IRON DEFICIENCY ANEMIA IN PREGNANCY

Nyoman Arya Adi Wangsa

030.09.177

FACULTY OF MEDICINE TRISAKTI UNIVERSITY

JAKARTA
DECEMBER 7, 2012

CONTENTS
PREFACE

................................................................................................. 1

CONTENTS ................................................................................................. 2
ABSTRACT ................................................................................................. 3
CHAPTER I
I.I

INTRODUCTION

..................................................................................... 4

CHAPTER II
II.I

IRON METABOLISM

..5

II.II

IRON DEFICIENCY ANEMIA

..8

CHAPTER III
III.I

IRON

DEFICIENCY

ANEMIA

IN

PREGNANCY

12
CONCLUSION

.................................................................................20

REFERENCES

.................................................................................................21

ABSTRACT
Anemia is one of the four major problem in Indonesia that experienced by approximately 51% of
pregnant women. According to WHO, anemia in pregnancy is the cause of 40% of deaths of
mothers in developing countries such as Indonesia. In addition to the mother, anemia in
pregnancy also adversely affects to the fetus. Deficiency of nutrients have been suggested as the
most common cause of anemia. About 75% of anemia in pregnancy caused by iron deficiency.
WHO reported the prevalence of pregnant mothers who experience iron deficiency approximately
35-75% and increases as you age pregnancy. This is really unfortunate, given the importance of
adequate nutrition, especially iron for growth and development of the fetus is getting more
complex as you age pregnancy.
Of the 80 patients with a restriction Hb less than 11 gr/dl are anemia on pregnant women, from
26 people who had anemia with distribution according to gestational age, 1 person in the first
trimester, 4 people in the second trimester and 21 people in the third trimester. Iron deficiency
anemia in pregnancy is a risk factor for preterm delivery and subsequent low birth weight, and
possibly for inferior neonatal health. For women with reasonable iron stores, iron supplements
improve iron status during pregnancy and for a considerable length of time postpartum, thus
providing some protection against iron deficiency in the subsequent pregnancy.
Key Words : Anemia, iron deficiency anemia, pregnancy, trimester, preterm delivery, birth
weight

CHAPTER I
Introduction
Iron deficiency anemia (IDA) is a type of anemia that affects most people in developing
countries, including in Indonesia. As many as 16-50% of men suffer from IDA in Indonesia with
the most common cause of hookworm infection (54%) and haemorrhoids (27%). 25-48% of adult
women in Indonesia suffer menorraghia IDA with the most common cause (33%), hemorrhoids
(17%) and hookworm infection (17%). 46-92% of pregnant women in Indonesia suffer from IDA
A woman loses about 500 mg of iron with each pregnancy. Menstrual losses are highly variable,
ranging from 10 to 250 mL (4-100 mg of iron) per period. These iron losses in women double
their need to absorb iron in comparison to males. A special effort should be made to identify and
treat iron deficiency during pregnancy and early childhood because of the effects of severe iron
deficiency upon learning capability, growth, and development. Race probably has no significant
effect upon the occurrence of iron deficiency anemia; however, because diet and socioeconomic
factors play a role in the prevalence of iron deficiency, it more frequently is observed in people of
various racial backgrounds living in poorer areas of the world. (2)
The limitation of the problem of this paper is about Iron Deficiency Anemia, pregnancy, and their
relation. The purpose of this paper is to give some information about it and prevent the
complication that may be occur to the pregnant women and the fetus. The method that the writer
uses is literature review. The material that will be written in this paper are about definition,
causes, symptom, diagnosis of iron metabolism, iron deficiency anemia then about physiology of
pregnancy, and also the relation between Iron Deficiency Anemia in Pregnancy. These all will be
written in chapter II and III.

CHAPTER II
IRON METABOLISM
Most of the iron within the body is found in hemoglobin within erythrocytes (about 1800 mg of
iron). Iron is stored in macrophages (and to a lesser extent in hepatocytes), which represents the
storage pool of iron (about 1600 mg of iron). Small amounts of iron are found in myoglobin and
in plasma (bound to transferrin. Iron is conserved within the body. The typical adult human body
contains about 3000-4000 mg of iron. Only about 1 mg of iron is lost from the body per day
(through blood loss or sloughed mucosal epithelial cells) and must be replaced through the diet.
The majority of iron required by the body is acquired by recycling iron from senescent red cells.
Iron Absorption in Gastrointestinal Tract
Pic 1. Iron Absorption in Intestine

Dietary iron is obtained either from inorganic

sources or animal sources (in heme from
breakdown of hemoglobin or myoglobin). Dietary
iron

enters

intestinal

cells

via

specific

transporters.The iron is then used by the cell

(incorporated into enzymes), stored as ferritin
(excreted in the feces when the intestinal epithelial
cell sloughs) or is transferred to the plasma.
Plasma transfer of iron from enterocytes to the transport protein, apotransferrin, occurs through
specific iron channels, called ferroportins, and is facilitated by a protein (with ferroxidase
activity) called hephaestin. When apotransferrin binds iron, it is called transferrin. Hephaestin
contains copper, so copper deficiency will decrease iron absorption (as the iron absorbed from the
4

diet cannot be transferred to plasma). Hepcidin, a main iron regulating protein, decreases
ferroportin and thus decreases iron absorption.
Iron Transfer/recycling
Iron is not free in the circulation but

Pic 2. Iron Transfer

exists as transferrin (bound to

apotransferrin). Most of the iron
used for red blood cell hemoglobin
production

is

obtained

from

hemoglobin breakdown of senescent

RBCs (called recycling). When red
blood cells reach the end of their lifespan (senescent), they are phagocytized by macrophages (in
the spleen, liver, bone marrow). Hydrolytic enzymes in macrophages degrade the ingested RBCs
and release hemoglobin. Proteolytic digestion of hemoglobin liberates heme and globins. Globins
are broken down to amino acids which can be used for protein production. The iron is released
from heme, leaving a porphyrin ring which is converted to bilirubin. Once iron is released from
the heme, it is utilized by the cell (iron is an essential component of many enzymes), exported
(via ferroportin), or stored as ferritin (like enterocytes - see above figure). In macrophages,
ceruloplasmin (which like hephaestin in intestinal cells also requires copper) is a ferroxidase and
facilitates the transfer of macrophage iron to transferrin. So copper deficiency decreases iron
release from macrophages and affects iron absorption. Like enterocytes, hepcidin downregulates
ferroportin causing iron sequestration in macrophages.

Iron Uptake by Eythroid Progenitors

Transferrin-bound iron (from absorption of dietary iron in the intestine or released by
macrophages) binds to transferrin receptors, which are highly expressed on the surface of red cell
precursors, and is taken up into the cells where it is used to form hemoglobin. Erythroid
progenitors cluster around macrophages in the bone marrow and spleen, because they are
obtaining their iron (required for hemoglobin synthesis) from these iron-storing cells, as well as
from circulating transferrin. Excess iron is dangerous, because it promotes free radical
production. Whole body iron levels are regulated primarily at the level of absorption by
enterocytes, there is no regulated pathway for active excretion of iron (can only occur by
bleeding or sloughing of iron-laden enterocytes). Regulation of iron uptake by enterocytes and
release of iron stores from macrophages and hepatocytes is mediated by the hormone hepcidin,
and its effect on ferroportin. Hepcidin decreases serum iron by decreasing iron absorption and
preventing macrophages from releasing iron (causing iron sequestration). Hepcidin is regulated
by iron levels and erythropoiesis. Increased iron will upregulate hepcidin which then decreases
iron and vice versa. Active erythropoiesis inhibits hepcidin (allowing iron to be absorbed/released
for hemoglobin synthesis). Hepcidin is increased by inflammatory cytokines, particularly IL-6,
and reduces available iron during inflammatory processes (see below). Inflammation thus causes
a "functional" iron deficiency because iron is not released from macrophages (results in increased
iron stores). This contributes to the anemia of inflammatory disease. (1)
Table 1. Normal Distribution of Iron Component in Men and Women (mg/kg)

6
Table 2. Comparison stage of negative iron balance

IRON DEFICIENCY ANEMIA

Iron deficiency is defined as a decreased total iron body content. Iron deficiency anemia occurs
when iron deficiency is severe enough to diminish erythropoiesis and cause the development of
anemia. Iron deficiency is the most prevalent single deficiency state on a worldwide basis. It is
important economically because it diminishes the capability of individuals who are affected to
perform physical labor, and it diminishes both growth and learning in children.(2)
Causes
Iron deficiency anemia occurs when your body doesnt have enough iron to produce hemoglobin.
Hemoglobin is the part of red blood cells that gives blood its red color and enables the red blood
cells to carry oxygenated blood throughout your body. If you arent consuming enough iron, or if
youre losing too much iron, your body cant produce enough hemoglobin, and iron deficiency
anemia will eventually develop. Causes of iron deficiency anemia include: Blood loss, a lack of
iron in diet, an inability to absorb iron, pregnancy.
Symptoms
Initially, iron deficiency anemia can be so mild that it goes unnoticed. But as the body becomes
more deficient in iron and anemia worsens, the signs and symptoms intensify. Iron deficiency
anemia symptoms may include:
Extreme fatigue
Pale skin
Weakness
Shortness of breath
Headache

Irritability
Inflammation or soreness of your tongue
Brittle nails
Fast heartbeat
Unusual cravings for non-nutritive substances,

Dizziness or lightheadedness
Cold hands and feet

such as ice, dirt or starch

Poor appetite, especially in infants and children
with iron deficiency anemia
An uncomfortable tingling or crawling feeling in
your legs (restless legs syndrome)

Table 3. Iron Deficiency Anemia Symptoms

Pathophysiology
Iron is required for the formation of the haem moiety in haemoglobin, myoglobin, and haem
enzymes, also known as cytochromes. Adults lose approximately 1 mg (men) to 1.5 mg
(premenopausal women) a day in faeces and desquamated mucosal and skin cells. The haem from
destroyed or senescent red blood cells is recycled back into new RBCs. Iron, which is absorbed
mostly in the jejunum, is transported by transferrin and stored in either ferritin or haemosiderin
forms. If more iron is lost or needed than can be absorbed, iron stores are used up, and the patient
becomes iron deficient. Poor iron stores result in impaired haemoglobin synthesis and a
hypochromic, microcytic anaemia. Anaemia then results in decreased oxygen-carrying capacity
and the resultant symptoms of fatigue, low energy level, and dyspnoea on exertion.(3)
Test and Diagnosis
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 levels. A low level of hemoglobin or hematocrit is a sign of
anemia. 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 volume (MCV) and the
mean corpuscular hemoglobin concentration (MCHC) have values below the normal
range for the laboratory performing the test. Reference range values for MCV and MCHC
are 83-97 fL and 32-36 g/dL, respectively.
Reticulocyte count : This test measures the number of reticulocytes 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. The
characterize of Iron Deficiency Anemia is microcytic hypochrom.
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

protein

that carries iron in

is

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.(2,3)

Table 4. Normal Hemoglobin Consentration (WHO)

10

CHAPTER III
IRON DEFICIENCY ANEMIA IN PREGNANCY
Physiology of Pregnancy
Pregnancy causes physiologic changes in all maternal organ systems such as cardiovascular,
hematologic, respiratory, endocrine, urinary, dermatology, and others; most return to normal after
delivery. In general, the changes are more dramatic in multifetal than in single pregnancies.
Hematologic: Total blood volume increases proportionally with CO, but the increase in plasma
volume is greater (close to 50%, usually by about 1600 mL for a total of 5200 mL) than that in
RBC mass (about 25%); thus, Hb is lowered by dilution, from about 13.3 to 12.1 g/dL. This
dilutional anemia decreases blood viscosity. With twins, total maternal blood volume increases
more (closer to 60%). WBC count increases slightly to 9,000 to 12,000/L. Marked leukocytosis
( 20,000/L) occurs during labor and the first few days postpartum.
Iron requirements increase by a total of about 1 g during the entire pregnancy and are higher
during the 2nd half of pregnancy6 to 7 mg/day. The fetus and placenta use about 300 mg of
iron, and the increased maternal RBC mass requires an additional 500 mg. Excretion accounts for
200 mg. Iron supplements are needed to prevent a further decrease in Hb levels because the
amount absorbed from the diet and recruited from iron stores (average total of 300 to 500 mg) is
usually insufficient to meet the demands of pregnancy.(4,10)
Regulation of Iron Transfer to The Fetus
Transfer of iron from the mother to the fetus is supported by a substantial increase in maternal
iron absorption during pregnancy and is regulated by the placenta. Serum ferritin usually falls

11

markedly between 12 and 25 week of gestation, probably as a result of iron utilization for
expansion of the maternal red blood cell mass. Most iron transfer to the fetus occurs after week
30 of gestation, which corresponds to the time of peak efficiency of maternal iron absorption.
Serum transferrin carries iron from the maternal circulation to transferrin receptors located on the
apical surface of the placental syncytiotrophoblast, holotransferrin is endocytosed, iron is
released, and apotransferrin is returned to the maternal circulation. The free iron then binds to
ferritin in placental cells where it is transferred to apotransferrin, which enters from the fetal side
of the placenta and exits as holotransferrin into the fetal circulation. This placental iron transfer
system regulates iron transport to the fetus. When maternal iron status is poor, the number of
placental transferrin receptors increases so that more iron is taken up by the placenta. Excessive
iron transport to the fetus may be prevented by the placental synthesis of ferritin. As discussed
later in this review, evidence is accumulating that the capacity of this system may be inadequate
to maintain iron transfer to the fetus when the mother is iron deficient.(5)
Pathogenesis Hemoglobin Concentration Changes in Pregnancy
Anemia in pregnancy is a condition with elevated maternal hemoglobin values below 11 gr % in
first trisemester and third trimester, or levels of hemobglobin values of less than 10,5 % in two
trisemester (Centers for Disease Control, 1998). Difference above the limit value associated with
the incidence of hemodilution
During pregnancy, blood volume increases dramatically in order to nourish and grow of the baby.
Plasma volume rises 50%, but red blood cells increase only about 30%, resulting in a physiologic
dilution of red blood cells called hemodilution of pregnancy that can look a lot like anemia.
This is a normal process that occurs throughout the first 28-30 weeks of pregnancy in the healthy,
well-nourished mother and is an excellent indicator of how well the blood volume is or is not
12

expanding. A falling hemoglobin

and a healthy well-grown fetus
often go together. After 28 weeks,
the hemoglobin values begin to
rise again as the plasma stops
expanding and red blood cells
continue to increase.
An expanded plasma volume
decrease

hematocrit,

blood

hemoglobin concentration and erythrocyte count, but did not reduce the absolute amount of
hemoglobin or red blood cells in circulation. Decrease in hematocrit, hemoglobin concentration,
erythrocyte count and can usually be seen at week-7-8 to the pregnancy, and continued until
week 16 to 22 when the balance point is reached.
A hemoglobin of 11 g/dl of whole blood or more at 8 weeks of pregnancy is a good starting point.
A gradual 2-gram drop by 28-30 weeks is normal and may be even greater for women carrying
twins. A value below 11 g/dl at 8 weeks merits treatment, since that 2-gram drop is anticipated.
We did not want to arrive at the end of pregnancy with a hemoglobin of 10 or less. It often takes
7-12 days for hemoglobin levels to start to respond to therapy.
Therefore, if the plasma volume expansion constant is not followed by increased production of
erythropoietin, this will be resulting in lower levels of hematocrit, hemoglobin concentration,
erythrocyte count below the normal levels, then anemia occurs. Pregnant women are generally
considered to be anemic if hemoglobin levels below 11 g / dl or hematocrit less than 33%.
The high incidence of iron deficiency underscores the need for iron supplementation in
pregnancy. Iron supplementation is especially important because the demand for iron by the
13

mother and the fetus increases during pregnancy. This increased demand cannot be met without
iron supplementation. During pregnancy the total maternal need for extra iron averages close to
800 - 1000 mg (elemental iron), of which about 300 mg is for the fetus and the placenta, 300-400
mg for increasing red blood cells (peaks at week 32), and about 190 mg is lost during delivery. (6)

Effects of Iron Deficiency Anemia in Pregnancy

1. Negative Effects on the Mother During Pregnancy and the Perinatal Period.
a) Reproduction-related mortality.
It has been clearly demonstrated that the anemic pregnant woman is at greater risk of death
during the perinatal period. Close to 500,000 maternal deaths ascribed to childbirth or early postpartum occur every year, the vast majority taking place in the developing countries. Mortality
decreased as Hb concentration rose. It is important to realize that severe anaemia is associated
with very poor overall socioeconomic and health conditions in certain countries and regions of
the developing world. As a rule malaria, other infections, and multiple nutritional deficiencies,
including folate and vitamin A are also endemic in these populations. Iron deficiency, however, is
responsible for, or contributes significantly to, the majority of anaemia cases during
pregnancy.The risk of complications during birth, including fetal mortality, is higher among
stunted populations who also exhibit poor pelvic development. General undernutrition and
specifically iron and folate deficiencies during childhood and adolescence impair physical
growth. Both iron and folate supplementation can result in improved growth in children and in
pregnant teenage girls.

14

b) Performance during pregnancy and delivery.

Iron deficient anemic women have shorter pregnancies than non-anemic, or even anemic but not
iron deficient pregnant women. Several studies showed that all anemic pregnant women had a
higher risk of pre-term delivery in relation to non-anemic women. The iron-deficient, anemic
group had twice the risk of those with anemia in general. Several studies showed that better
nutrition, including lesser prevalence of anemia, was associated with better newborn weights and
lower rates of pre-term deliveries The more severe the anemia the greater the risk of low-birth
weight.
c) Immunity status.
Two studies in India demonstrate that severely anemic as well as iron deficient pregnant women
have impaired cell mediated immunity that is reversible with iron treatment. An important control
variable lacking in these studies is documentation of folate nutrition.
2. Negative Effects on the Infant.
a) Health and development.
There is mounting evidence that in infants iron deficiency anaemia may produce long-lasting
defects in mental development and performance that my further impair the childs learning
capacity.(7,9)
Test and Diagnosis(8)
The U.S. Preventive Services Task Force (USPSTF) and the Centers for Disease Control and
Prevention (CDC) recommend routine screening for iron deficiency anemia in pregnant women.
During pregnancy the hemoglobin concentration declines during the first and second trimesters

15

because of an increase in blood volume. Therefore, it is recommended anemia criteria for the
specific stage of pregnancy be used :
Trimester
First
Second
Third

Hemoglobin (g/dl)
<11
<10,5
<11

Hematocrit (%)
<33
<32
<33

Table 5. Iron Deficiency Anemia Criteria in Pregnancy (CDC)

Parameter
MCV
MCHC
Serum Iron (SI)
TIBC
Jenuh Transferin
Serum Feritin

Iron Deficiency Anemia

<80 fL
< 31 %
< 50 ugr%
> 400 ugr%
< 15 %
< 12 ugr/l

Normal level
82 92 fL
32 35 %
80 160 ugr%
250 400 ugr%
30 35 %
12 200 ugr/l

Table 6. Iron Deficiency Anemia Criteria

Treatment and Prevention(6)

The iron requirement increases from a 0.8 mg/day in the first trimester to 6 to 7 mg/day in the
second half of pregnancy. Overall, a pregnant woman needs about 2 to 4.8 mg of iron per day.
The woman must consume 20 to 48 mg of dietary iron to absorb this quantity of iron daily. An
average vegetarian diet does not provide more than 10 to 15 mg of iron per day. Thus, the amount
of iron absorbed from diet, coupled with that mobilized from body iron stores, is usually
insufficient to meet the demands imposed by pregnancy. This is true even though the
bioavailability of iron from the gastrointestinal (GI) tract is moderately increased during
pregnancy and menstrual iron loss ceases. Therefore, iron supplementation during pregnancy is
recommended universally even in nonanemic women.

16

Table 7. Selected Recommended Daily Intakes for Iron, by Estimated Dietary Iron Bioavailability

Childre
n (13
years)

Childre
n (46
years)

Women
(1950
years)

Women
during
pregnancy
(second
trimester)

Women during
breastfeeding
(03 months
lactation)

Men
(1950
years)

15
%

3.9

4.2

19.6

> 50.0

10.0

9.1

10
%

5.8

6.3

29.4

> 50.0

15.0

13.7

5%

11.6

12.6

58.8

> 50.0

30.0

27.4

Numbers are mg per day.

There are 3 main strategies for correcting iron deficiency in populations, which can be used alone
or in combination:
1. Education combined with dietary modification or diversification to improve iron intake
and bioavailability.
2. Iron supplementation (provision of iron, usually in higher doses, without food): Iron
supplementation is the most common strategy currently used to address iron deficiency in
developing countries. Iron supplementation can be targeted to high-risk groups (eg,
pregnant women) and can be cost-effective, but the logistics of distribution and
compliance issues are major limitations. For oral supplementation, ferrous iron salts
(ferrous sulphate and ferrous gluconate) are preferred because of their low cost and high
bioavailability. Standard therapy for iron-deficiency anemia in adults is a 300-mg tablet of
ferrous sulphate (60 mg of iron) 3 or 4 times per day. In studies supported by WHO in
southeast Asia, iron and folic acid supplementation every week to women of childbearing
age improved iron nutrition and reduced iron-deficiency anemia. Iron supplementation

17

during pregnancy is advisable in developing countries, where women often enter

pregnancy with low iron stores.
3. Food-based Approaches and Iron fortification of foods : Food-based approaches can
broadly be categorized into 2 interventions: dietary improvement and food fortification.
Efforts to reduce iron deficiency should be directed toward promoting the availability of
and access to iron-rich foods. Bioavailability of iron-containing foods is strongly
influenced by enhancers in the diet and inhibitors. Examples of simple alterations in food
habits that may improve iron bioavailability include:

Including fresh fruits or fruit juices and other sources of vitamin C such as tomatoes,
spinach, cabbage, cauliflower, potatoes, and other green leafy vegetables and tubers in the
meal;

Consuming milk, cheese, and other dairy products as between-meal snacks rather than at
mealtimes;

Separating tea drinking from mealtime by at least 2 hours; and

Consuming foods that contain inhibitors of iron absorption with tea or milk at those meals
that are inherently low in iron such as a breakfast of a low-iron cereal (eg, bread,
cornflakes).

Iron fortification is probably the most practical sustainable and cost-effective long-term
solution to control iron deficiency at the national level. Fortification of foods with iron is
more difficult than it is with other nutrients, such as iodine in salt and vitamin A in cooking
oil. The most bioavailable iron compounds are soluble in water or diluted acid, but these
compounds often react with other food components to cause off flavors and color changes or
18

fat oxidation or both. Thus, less-soluble forms of iron, although less well absorbed, are often
chosen for fortification to avoid unwanted sensory changes. Fortification with low iron doses
is more similar to the physiologic environment than is supplementation and might be the
safest intervention.
4. Pregnant women should receive 1 adult tablet per day for 100 days. Each tablet contains 100
mg of elemental iron and 500 mcg of folic acid. These tablets should be provided to women
after the first trimester of pregnancy.

Conclusion
Anemia is one of the four major problem in Indonesia that experienced by approximately 51% of
pregnant women. About 75% of anemia in pregnancy caused by iron deficiency. Iron is very
important in formation of red blood cells. If someone has iron deficiency, they will suffer anemia.
Anemia in pregnancy adversely affects to the mother and to the fetus. Iron deficiency anemia is
diagnosed by clinical history, examination, and laboratory test. The treatment of iron deficiency
anemia in pregnancy include education, iron supplementation, food-based approaches,
fortification, and folic acid supplementation.

19

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21