Download iron rich foods

Iron-deficiency anemia (or iron-deficiency anaemia)
is a common anemia (low red blood cell or hemoglobin
levels) caused by insufficient dietary intake and
absorption of iron, and/or iron loss from bleeding which
can originate from a range of sources such as the
intestinal, uterine or urinary tract.
Iron deficiency causes approximately half of all anemia
cases worldwide, and affects women more often than
men. World estimates of iron deficiency occurrence are
somewhat vague, but the true number probably exceeds
one billion people. This can result if:
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The body does not make enough red blood cells
Bleeding causes loss of red blood cells more
quickly than they can be replaced
The most significant cause of iron-deficiency anemia in
developing world children is parasitic worms:
hookworms, whipworms, and roundworms. Worms
cause intestinal bleeding, which is not always
noticeable in faeces, and is especially damaging to
growing children.[ Malaria, hookworms and vitamin A
deficiency contribute to anemia during pregnancy in
most underdeveloped countries. 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.
Anemia is one result of advanced-stage 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.[4]
Signs and symptoms
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 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).[5] 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. Irondeficiency 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 anaemia 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:
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Anxiety often resulting in OCD-type compulsions
and obsessions
Irritability or a low feeling
Angina
Constipation
Sleepiness
Tinnitus
Mouth ulcers
Palpitations
Hair loss
Fainting or feeling faint
Depression
Breathlessness
Twitching muscles
Pale yellow skin
Tingling, numbness, or burning sensations
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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[6]
Infant development
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. Irondeficiency anemia affects neurological development by
decreasing learning ability, altering motor functions,
and permanently reducing the number of dopamine
receptors 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
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,
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 anaemia
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. In women of
childbearing age, heavy or long menstrual periods can
also cause mild iron-deficiency anemia.
Parasitosis
The leading cause of iron deficiency worldwide is
infestation with parasitic worms (hookworms,
whipworms, roundworms). Estimates of infection in the
world population vary from a minimum of a billion
humans to as many as 5 or 6 billion. Paracitic worms
cause both inflammation as well as chronic blood loss.
Blood loss
Blood contains iron within red blood cells. So if a
person loses blood, he or she will lose some iron. There
are several common causes of blood loss: Women with
menorrhagia (heavy periods) are at risk of iron
deficiency anemia because they lose a larger amount
blood during menstruation than is replaced from their
diet. Slow, chronic blood loss within the body — such
as from a peptic ulcer, angiodysplasia, a colon polyp or
gastrointestinal cancer — can cause iron-deficiency
anemia. Gastrointestinal bleeding can result from
regular use of some groups of medication, such as non
steroidal anti inflammatory drugs (NSAIDs) e.g.
Aspirin, anticoagulants such as clopidogrel and
warfarin although these are required in some patients,
especially those with states causing thrombophilia.
A lack of iron in the diet
The body regularly gets iron from the foods eaten. If a
person consumes too little iron, or iron that is poorly
absorbed (non-heme iron), over time the body can
become iron-deficient. Examples of iron-rich foods
include meat, eggs, leafy green vegetables and ironfortified foods. For proper growth and development,
infants and children need iron from their diet, too.
An inability to absorb iron
Iron from food is absorbed into the bloodstream in the
small intestine, especially the duodenum and proximal
illeum. Many intestinal disorders can reduce the body's
ability to absorb iron. There are different mechanisms
that be present.
In cases where there has been a reduction in surface
area of the bowel, such as in celiac disease, inflamatory
bowel disease or post surgical resection the body can
absorb iron, but there is simply insiffucient surface area.
If there is insufficient production of hydrochloric acid
in the stomach, hypochlorhydria/achlorhydria (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 both mechanism
may occur.
Pregnancy
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.
Other less common causes are intravascular hemolysis
and hemoglobinuria.
Diagnosis
Anemia may be diagnosed from symptoms and signs,
but when it is mild, it may not be diagnosed from mild
nonspecific symptoms. Pica, an abnormal craving for
dirt, ice, or other "odd" foods occurs variably in iron
and zinc deficiency, but is neither sensitive or specific
to the problem, so is of little diagnostic help
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, 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 and/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.
Blood smear of a patient with iron-deficiency anemia at
40X enhancement
The blood smear of a patient 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 target cells,
hypochromic pencil-shaped cells, and occasionally
small numbers of nucleated red blood cells.[9] 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.
The diagnosis of iron-deficiency anemia will be
suggested by appropriate history (e.g., anemia in a
menstruating woman or an athlete engaged in longdistance running), the presence of occult blood (i.e.,
hidden blood) in the stool, and often by other history.[10]
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.
Body-store iron deficiency is diagnosed by diagnostic
tests, such as a low serum ferritin, a low serum iron
level, an elevated serum transferrin and a high total iron
binding capacity. A low serum 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 ironbinding 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. Saturations over 12% (taken alone)
make 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.
Change in lab values in iron deficiency anemia
Change
Parameter
Decrease
ferritin, hemoglobin, MCV
Increase
TIBC, transferrin, RDW
Iron-deficiency anemia and thalassemia minor present
with many of the same lab results. It is very important
not to treat a patient 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.
Gold standard
Conventionally, a definitive diagnosis requires a
demonstration of depleted body iron stores obtained by
bone marrow aspiration, with the marrow stained for
iron. 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 questions the value of stainable bone marrow iron
following parenteral iron therapy.
Treatment
Anemia is sometimes treatable, but certain types of
anemia may be lifelong. If the cause is dietary iron
deficiency, eating more iron-rich foods, such as beans,
lentils or red meat, or taking iron supplements, usually
with iron(II) sulfate, ferrous gluconate, or iron amino
acid chelate ferrous bisglycinate, or synthetic chelate
NaFerredetate EDTA, will usually correct the anemia.
Alternatively, intravenous iron can be administered.
Recent research suggests the replacement dose of iron,
at least in the elderly with iron deficiency, may be as
little as 15 mg per day of elemental iron. An experiment
done in a group of 130 anemia patients showed a 98%
increase in iron count when using an iron supplement
with an average of 100 mg of iron. Women who
develop iron deficiency anemia in midpregnancy can be
effectively treated with low doses of iron (20–40 mg
per day). The lower dose is effective and produces
fewer gastrointestinal complaints. The body apparently
adapts to oral iron supplementation, so iron is often
effectively started at a comparatively low dose, then
slowly increased.
The difference between iron intake and iron absorption,
also known as bioavailability, can be great. Scientific
studies indicate 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:
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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
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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.[14][15]
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 essential 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
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 that Parenteral 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 chronic
osteomyelitis.
Iron deficiency protects against infection by creating an
unfavorable environment for bacterial growth. Some
studies have found iron supplementation can lead to an
increase in infectious 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.
Epidemiology
Disability-adjusted life year for iron-deficiency anemia
per 100,000 inhabitants in 2004.[16]
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.[17] It is slightly more common in
female (9.9%) than males (7.8%).[17] Mild iron
deficiency anemia affects another 375 million.
IRON RICH FOODS
The best way to prevent and treat anemia is to consume
iron rich foods. The treatment of anemia may also be
successful with the usage of iron supplements. When it
comes to iron-rich nutrition, we can recognize two
types of iron:
Heme iron: Iron found in hemoglobin in blood,
therefore red meat
Non-heme iron: Iron found in vegetables, dairy
products and eggs
Non-heme iron: (iron found in vegetables) is harder to
absorb than heme iron (found in meat) and that is why
vegetarians are at a greater risk of developing iron
deficiency anemia.
Iron rich foods that are good sources of heme iron
include:
- Beef, chicken and pork liver
- Clams and oysters
- Fish and shrimp
- Turkey, chicken, beef and pork
Iron rich foods that are good sources of non-heme
iron include:
- Fortified cereals, grains and pasta
- Beans and lentils
- Pumpkin seeds
- Canned beans
Today we are able to choose between a variety of iron
rich foods and even the picky ones have an opportunity
to have a healthy nutrition. First we will start by
mentioning the best ones:
TOP TEN IRON RICH FOODS
- Red meat
- - Turkey and chicken
- Iron fortified foods (grains and cereals)
- Dark green vegetables such as spinach and kale
- Beans (kidney, lima, navy etc.) soybeans and lentils
- Liver
- Egg yolks
- Seafood such as fish, oysters, clams and shrimp
Not only do we have a plentiful of iron rich foods today
but we also have iron fortified foods. These foods
contain iron that has been added to them and they are
especially good when it comes to “picky eaters” since
some of the natural resources of iron may sometimes
appear tasteless. These foods include:
- Cereals
- Oatmeal
- Pasta
- Iron fortified bread
There are many other iron fortified foods as well, so
make sure you look for them on labels while shopping
for groceries.But why should we stop here. As we
mentioned before there is a variety of choices when it
comes to iron rich foods. For example: nuts, hazelnuts
and almonds are a good source of iron and we can add
curry, rosemary, cinnamon and sesame seeds to our
daily diet to improve iron levels in our body. There are
also many vegetables that can be added to this list of
iron-rich foods and they include broccoli, parsley,
brussel sprouts, swiss chard etc.
The biggest intake of iron is necessary during
pregnancy, childhood and adolescence. These are the
most sensitive stages of life and proper nutrition is the
key for preventing anemia. Women in pregnancy, for
example, need up to 27 mg of iron in their daily diet so
it is crucial for them to eat iron rich foods, not only for
them to be healthy, but for the baby’s development as
well. Women who have two pregnancies close together
or are pregnant with more than one child are at a greater
risk for having anemia if they are not careful during
their pregnancy.
Iron from iron rich foods is best absorbed if those foods
are consumed with vitamin C. And it is best if these two
are combined together in your meals.
Here are some foods rich in vitamin
C:
- Citrus fruit
- Green vegetables
- Apples
- Bananas
- Fortified juices
- Green vegetables
Proper nutrition is especially important for persons who
have lost larger amounts of blood. This is why women
need more iron during their periods. The dominating
iron – rich foods in their nutrition should be fish, red
meat, clams and oysters, dried fruit and beans. Some
iron – rich foods are not only rich in iron, but they are
also rich in copper which helps enormously with the
absorption of iron. These foods include seafood, liver,
green vegetables, dried figs, apricots, etc.
You should note that it is best not to eat whole grains,
which are rich in iron, in combination with other iron
rich foods since they contain phytates that decrease iron
absorption through food. The same note goes for
spinach, which is rich in oxalate substances which
decrease the absorption of iron.
Unvarying nutrition, an exaggerated use of alcohol and
coffee, vegetarianism, drastic diets for losing weight
and an insufficient intake of iron through food are all
possible causes of iron deficiency anemia. The
consummation of groceries rich in vitamin C enlarges
the absorption of iron, and it is highly recommendable
to use vitamin C supplements (up to 2g daily). It would
be best if every meal contained fish or meat and vitamin
C.
Anemic persons should also spend much time in fresh
air and walk at least one hour daily. Diverse nutrition, a
regular intake of fresh fruits and vegetables as well as
minimal consummation of alcohol, coffee, cocoa,
aerated drinks and tea, are the best way to prevent
anemia. If the iron intake through food is not sufficient,
people suffering from anemia may also use
supplements, which work best if taken on an empty
stomach. Some may also use vitamin B and vitamin C
supplements in addition to the corresponding therapy
recommended by their doctor.
You can combine iron – rich foods into many delicious
meals. You can take fresh apples beetroot and carrots
and make a tasteful juice out of them by adding honey.
Nettle is also very useful as you can make a salad out of
it which you can combine with lemon juice and olive oil
or you can drink nettle tea which is also very useful in
fighting anemia.
If you suspect that you have anemia, you should
definitely talk to your doctor because sometimes an
underlying illness may be the cause of your anemia.
You should also be very careful with food allergies
since some of the mentioned iron–rich foods may pose
a threat of an allergic reaction. For example, many
people are allergic to nuts and seafood and this is
especially important to know when it comes to children
since they are the most sensitive age group.
Children and toddlers also consume a lot of milk, and
dairy products are not that good for the absorption of
iron through iron–rich foods, so they are a risk factor
for iron deficiency anemia. Toddlers need about 7 to 10
mg of iron a day which is a lot less from the needs of 18
mg in adults so you should be careful, when giving iron
rich foods to your child, not to exaggerate since too
much iron can be toxic and very dangerous for
children.
IRON RICH BABY FOODS
The most important thing to remember when it comes
to your child’s healthy nutrition is that iron is best
absorbed when combined with vitamin C. Foods that
are high in vitamin C help with the absorption of non
heme iron and this is very useful, especially when it
comes to children. Having this in mind, you can easily
combine meals for your child. For example, cereals
with fruit rich in vitamin C, or with vitamin C fortified
juices is certainly a good choice for breakfast. Here you
have iron from the cereals and vitamin C from the fruit
or juice which makes it a great combination.
At first, your newborn will receive all the amounts of
iron it needs through breast milk which also contains
vitamin C. Later your child will have the need for
additional iron which can be compensated through iron
fortified baby cereal. From this point your child will
need extra iron which you can find in iron rich baby
foods so make sure you check food labels in order to
find the best of them. You can make iron rich baby
foods in your own kitchen as well. Choose the best iron
rich foods and turn them into mash or adjust the
portions to your child’s needs.
Rho(D) Immune Globulin is a medicine given by
intramuscular injection that is used to prevent the
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.immunological condition known as Rhesus disease (or
hemolytic disease of newborn). The medicine is a
solution of IgG anti-D (anti-RhD) antibodies that
suppresses the mother's immune system from attacking
Rh-positive blood cells which have entered the maternal
blood stream from fetal circulation. In a Rhesus
negative mother Rho(D) Immune Globulin can prevent
temporary sensitization of the maternal immune system
to Rh D antigens, which can cause rhesus disease in the
current or in subsequent pregnancies. With the
widespread use of Rho(D) Immune Globulin, Rh
disease of the fetus and newborn has almost
disappeared. The risk that a D-negative mother can be
alloimmunized by a D-positive fetus can be reduced
from approximately 16% to less than 0.1% by the
appropriate administration of RhIG.,
Rho(D) Immune Globulin is composed of IgG
antibodies and therefore is able to cross the placenta. In
rare cases this can cause a baby to have a weakly
positive DAT (direct antiglobulin test) due to
sensitization of fetal cells from mothers who have
received multiple doses of Rho(D) Immune Globulin.
However, no treatment is necessary as the clinical
course is benign.
History
The first Rho(D) Immuno Globulin treatment
"RhoGAM" was introduced by Ortho-Clinical
Diagnostics, a subsidiary holding of Johnson and
Johnson, and was first administered on May 29, 1968 to
a woman in Teaneck, NJ.
In 1996 ZLB Bioplasma (part of CSL Behring) was
given approval to sell Rhophylac in Europe, and in
2004 Rhophylac was approved in the United States.
Manufacturing and prion transmission
Rho(D) Immune Globulin is a derivative of human
plasma. In the manufacturing process steps are taken to
eliminate bacterial and viral contamination. The most
common way anti-D products are manufactured is by a
form of the Cohn cold ethanol fractionation method
developed in the 1950s. Variations of the Cohn method
developed in the 1950s may not completely clear
aggregates of immunoglobulins, which can cause
problems for patients if administered intravenously, and
is a primary reason why most anti-Ds are for
intramuscular use only. A non-Cohn manufacturing
variation is ChromaPlus process approved by the U.S.
Food and Drug Administration (FDA) that is used to
make Rhophylac.[8] Rho(D) immune globulin may
trigger an allergic reaction, and there is the possibility
of transmission of Creutzfeldt-Jakob disease as a
residual risk.
Antepartum Administration
In a pregnancy where the mother is D-negative and the
father is D-positive, there is a 50% chance that the fetus
will be D-positive and the mother is therefore at risk for
D alloimmunization. These women are candidates for
RhIG prophylaxis.
The medication has an FDA Pregnancy Category C. It
is given by intramuscular injection as part of modern
routine antenatal care at about 28 weeks of pregnancy,
as recommended by the American College of
Obstetricians and Gynecologists (ACOG). The '28
weeks' recommendation comes from the fact that it has
been observed that 92% of women who develop an antiD during pregnancy do so at or after 28 weeks
gestation.
RhIG should also be given after antenatal pathological
events that are likely to cause a feto-maternal
hemorrhage. Applicable 'pathologic events' include
accidents which may induce fetomaternal hemorrhage
(motor vehicle accidents, falls, abdominal trauma),
following procedures during pregnancy, and following
spontaneous or therapeutic abortions.
Postpartum Administration
A D-negative mother who is not alloimmunized to D
should also receive an appropriate dose of RhIG after
delivery of a D-positive infant. After delivery, a cord
blood sample from infants born to D-negative mothers
should be tested for the D antigen. If the neonate is Dnegative, no further RhIG is needed. However, if the
infant is D-positive, the mother should have a
postpartum blood sample screened for fetomaternal
hemorrhage in order to determine the appropriate
dosage of RhIG to be administered. (the presence of
residual anti-D from antepartum RhIG administration
does NOT indicate ongoing protection from
alloimmunization- repeat administration of RhIG is
necessary).
The rosette test (see: erythrocyte rosetting) is a sensitive
method to detect fetomaternal hemorrhage of 10 cc or
more. A rosette test will be positive if fetal D-positive
cells are present in the maternal sample, indicating a
significantly large fetomaternal hemorrhage has
occurred. A rosette test may be falsely positive if the
mother is positive for the weak D phenotype and falsely
negative if the neonate is weak D. (See Rh Blood Group
System section on Weak D:
If the rosette test is negative, then a dose of 300
micrograms of RhIG is given (sufficient to prevent
alloimmunization after delivery in 99% of cases)., The
RhIG dose suppresses by up to 30 cc of whole blood.
If a fetomaternal hemorrhage in excess of 30 cc has
occurred, additional testing is mandatory in order to
determine the appropriate dosage of RhIG to prevent
alloimmunization. A positive rosette test should be
followed by a quantitative test such as the KleihauerBetke test (acid/elution) or an alternative approach such
as flow cytometry. See article on Kleihauer-Betke test
for details on how the volume of fetomaternal
hemorrhage is calculated.
The dosage of RhIG is calculated from the volume of
fetal hemorrhage (in mL). Ex: 50 mL fetal hemorrhage /
30 ml = 1.667 (round up to 2) then add 1 = 3 vials of
RhIG.
Postpartum RhIG should be administered within 72
hours of delivery. If prophylaxis is delayed, the
likelihood that alloimmunization will be prevented is
decreased. However, ACOG still recommends that
RhIG be administered because partial protection still
occurs., If the D-type of a newborn or stillborn is
unknown or cannot be determined, RhIG should be
administered.
Immune Thrombocytopenia (ITP)
Primary Immune Thrombocytopenia (ITP) is an
acquired immune mediated disorder characterized by
isolated thrombocytopenia, defined as a peripheral
blood platelet count less than 100 x 109/L, and the
absence of any obvious initiating and/or underlying
cause of the thrombocytopenia. Symptoms of ITP
include abnormal bleeding and bruising due to the
reduction in platelet count. Rho(D) Immune Globulin
Intavenous [Human; Anti-D] is indicated for use in nonsplenectomized, Rho(D)-positive children with chronic
or acute ITP, adults with chronic ITP, and children and
adults with ITP secondary to HIV infection. Anti-D
must be administered via the intravenous route when
used in clinical situations requiring an increase in
platelet count. The mechanism of action of anti-D is not
fully understood however, after administration the antiD coated red blood cell complexes saturate Fcγ
receptors sites on macrophages, resulting in preferential
destruction of red blood cells (RBCs), therefore sparing
antibody-coated platelets.[21] Anti-D is recommended as
a first-line therapy for ITP, along with corticosteroids
and intravenous immune globulin (IVIG).[22][23] WinRho
SDF is an anti-D manufactured, distributed and
marketed by Cangene Corporation in the US.
Contraindications
The following females are NOT candidates for RhIG:



D-negative females whose infant is known to be Dnegative
D-negative females who have been previously
alloimmunized to D (they have an anti-D antibody)
Any D-positive females (NOTE: women who test
positive for the weak D phenotype should be
considered D-positive and not receive RhIG.
Rhophylac manufactured by CSL Limited Brand
names
. RhoGAM and MICRhoGam are brand names of
Johnson and Johnson. Other brand names are: BayRHoD, Gamulin Rh, HypRho-D Mini-Dose, Mini-Gamulin
Rh, WinRho SDF (Cangene), Partobulin SDF (Baxter)
and Rhesonativ (Octapharma). RhesuGam (NBI)
Routes of Administration
RhIG can be administered either by either intramuscular
(IM) or intravenous (IV) injection, depending on the
preparation. The IM-only preparation should never be
administered IV due to the risk of complement system
activation. Multiple IM doses should be given at
different sites or at different times within the 72 hour
window. Or, multiple IV doses can be administered
according to the instructions in the package insert.
RhoGAM (rhod immune globulin human) ® and
MICRhoGAM (rhod immune globulin human) ®
Rho(D) Immune Globulin (Human) are sterile solutions
containing IgG anti-D (anti-Rh) for use in preventing
Rh immunization. They are manufactured from human
plasma containing anti-D. A single dose of RhoGAM
(rhod immune globulin human) contains sufficient antiD (approximately 300 μg or 1500 IU)* to suppress the
immune response to 15 mL (or less) of Rh-positive red
blood cells. A single dose of MICRhoGAM (rhod
immune globulin human) contains sufficient anti-D
(approximately 50 μg or 250 IU)* to suppress the
immune response to 2.5 mL (or less) of Rh-positive red
blood cells.
Rho(D) Immune Globulin (Human) intended for
intramuscular use and prepared by cold alcohol
fractionation has not been reported to transmit hepatitis
or other infectious diseases.7