deadly," and was used as before the availability of
treatment the disease was often fatal.[5][15]
The symptoms of pernicious anemia come on slowly. Untreated, it can lead to neurological
complications, and in serious cases, death. Many of the signs and symptoms are due to anemia
itself, when anemia is present.[16] Symptoms may consist of the triad of tingling or other skin
sensations (paresthesia), tongue soreness (glossitis), and fatigue and general
weakness.[17][18][19][page needed] It presents with a number of further common
symptoms,[19][page needed][20][page needed] including depressive mood, low-grade fevers,diarrhea, dyspepsia,
weight loss,[17] neuropathic pain, jaundice, sores at the corner of the mouth (angular cheilitis), a look
of exhaustion with pale and dehydrated or cracked lips and dark circles around the eyes, as well as
brittle nails,[18] and thinning and early greying of the hair.[18] Because PA may affect the nervous
system, symptoms may also include difficulty in proprioception,[21]memory changes,[20][page needed] mild
cognitive impairment (including difficulty concentrating and sluggish responses, colloquially referred
to as brain fog), and even psychoses, impaired urination,[17] loss of sensation in the feet, unsteady
gait,[21] difficulty in walking,[18] muscle weakness[19][page needed] and clumsiness.[17] Anemia may also lead to
tachycardia (rapid heartbeat),[17] cardiac murmurs, a yellow waxy pallor,[18] altered blood pressure
(low or high), and a shortness of breath (known as "the sighs").[19][page needed] The deficiency also may
present with thyroid disorders.[19][page needed] In severe cases, the anemia may cause evidence of
congestive heart failure.[20][page needed] A complication of severe chronic PA is subacute combined
degeneration of spinal cord, which leads to distal sensory loss (posterior column), absent ankle
reflex, increased knee reflex response, and extensor plantar response.[22] Other than anemia,
hematological symptoms may include cytopenias, intramedullary hemolysis, and pseudothrombotic
microangiopathy.[1] Pernicious anemia can contribute to a delay in physical growth in children, and
may also be a cause for delay in puberty for adolescents.

Causes[edit]
Vitamin B12 cannot be produced by the human body, and must be obtained from the diet. When
foods containing B12 are eaten, the vitamin is usually bound to protein and is released by stomach
acid. Following its release, most B12 is absorbed by the body in the small bowel (ileum) after binding
to a protein known as intrinsic factor. Intrinsic factor is produced by parietal cells of
the gastric mucosa (stomach lining) and the intrinsic factor-B12 complex is absorbed by cubilin
receptors on the ileum epithelial cells.[23][24] PA is characterised by B12 deficiency caused by the
absence of intrinsic factor.[25]
PA may be considered as an end stage of immune gastritis, a disease characterised by stomach
atrophy and the presence of antibodies to parietal cells and intrinsic factor.[26] A specific form of
chronic gastritis, type A gastritis or atrophic body gastritis, is highly associated with PA. This
autoimmune disorder is localised to the body of the stomach, where parietal cells are
located.[25] Antibodies to intrinsic factor and parietal cells cause the destruction of the oxyntic gastric
mucosa, in which the parietal cells are located, leading to the subsequent loss of intrinsic factor
synthesis. Without intrinsic factor, the ileum can no longer absorb the B12.[27]
Although the exact role of Helicobacter pylori infection in PA remains controversial, evidence
indicates H. pylori is involved in the pathogenesis of the disease. A long-standing H. pylori infection
may cause gastric autoimmunity by a mechanism known as molecular mimicry. Antibodies produced
by the immune system can be cross-reactive and may bind to both H. pylori antigens and those
found in the gastric mucosa. The antibodies are produced by activated B cells that recognise both
pathogen and self-derived peptides. Theautoantigens believed to cause the autoreactivity are the
alpha and beta subunits of the H+/K+-ATPase.[27][28]
Less commonly, H. pylori and Zollinger-Ellison syndrome may also cause a form of nonautoimmune
gastritis that can lead to pernicious anemia.[29]
Impaired B12 absorption can also occur following gastric removal (gastrectomy) or gastric bypass
surgery. In these surgeries, either the parts of the stomach that produce gastric secretions are
removed or they are bypassed. This means intrinsic factor, as well as other factors required for
B12 absorption, are not available. However, B12 deficiency after gastric surgery does not usually
become a clinical issue. This is probably because the body stores many years' worth of B12 in the
liver and gastric surgery patients are adequately supplemented with the vitamin.[30][31]
Although no specific PA susceptibility genes have been identified, a genetic factor likely is involved
in the disease. Pernicious anemia is often found in conjunction with other autoimmune disorders,
suggesting common autoimmune susceptibility genes may be a causative factor.[25] In spite of that,
previous family studies and case reports focusing on PA have suggested that there is a tendency of
genetic heritance of PA in particular, and close relatives of the PA patients seem to have higher
incidence of PA and associated PA conditions.[32][33][34] Moreover, it was further indicated that the
formation of antibodies to gastric cells was autosomal dominant gene determined, and the presence
of antibodies to the gastric cells might not be necessarily related to the occurrence of atrophic
gastritis related to PA.[32][34]

Pathophysiology[edit]
Although the healthy body stores three to five years' worth of B12 in the liver, the usually undetected
autoimmune activity in one's gut over a prolonged period of time leads to B12depletion and the
resulting anemia. B12 is required by enzymes for two reactions: the conversion of methylmalonyl
CoA to succinyl CoA, and the conversion of homocysteine tomethionine. In the latter reaction,
the methyl group of 5-methyltetrahydrofolate is transferred to homocysteine to
produce tetrahydrofolate and methionine. This reaction is catalyzed by the enzyme methionine
synthase with B12 as an essential cofactor. During B12 deficiency, this reaction cannot proceed, which
leads to the accumulation of 5-methyltetrahydrofolate. This accumulation depletes the other types of
folate required for purine and thymidylate synthesis, which are required for the synthesis of DNA.
Inhibition of DNA replication in red blood cells results in the formation of large, fragile
megaloblastic erythrocytes. The neurological aspects of the disease are thought to arise from the
accumulation of methylmalonyl CoA due to the requirement of B12 as a cofactor to the enzyme
methylmalonyl CoA mutase.[23][35][36][37]

Diagnosis[edit]

Immunofluorescence staining pattern of gastric parietal cell antibodies on a stomach section

PA may be suspected when a patient's blood smear shows large, fragile, immature erythrocytes,
known as megaloblasts. A diagnosis of PA first requires demonstration of megaloblastic anemia by
conducting a full blood count and blood smear, which evaluates the mean corpuscular
volume (MCV), as well the mean corpuscular hemoglobin concentration (MCHC). PA is identified
with a high MCV (macrocytic anemia) and a normal MCHC (normochromic anemia).[38] Ovalocytes
are also typically seen on the blood smear, and a pathognomonicfeature of megaloblastic anemias
(which include PA and others) is hypersegmented neutrophils.[18]
Serum vitamin B12 levels are used to detect its deficiency, but they do not distinguish its causes.
Vitamin B12 levels can be falsely high or low and data for sensitivity and specificity vary widely.
Normal serum levels may be found in cases of deficiency where myeloproliferative disorders, liver
disease, transcobalamin II deficiency, or intestinal bacterial overgrowth are present. Low levels of
serum vitamin B12 may be caused by other factors than B12 deficiency, such as folate
deficiency, pregnancy, oral contraceptive use, haptocorrin deficiency, andmyeloma.[39][40]
The presence of antibodies to gastric parietal cells and intrinsic factor is common in PA. Parietal cell
antibodies are found in other autoimmune disorders and also in up to 10% of healthy individuals,
making the test nonspecific. However, around 85% of PA patients have parietal cell antibodies,
which means they are a sensitive marker for the disease. Intrinsic factor antibodies are much less
sensitive than parietal cell antibodies, but they are much more specific. They are found in about half
of PA patients and are very rarely found in other disorders. These antibody tests can distinguish
between PA and food-B12 malabsorption.[40] The combination of both tests of intrinsic factor
antibodies and parietal cell antibodies may improve overall sensitivity and specificity of the
diagnostic results.[41]
A buildup of certain metabolites occurs in B12 deficiency due to its role in cellular physiology.
Methylmalonic acid (MMA) can be measured in both the blood and urine, whereas homocysteine is
only measured in the blood. An increase in both MMA and homocysteine can distinguish between
B12 deficiency and folate deficiency because only homocysteine increases in the latter.[40][42]
Elevated gastrin levels can be found in around 80-90% of PA cases, but they may also be found in
other forms of gastritis. Decreased pepsinogen I levels or a decreased pepsinogen I to pepsinogen II
ratio may also be found, although these findings are less specific to PA and can be found in food-
B12 malabsorption and other forms of gastritis.[42]
The diagnosis of atrophic gastritis type A should be confirmed by gastroscopy and stepwise
biopsy.[43] About 90% of individuals with PA have antibodies for parietal cells; however, only 50% of
all individuals in the general population with these antibodies have pernicious anemia.[44]
Forms of vitamin B12 deficiency other than PA must be considered in the differential diagnosis of
megaloblastic anemia. For example, a B12-deficient state which causes megaloblastic anemia and
which may be mistaken for classical PA may be caused by infection with
the tapeworm Diphyllobothrium latum, possibly due to the parasite's competition with host for vitamin
B12.[45]
The classic test for PA, the Schilling test, is no longer widely used, as the foregoing more efficient
methods to are available. This historic test consisted, in its first step, of taking an oral dose
of radiolabelled vitamin B12, followed by quantitation of the vitamin in the patient's urine over a 24-
hour period via measurement of the radioactivity. A second step of the test repeats the regimen and
procedure of the first step, with the addition of oral intrinsic factor. A patient with PA presents lower
than normal amounts of intrinsic factor; hence, addition of intrinsic factor in the second step results in
an increase in vitamin B12 absorption (over the baseline established in the first). The Schilling test
distinguished PA from other forms of B12 deficiency,[23] specifically, from Imerslund-Grasbeck
Syndrome (IGS), a vitamin B12-deficiency caused by mutations in the cobalamin receptor.[46]

Treatment[edit]

Hydroxocobalamin injection usp(1000 mcg/ml) is a clear red liquid solution of hydoxocobalamin which is
available in a 30-ml brown glass multidose vial packaged in a paper box. Shown is 500 mcg B-12 (as 1/2 cc)
drawn up in a 0.5-cc U-100 27 gauge x 1/2" insulin syringe, as prepared for subcutaneous injection.
The treatment of PA varies by country and area. Opinions vary over the efficacy of administration
(parenteral/oral), the amount and time interval of the doses, or the forms of vitamin B12 (e.g.
cyanocobalamin/hydrocobalamin). More comprehensive studies are still needed in order to validate
the feasibility of a particular therapeutic method for PA in clinical practices. A permanent cure for PA
is lacking, although repletion of B12 should be expected to result in cessation of anemia-related
symptoms, a halt in neurological deterioration, and in cases where neurological problems are not
advanced, neurological recovery and a complete and permanent remission of all symptoms, so long
as B12 is supplemented. Repletion of B12 can be accomplished in a variety of ways.

Intramuscular injections[edit]
The standard treatment for PA has been intramuscular injections of cobalamin in the form of
cyanocobalamin (CN-Cbl) and hydroxocobalamin (OH-Cbl).[47]

Oral doses[edit]
Treatment with high-dose vitamin B12 by mouth also appears effective.[47][48][49]

Prognosis[edit]
A person with well-treated PA can live a healthy life. Failure to diagnose and treat in time, however,
may result in permanent neurological damage, excessive fatigue, depression, memory loss, and
other complications. In severe cases, the neurological complications of pernicious anemia can lead
to death - hence the name, "pernicious", meaning deadly.
An association has been observed between pernicious anemia and certain types of gastric cancer,
but a causal link has not been established.[27]

Epidemiology[edit]
PA is estimated to affect 0.1% of the general population and 1.9% of those over 60, accounting for
20-50% of B12 deficiency in adults.[1] A review of literature shows that the prevalence of PA is higher
in Northern Europe, especially in Scandinavian countries, and among people of African descent, and
that increased awareness of the disease and better diagnostic tools might play a role in apparently
higher rates of incidence.[50]

History[edit]
The symptoms are first described in 1822 by Dr James Scarth Combe in the Transactions of the
Medico-Chirurgical Society of Edinburgh, under the title of History of a Case of Anaemia.[51]
However, this was not investigated in more depth until 1849, by British physician Thomas Addison,
from which it acquired the common name of Addison's anemia. In 1871, German physician Michael
Anton Biermer (1827–1892) noticed the particular characteristic of the anemia in one of his patients;
he later coined the term "progressive pernicious anemia".[52][better source needed] In 1907, Richard Clarke
Cabot reported on a series of 1200 patients with PA; their average survival was between one and
three years.[citation needed]William Bosworth Castle performed an experiment whereby he ingested raw
hamburger meat and regurgitated it after an hour, and subsequently fed it to a group of 10
patients.[53][full citation needed] Untreated raw hamburger meat was fed to the control group. The former group
showed a disease response, whereas the latter group did not. This was not a sustainable practice,
but it demonstrated the existence of an 'intrinsic factor' from gastric juice.
Pernicious anemia was a fatal disease before about the year 1920, when George
Whipple suggested raw liver as a treatment.[citation needed] The first workable treatment for pernicious
anemia began when Whipple made a discovery in the course of experiments in which he bled dogs
to make them anemic, then fed them various foods to see which would make them recover most
rapidly (he was looking for treatments for anemia from bleeding, not pernicious anemia). Whipple
discovered ingesting large amounts of liver seemed to cure anemia from blood loss, and tried liver
ingestion as a treatment for pernicious anemia, reporting improvement there, also, in a paper in
1920.[citation needed] George Minot and William Murphy then set about to partly isolate the curative
property in liver, and in 1926 showed it was contained in raw liver juice (in the process also showing
it was the iron in liver tissue, not the soluble factor in liver juice, which cured the anemia from
bleeding in dogs); thus, the discovery of the liver juice factor as a treatment for pernicious anemia
had been by coincidence.[citation needed] Frieda Robscheit-Robbins worked closely with Whipple, co-
authoring 21 papers from 1925-30.[citation needed] For the discovery of the cure of a previously fatal
disease of unknown etiology, Whipple, Minot, and Murphy shared the 1934 Nobel Prize in
Medicine.[54][full citation needed]
After Minot and Murphy's verification of Whipple's results in 1926, pernicious anemia victims ate or
drank at least one-half pound of raw liver, or drank raw liver juice, every day.[citation needed] This continued
for several years, until a concentrate of liver juice became available. In 1928, chemist Edwin
Cohn prepared a liver extract that was 50 to 100 times more potent than the natural food (liver).[citation
needed]
The extract could even be injected into muscle, which meant patients no longer needed to eat
large amounts of liver or juice. This also reduced the cost of treatment considerably.[citation needed]
The active ingredient in liver remained unknown until 1948, when it was isolated by two
chemists, Karl A. Folkers of the United States and Alexander R. Todd of Great Britain.[citation needed] The
substance was a cobalamin, which the discoverers named vitamin B12. The new vitamin in liver juice
was eventually completely purified and characterized in the 1950s, and other methods of producing
it from bacteria were developed.[citation needed] It could be injected into muscle with even less irritation,
making it possible to treat PA with even more ease.[citation needed] Pernicious anemia was eventually
treated with either injections or large oral doses of B12, typically between 1 and 4 mg daily.[citation needed]
Mary Todd Lincoln, the wife of American President Abraham Lincoln, had symptoms of pernicious
anemia for at least 25 years, and perhaps 40 years, and died of it.[55]
Iron-deficiency anemia, also spelled iron-deficiency anaemia,[help 1] is anemia caused by a lack of
iron. Anemia is defined as a decrease in the amount of red blood cells (RBCs) or hemoglobin in
the blood.[1] When anemia comes on slowly, the symptoms are often vague and may include feeling
tired, weakness, shortness of breath or poor ability to exercise. Anemia that comes on quickly often
has greater symptoms which may include: confusion, feeling like one is going to pass out, and
increased thirst. There needs to be significant anemia before a person becomes noticeably pale.
There may be additional symptoms depending on the underlying cause.[2][3]
It is caused by insufficient dietary intake and absorption of iron, or iron loss from bleeding. Bleeding
can be from a range of sources such as the intestinal, uterine or urinary tract. The most common
cause of iron-deficiency anemia in children in developing countriesis parasitic worms.[citation
needed]
Worms cause intestinal bleeding, which is not always noticeable in feces, and is especially
damaging to children.[4] Malaria, hookworms and vitamin A deficiency contribute to anemia during
pregnancy in most underdeveloped countries.[5] In women over 50 years old, the most common
cause of iron-deficiency anemia is chronic gastrointestinal bleeding from nonparasitic causes, such
as gastric ulcers, duodenal ulcers or gastrointestinal cancer.
Iron deficiency causes approximately half of all anemia cases worldwide, and affects women more
often than men. Iron-deficiency anemia affected 1.2 billion people in 2013.[6] In 2013 anemia due to
iron deficiency resulted in about 183,000 deaths – down from 213,000 deaths in 1990.[7]

Iron-deficiency anemia is characterized by the sign of pallor (reduced oxyhemoglobin in skin or

mucous membranes), and the symptoms of fatigue, lightheadedness, and weakness. None of the
symptoms (or any of the others below) are sensitive or specific. Pallor of mucous membranes
(primarily the conjunctiva) in children indicates anemia with the best correlation to the actual
disease, but in a large study was found to be only 28% sensitive and 87% specific (with high
predictive value) in distinguishing children with anemia [hemoglobin (Hb) <11.0 g/dl] and 49%
sensitive and 79% specific in distinguishing severe anemia (Hb < 7.0 g/dl).[8] Thus, this sign is
reasonably predictive when present, but not helpful when absent, as only one-third to one-half of
children who are anemic (depending on severity) will show pallor. Iron-deficiency must be diagnosed
by laboratory testing.
Because iron deficiency tends to develop slowly, adaptation occurs and the disease often goes
unrecognized for some time, even years; patients often adapt to the systemic effects that anemia
causes. In severe cases, dyspnea (trouble breathing) can occur. Unusual obsessive food cravings,
known as pica, may develop. Pagophagia or pica for ice has been suggested to be specific, but is
actually neither a specific or sensitive symptom, and is not helpful in diagnosis. When present, it may
(or may not) disappear with correction of iron-deficiency anemia.
Other symptoms and signs of iron-deficiency anemia include:

 Anxiety often resulting in OCD-type compulsions and obsessions

 Irritability or a low feeling
 Angina
 Constipation
 Sleepiness/Hypersomnia
 Tinnitus
 Mouth ulcers
 Palpitations
 Hair loss
 Fainting or feeling faint
 Depression
 Breathlessness
 Twitching muscles
 Pale yellow skin
 Tingling, numbness, or burning sensations
 Missed menstrual cycle
 Slow social development
 Glossitis (inflammation or infection of the tongue)
 Angular cheilitis (inflammatory lesions at the mouth's corners)
 Koilonychia (spoon-shaped nails) or nails that are weak or brittle
 Poor appetite
 Pruritus (itchiness)
 Dysphagia due to formation of esophageal webs (Plummer-Vinson syndrome)
 Insomnia
 Restless legs syndrome[9]
Infant development[edit]
Iron-deficiency anemia for infants in their earlier stages of development may have greater
consequences than it does for adults. An infant made severely iron-deficient during its earlier life
cannot recover to normal iron levels even with iron therapy. In contrast, iron deficiency during later
stages of development can be compensated with sufficient iron supplements. Iron-deficiency anemia
affects neurological development by decreasing learning ability, altering motor functions, and
permanently reducing the number of dopaminereceptors and serotonin levels. Iron deficiency during
development can lead to reduced myelination of the spinal cord, as well as a change in myelin
composition. Additionally, iron-deficiency anemia has a negative effect on physical growth. Growth
hormone secretion is related to serum transferrin levels, suggesting a positive correlation between
iron-transferrin levels and an increase in height and weight. This is also linked to pica, as it can be a
cause.

Cause[edit]
A diagnosis of iron-deficiency anemia then requires further investigation as to its cause. It can be
caused by increased iron demand / loss or decreased iron intake,[10] and can occur in both children
and adults. The cause of chronic blood loss should all be considered, according to the patient's sex,
age, and history, and anemia without an attributable underlying cause is sufficient for an urgent
referral to exclude underlying malignancy. In babies and adolescents, rapid growth may outpace
dietary intake of iron, and result in deficiency without disease or grossly abnormal diet.[10] In women
of childbearing age, heavy or long menstrual periods can also cause mild iron-deficiency anemia.

Parasitic disease[edit]
The leading cause of iron deficiency worldwide is a parasitic disease known as
a helminthiasis caused by infestation with parasitic worms (helminths) such as tapeworms, flukes,
and roundworms).[citation needed] The World Health Organization estimates that "approximately two billion
people are infected with soil-transmitted helminths worldwide."[11] Parasitic worms cause both
inflammation and chronic blood loss.

Blood loss[edit]
Blood contains iron within red blood cells, so blood loss leads to a loss of iron. There are several
common causes of blood loss: Women with menorrhagia (heavy menstrual periods) are at risk of
iron-deficiency anemia because they are at higher-than-normal risk of losing a larger amount blood
during menstruation than is replaced in their diet. Slow, chronic blood loss within the body — such
as from a peptic ulcer, angiodysplasia, a colon polyp or gastrointestinal cancer, excessively heavy
periods — can cause iron-deficiency anemia. Gastrointestinal bleeding can result from regular use of
some groups of medication, such as NSAIDs (e.g. aspirin), anticoagulants such
as clopidogrel and warfarin, although these are required in some patients, especially those with
states causing thrombophilia.

Diet[edit]
The body normally gets the iron it requires from foods. If a person consumes too little iron, or iron
that is poorly absorbed (non-heme iron), they can become iron deficient over time. Examples of iron-
rich foods include meat, eggs, leafy green vegetables and iron-fortified foods. For proper growth and
development, infants and children need iron from their diet, too.[12] A high intake of cow’s milk is
associated with an increased risk of iron deficiency anemia.[13] Other risk factors for iron deficiency
include low meat intake and low intake of iron-fortified products.[13]

Iron absorption[edit]
Iron from food is absorbed into the bloodstream in the small intestine, especially the duodenum and
proximal ileum. Many intestinal disorders can reduce the body's ability to absorb iron. There are
different mechanisms that may be present.
In cases where there has been a reduction in surface area of the bowel, such as in celiac
disease, inflammatory bowel disease or post surgical resection, the body can absorb iron, but there
is simply insufficient surface area.[citation needed]
If there is an insufficient production of hydrochloric acid in the stomach,
hypochlorhydria/achlorhydria can occur (often due to chronic H. pylori infections or long-term proton
pump inhibitor therapy). Ferrous and Ferric iron salts will precipitate out of solution in the bowel
which are poorly absorbed.
In cases where systemic inflammation is present, iron will be absorbed into enterocytes, but due to
the reduction in basolateral ferroportin molecules which allow iron to pass into the systemic
circulation, iron is trapped in the enterocytes and is lost from the body when the enterocytes are
sloughed off.Depending on the disease state, one or more mechanisms may occur.[citation needed]

Pregnancy[edit]
Without iron supplementation, iron deficiency anemia occurs in many pregnant women because their
iron stores need to serve their own increased blood volume as well as be a source of hemoglobin for
the growing fetus, and for placental development.[12]
Other less common causes are intravascular hemolysis and hemoglobinuria.

Mechanism[edit]
Anemia is one result of significant iron deficiency. When the body has sufficient iron to meet its
needs (functional iron), the remainder is stored for later use in all cells, but mostly in the bone
marrow, liver, and spleen. These stores are called ferritin complexes and are part of the human (and
other animals) iron metabolism systems. Ferritin complexes in humans carry about 4500 iron atoms
and form into 24 protein subunits of two different types.[14]

Diagnosis[edit]

Blood smear of a person with iron-deficiency anemia at 40X enhancement

History[edit]
Anemia may be diagnosed from symptoms and signs, but when it is mild, it may not be diagnosed
from mild nonspecific symptoms.
The diagnosis of iron-deficiency anemia will be suggested by appropriate history (e.g., anemia in a
menstruating woman or an athlete engaged in long-distance running), the presence of occult
blood (i.e., hidden blood) in the stool, and often by additional history.[15] For example, known celiac
disease can cause malabsorption of iron. A travel history to areas in which hookworms and
whipworms are endemic may be helpful in guiding certain stool tests for parasites or their eggs.[citation
needed]

Blood tests[edit]
Change in lab values in iron deficiency anemia
 Change Parameter

↓ ferritin, hemoglobin, MCV

↑ TIBC, transferrin, RDW

Anemia is often first shown by routine blood tests, which generally include a complete blood
count (CBC) which is performed by an instrument which gives an output as a series of index
numbers. A sufficiently low hemoglobin (Hb) by definition makes the diagnosis of anemia, and a
low hematocrit value is also characteristic of anemia. Further studies will be undertaken to determine
the anemia's cause. If the anemia is due to iron deficiency, one of the first abnormal values to be
noted on a CBC, as the body's iron stores begin to be depleted, will be a high red blood cell
distribution width (RDW), reflecting an increased variability in the size of red blood cells (RBCs). In
the course of slowly depleted iron status, an increasing RDW normally appears even before anemia
appears.
A low mean corpuscular volume (MCV) often appears next during the course of body iron depletion.
It corresponds to a high number of abnormally small red blood cells. A low MCV, a low mean
corpuscular hemoglobin or mean corpuscular hemoglobin concentration, and the appearance of the
RBCs on visual examination of a peripheral blood smear narrows the problem to a microcytic
anemia (literally, a "small red blood cell" anemia). The numerical values for these measures are all
calculated by modern laboratory equipment.
The blood smear of a person with iron deficiency shows many hypochromic (pale and relatively
colorless) and rather small RBCs, and may also show poikilocytosis (variation in shape)
and anisocytosis (variation in size). With more severe iron-deficiency anemia, the peripheral blood
smear may show hypochromic pencil-shaped cells, and occasionally small numbers of nucleated red
blood cells.[16] Very commonly, the platelet count is slightly above the high limit of normal in iron
deficiency anemia (this is mild thrombocytosis). This effect was classically postulated to be due to
high erythropoietin levels in the body as a result of anemia, cross-reacting to
activate thrombopoietin receptors in the precursor cells that make platelets; however, this process
has not been corroborated. Such slightly increased platelet counts present no danger, but remain
valuable as an indicator even if their origin is not yet known.[citation needed]
Body-store iron deficiency is diagnosed by tests such as a low serum ferritin, a low serum iron level,
an elevated serum transferrin and a high total iron binding capacity. A lowserum ferritin is the
most sensitive lab test for iron deficiency anemia. However, serum ferritin can be elevated by any
type of chronic inflammation and so is not always a reliable test of iron status if it is within normal
limits (i.e. this test is meaningful if abnormally low, but less meaningful if normal).
Serum iron levels (i.e. iron not part of the hemoglobin in red cells) may be measured directly in the
blood, but these levels increase immediately with iron supplementation (the patient must stop
supplements for 24 hours), and pure blood-serum iron concentration, in any case, is not as sensitive
as a combination of total serum iron, along with a measure of the serum iron-binding protein levels
(TIBC). The ratio of serum iron to TIBC (called iron saturation or transferrin saturation index or
percent) is the most specific indicator of iron deficiency when it is sufficiently low. The iron saturation
(or transferrin saturation) of < 5% almost always indicates iron deficiency, while levels from 5% to
10% make the diagnosis of iron deficiency possible but not definitive. A transferrin saturation of 12%
or more (taken alone) makes the diagnosis unlikely. Normal saturations are usually slightly lower for
women (>12%) than for men (>15%), but this may indicate simply an overall slightly poorer iron
status for women in the "normal" population.[citation needed]
Iron-deficiency anemia and thalassemia minor present with many of the same lab results. It is very
important not to treat a people with thalassemia with an iron supplement, as this can lead
to hemochromatosis (accumulation of iron in various organs, especially the liver). A hemoglobin
electrophoresis provides useful evidence for distinguishing these two conditions, along with iron
studies.[citation needed]

Screening[edit]
It is unclear if screening pregnant women for iron deficiency during pregnancy improves outcomes in
the developing world.[17]

Gold standard[edit]
Conventionally, a definitive diagnosis requires a demonstration of depleted body iron stores obtained
by bone marrow aspiration, with the marrow stained for iron.[18][19] Because this is invasive and
painful, while a clinical trial of iron supplementation is inexpensive and not traumatic, patients are
often treated based on clinical history and serum ferritin levels without a bone marrow biopsy.
Furthermore, a study published April 2009[20] questions the value of stainable bone marrow iron
following parenteral iron therapy.

Treatment[edit]
This section needs more medical references for verification or
relies too heavily on primary sources. Please review the contents
of the section and add the appropriate references if you can.
Unsourced or poorly sourced material may be challenged
and removed. (July 2016)

See also: Lucky iron fish

Anemia is sometimes treatable, but certain types of anemia may be lifelong. If the cause is a dietary
iron deficiency, eating more iron-rich foods, such as beans, lentils or red meat, or taking iron
supplements will usually correct the anemia. Alternatively, intravenous iron (or blood transfusions)
can be administered.

Ascorbic acid

The difference between iron intake and iron absorption, also known as bioavailability, can be great.
Iron absorption problems are worsened when iron is taken in conjunction with milk, tea, coffee and
other substances. A number of methods that can help mitigate this, including:

 Fortification with ascorbic acid increases bioavailability in both presence and absence of
inhibiting substances, but is subject to deterioration from moisture or heat. Ascorbic acid
fortification is usually limited to sealed, dried foods, but individuals can easily take ascorbic acid
with a basic iron supplement for the same benefits. The primary benefit over ascorbic acid is
durability and shelf life, particularly for products like milk, which undergo heat treatment.
 Microencapsulation with lecithin binds and protects the iron particles from the action of inhibiting
substances.
 Using an iron amino acid chelate, such as NaFeEDTA, similarly binds and protects the iron
particles. A study by the hematology unit of the University of Chile indicated chelated iron
(ferrous bis-glycine chelate) can work with ascorbic acid to achieve even higher absorption
levels.
 Separating intake of iron and inhibiting substances by a few hours
 Using nondairy milk (such as soy, rice, or almond milk) or goats' milk instead of cows' milk
 Gluten-free diets can resolve some instances of iron-deficiency anemia if it is a result of celiac
disease.
 Heme iron, found only in animal foods, such as meat, fish, and poultry, is more easily absorbed
than nonheme iron, found in plant foods and supplements.[21][22]
Iron bioavailability comparisons require stringent controls because the largest factor affecting
bioavailability is the subject's existing iron level. Informal studies on bioavailability usually do not take
this factor into account, so exaggerated claims from health supplement companies based on this
sort of evidence should be ignored. Scientific studies are still in progress to determine which
approaches yield the best results and the lowest costs.
If anemia does not respond to oral treatments, it may be necessary to administer
iron parenterally using a drip or hemodialysis. Parenteral iron involves risks of fever, chills,
backache, myalgia, dizziness, syncope, rash, and with some preparations, anaphylactic shock. The
total incidence of adverse events is much lower than that with oral tablets (where the dose needs to
be reduced or treatment stopped in over 40% of subjects) and blood transfusions.
A follow-up blood test is important to demonstrate whether the treatment has been effective; it can
be undertaken after two to four weeks. With oral iron, this usually requires a delay of three months
for tablets to have a significant effect.

Iron supplementation and infection risk[edit]

Because one of the functions of elevated ferritin (an acute phase reaction protein) in acute infections
is thought to be to sequester iron from bacteria, it is generally thought thatParenteral
iron supplementation (which circumvents this mechanism) should be avoided in patients who have
active bacterial infections bacteraemia. Replacement of iron stores is seldom such an emergency
situation that it cannot wait for such infections to be treated, although occasionally cases will arise
where this is not possible, such as chronicosteomyelitis.
Iron deficiency protects against infection by creating an unfavorable environment for bacterial
growth. Some studies have found iron supplementation can lead to an increase ininfectious
disease morbidity in areas where bacterial infections or where malaria are common. For example,
children receiving iron-enriched foods have demonstrated an increased rate in diarrhea overall and
enteropathogen shedding. Nevertheless, while iron deficiency might lessen infections by certain
pathogenic diseases, it also leads to a reduction in resistance to other strains of viral or bacterial
infections, such as Salmonella typhimurium or Entamoeba histolytica. Overall, it is sometimes
difficult to decide whether iron supplementation will be beneficial or harmful to an individual in an
environment prone to many infectious diseases; however, this is a different question than the
question of supplementation in individuals who are already ill with a bacterial infection.[citation needed]

Iron replacement[edit]
When adjusting daily iron supplementation regimens, lowering the daily iron dose requires a longer
duration of therapy. The estimated total dose of elemental iron may be used to guide therapy, and
replacement may be provided in cycles. Based on this approach, the person should participate in
their own care by determining the iron formulation and dose schedule that they are able to tolerate.
The amount of elemental iron that is absorbed in the gut is not constant, and can change
significantly depending on several factors, including hemoglobin level and body iron stores. The
amount of iron absorbed decreases as the iron deficiency is corrected. Therefore, it is not possible to
predict the exact amount of iron that will be absorbed, but it is recommended that approximately
10%-20% of an oral iron dose will be absorbed in the beginning of the therapy.
For ferrous sulfate, one cycle consists of 75 pills or three pills daily for 25 days. Among people with
moderate levels of anemia, a single cycle of should be enough and partial replacement of iron
stores. If the anemia is not severe and there is no complicating feature such as ongoing blood loss
or enteropathies, additional iron supplementation cycles are not going to be required for correcting
the anemia. Re-evaluation of the anemia after completion of the first cycle should be performed to
see if additional iron supplementation is necessary. If a person is predicted to have ongoing iron
deficits (e.g. menorrhagia), maintenance dosing of iron supplements can easily be devised. The key
feature of the cycled dosing strategy proposed here is that several factors including the cause of iron
deficiency Anemia, the total iron deficit, replacement iron formulations, and the predicted duration of
replacement therapy are integrated for implementation of an individualized therapeutic plan.[23]

Epidemiology[edit]

Deaths due to iron-deficiency anaemia per million persons in 2012

0-0

1-1

2-3

4-5

6-8

9-12

13-19

20-30

31-74

75-381
Disability-adjusted life year for iron-deficiency anemia per 100,000 inhabitants in 2004.[24]

no data

less than 50

50-100

100-150

150-200

200-250

250-300

300-350

350-400

400-450

450-500

500-1000

more than 1000

A moderate degree of iron-deficiency anemia affected approximately 610 million people worldwide or
8.8% of the population.[25] It is slightly more common in female (9.9%) than males (7.8%).[25] Mild iron
deficiency anemia affects another 375 million.[25]
Within the U.S iron-deficiency anemia affects about 2% of adult males, 10.5% of Caucasian women,
and 20% of African-American and Mexican-American women.[26]

Notes[edit]
1. Jump up^ The anemia and anaemia difference is a regional variation; the hyphen is optional (several
major dictionaries use it and several do not).
Treating anemia entails treating the condition of low haemoglobin and red blood cells in
blood as well as detecting and treating the disease process that has led to the anemia.

Unless the underlying cause of anemia, which may be continuous blood loss, haemolytic
anemias, iron deficiency or increased demand states like pregnancy, are assessed and
managed, the treatment remains incomplete.

Types of treatment for anemia

Treatment of anemia may depend on what type of anemia the patient has. (1-6)–

Iron deficiency anemia treatment

This usually involves taking iron supplements to replace the lack of intake of iron in diet or
excess loss of iron.

The most commonly prescribed supplement is ferrous sulphate. It is taken as pills two or
three times a day.

Oral iron preparations come with a host of side effects that include nausea, vomiting,
abdominal pain, heartburn, constipation, diarrhea, black stool and blackening of teeth,
gums and tongue.

Taking ferrous sulphate along with food or shortly after eating helps to reduce the side
effects.

Another alternative is ferrous gluconate.

Iron can be replaced by taking diet rich in iron. This includes dark-green leafy vegetables,
iron-fortified bread and cereal, beans, meat, nuts, apricots, prunes, raisins, dates etc.

Tea, coffee, calcium, found in dairy products such as milk, antacids etc. reduce the iron
absorption from the gut and should be avoided.

Vitamin C supplements helps absorb iron better. Patient is checked up after two to four
weeks to see if there is a response.

Vitamin B12 deficiency anaemia treatment

This can be treated by injections of vitamin B12. The vitamin is in the form of a substance
known as hydroxocobalamine. The injections are given on alternate days for two weeks.

If there is a dietary lack of the vitamin, tablets may be prescribed. Vitamin B12 can be
found in meat, milk, eggs, salmon etc.

Vegetarians or vegans may need supplementation as tablets or fortified cereals or soy

products.

Anemia due to folate deficiency

For folate deficiency anemia daily folic acid tablets are prescribed.

Folate tablets are usually prescribed along with Vitamin B12 supplements. This is because
folic acid treatment can sometimes improve the symptoms masking an underlying vitamin
B12 deficiency.

If a vitamin B12 deficiency is not detected and treated at this stage there could be severe
damage to the brain, nerves and spinal cord due to vitamin B12 deficiency.

Folate is found in broccoli, green cabbage, wheatgerm, pulses, nuts, green leafy vegetables
etc.

Treatment for severe anemia

When the anaemia is more severe, a blood transfusion is often necessary.

Sickle cell anemia treatment

Patients with sickle cell anemia need a healthy diet, supplements of folic acid, vitamin D and
zinc and avoid triggers for crises.

This includes smoking, alcohol, overexertion, dehydration, cold and hot temperatures,
constricting clothes etc.

There is no cure for sickle cell anaemia, but the frequency and severity of crises and their
complications can be reduced. They need complete vaccinations against flu, pneumococcus
meningitis, Hepatitis B and other diseases to prevent infections.

Anemia due to infection

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Anemia caused by an infection will usually improve when the infection is treated. This is
especially true for newborns with severe infections called sepsis.

Treatment for an enlarged spleen

In some forms of haemolytic anemia there may be an enlarged spleen.

The spleen may be surgically removed to prevent RBCs from being removed from circulation
or destroyed too rapidly.

Anemia in pregnancy
If the hemoglobin concentration is less than 9.0 g per dL anemia in pregnancy is diagnosed.
Anemia is managed with oral dose of 60 to 120 mg per day of iron. Patient is evaluated
after four weeks of therapy.

Anemia and bone marrow treatment

Some medications are prescribed to stimulate the bone marrow to produce more RBCs. This
is useful in aplastic anemia and leukemias.

Bone marrow transplantation may also be used. In this procedure, bone marrow cells taken
from a matching donor (usually with a genetic match e.g. a sibling or blood relation).

This is then injected into the vein. This then travels through the bloodstream to the bone
marrow and produced new blood cells.

Prevention of anemia

Prevention of anemia (4):

 In infants and preschool children anemia can be prevented by encouraging exclusive

breast feeding of infants (without supplementary liquids, water, formula or food) for
four to six months after birth.

During weaning from the breast to solids additional source of iron (approximately 1
mg per kg per day of iron) should be introduced in supplementary foods. If the infant
is not breast fed, only an iron-fortified formula as a substitute for breast milk is
recommended.

In breast fed infants who have iron deficient diet 1 mg per kg per day of iron drops
are recommended if not supplemented in other foods.

Since milk hampers the absorption of iron from gut, it should be suggested that
children aged one to five years need no more than 24 oz of cow's milk, goat's milk
and soy milk per day.

Foods rich in vitamin C (e.g., fruits, vegetables and juice) are recommended beyond
six months to increase iron absorption.

 For adolescent girls and women prevention of iron deficiency includes a healthy iron
rich diet. All adolescent girls and nonpregnant women need to be screened for
anemia every five to 10 years until menopause.
 In pregnancy oral low-dose (30 mg per day) supplements of iron at the first prenatal
visit may be started to prevent anemia. Pregnant women are encouraged to eat iron-
rich foods and foods that enhance iron absorption.