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Ni Nyoman Nami Arthisari
MAY )"* )0#)
Firstly I would say thanks to Ida Sang Hyang Widhi Wasa, finally my paper has been completed
to fulfill the english assignment.
I would also say thanks to Dr. Fajar rifin !unawijaya, "S as my super#isor. With his guidance,
this paper has been done.
In this paper, I would present a discussion about $he %elationship &etween Iron Deficiency
nemia and 'regnancy. I hope that this paper can pro#ide ade(uate information for the readers.
Finally, I apologi)e if there are some mistakes in this paper, and I am looking forward any
suggestions and criticisms to impro#e in the future.
(a.arta* May )"* )0#)
Ni Nyoman Nami A
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nemia is one of the four major problem in Indonesia that e9perienced by appro9imately 5,: of
pregnant women. ccording to WH-, anemia in pregnancy is the cause of 28: of deaths of
mothers in de#eloping countries such as Indonesia. In addition to the mother, anemia in
pregnancy also ad#ersely affects to the fetus. Deficiency of nutrients ha#e been suggested as the
most common cause of anemia. bout ;5: of anemia in pregnancy caused by iron deficiency.
WH- reported the pre#alence of pregnant mothers who e9perience iron deficiency appro9imately
05<;5: and increases as you age pregnancy. $his is really unfortunate, gi#en the importance of
ade(uate nutrition, especially iron for growth and de#elopment of the fetus is getting more
comple9 as you age pregnancy.
-f the 78 patients with a restriction Hb less than ,, gr=dl are anemia on pregnant women, from
/> people who had anemia with distribution according to gestational age, , person in the first
trimester, 2 people in the second trimester and /, people in the third trimester. Iron deficiency
anemia in pregnancy is a risk factor for preterm deli#ery and subse(uent low birth weight, and
possibly for inferior neonatal health. For women with reasonable iron stores, iron supplements
impro#e iron status during pregnancy and for a considerable length of time postpartum, thus
pro#iding some protection against iron deficiency in the subse(uent pregnancy.
&+y Wor0s ? nemia, iron deficiency anemia, pregnancy, trimester, preterm deli#ery, birth
Iron deficiency anemia @IDA is a type of anemia that affects most people in de#eloping
countries, including in Indonesia. s many as ,><58: of men suffer from ID in Indonesia with
the most common cause of hookworm infection @52:A and haemorrhoids @/;:A. /5<27: of adult
women in Indonesia suffer menorraghia ID with the most common cause @00:A, hemorrhoids
@,;:A and hookworm infection @,;:A. 2><B/: of pregnant women in Indonesia suffer from ID
woman loses about 588 mg of iron with each pregnancy. "enstrual losses are highly #ariable,
ranging from ,8 to /58 m3 @2<,88 mg of ironA per period. $hese iron losses in women double
their need to absorb iron in comparison to males. special effort should be made to identify and
treat iron deficiency during pregnancy and early childhood because of the effects of se#ere iron
deficiency upon learning capability, growth, and de#elopment. %ace probably has no significant
effect upon the occurrence of iron deficiency anemiaC howe#er, because diet and socioeconomic
factors play a role in the pre#alence of iron deficiency, it more fre(uently is obser#ed in people of
#arious racial backgrounds li#ing in poorer areas of the world.
$he limitation of the problem of this paper is about Iron Deficiency nemia, pregnancy, and their
relation. $he purpose of this paper is to gi#e some information about it and pre#ent the
complication that may be occur to the pregnant women and the fetus. $he method that the writer
uses is literature re#iew. $he 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 nemia in 'regnancy. $hese all will be
written in chapter II and III.
"ost of the iron within the body is found in hemoglobin within erythrocytes @about ,788 mg of
ironA. Iron is stored in macrophages @and to a lesser e9tent in hepatocytesA, which represents the
storage pool of iron @about ,>88 mg of ironA. Small amounts of iron are found in myoglobin and
in plasma @bound to transferrin. Iron is conser#ed within the body. $he typical adult human body
contains about 0888<2888 mg of iron. -nly about , mg of iron is lost from the body per day
@through blood loss or sloughed mucosal epithelial cellsA and must be replaced through the diet.
$he majority of iron re(uired by the body is ac(uired by recycling iron from senescent red cells.
Iron A/sor2tion in Gastroint+stina3 Tra-t
Dietary iron is obtained either from inorganic
sources or animal sources @in heme from
breakdown of hemoglobin or myoglobinA. Dietary
iron enters intestinal cells #ia specific
transporters.$he iron is then used by the cell
@incorporated into en)ymesA, stored as ferritin
@e9creted in the feces when the intestinal epithelial
cell sloughsA or is transferred to the plasma.
'lasma transfer of iron from enterocytes to the transport protein, apotransferrin, occurs through
specific iron channels, called ferroportins, and is facilitated by a protein @with ferro9idase
acti#ityA 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
Pic 1. Iron Absorption in Intestine
diet cannot be transferred to plasmaA. Hepcidin, a main iron regulating protein, decreases
ferroportin and thus decreases iron absorption.
Iron Trans,+r4r+-y-3in5
Iron is not free in the circulation but
e9ists as transferrin @bound to
apotransferrinA. "ost of the iron
used for red blood cell hemoglobin
production is obtained from
hemoglobin breakdown of senescent
%&+s @called recyclingA. When red
blood cells reach the end of their lifespan @senescentA, they are phagocyti)ed by macrophages @in
the spleen, li#er, bone marrowA. Hydrolytic en)ymes in macrophages degrade the ingested %&+s
and release hemoglobin. 'roteolytic digestion of hemoglobin liberates heme and globins. !lobins
are broken down to amino acids which can be used for protein production. $he iron is released
from heme, lea#ing a porphyrin ring which is con#erted to bilirubin. -nce iron is released from
the heme, it is utili)ed by the cell @iron is an essential component of many en)ymesA, e9ported
@#ia ferroportinA, or stored as ferritin @like enterocytes < see abo#e figureA. In macrophages,
ceruloplasmin @which like hephaestin in intestinal cells also re(uires copperA is a ferro9idase and
facilitates the transfer of macrophage iron to transferrin. So copper deficiency decreases iron
release from macrophages and affects iron absorption. 3ike enterocytes, hepcidin downregulates
ferroportin causing iron se(uestration in macrophages.
Iron %2ta.+ /y Eythroi0 Pro5+nitors
Pic 2. Iron Transfer
$ransferrin<bound iron @from absorption of dietary iron in the intestine or released by
macrophagesA binds to transferrin receptors, which are highly e9pressed on the surface of red cell
precursors, and is taken up into the cells where it is used to form hemoglobin. *rythroid
progenitors cluster around macrophages in the bone marrow and spleen, because they are
obtaining their iron @re(uired for hemoglobin synthesisA from these iron<storing cells, as well as
from circulating transferrin.
*9cess iron is dangerous, because it promotes free radical production. Whole body iron le#els are
regulated primarily at the le#el of absorption by enterocytes, there is no regulated pathway for
acti#e e9cretion of iron @can only occur by bleeding or sloughing of iron<laden enterocytesA.
%egulation 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 pre#enting macrophages from releasing
iron @causing iron se(uestrationA. Hepcidin is regulated by iron le#els and erythropoiesis.
Increased iron will upregulate hepcidin which then decreases iron and #ice #ersa. cti#e
erythropoiesis inhibits hepcidin @allowing iron to be absorbed=released for hemoglobin synthesisA.
Hepcidin is increased by inflammatory cytokines, particularly I3<>, and reduces a#ailable iron
during inflammatory processes @see belowA. Inflammation thus causes a DfunctionalD iron
deficiency because iron is not released from macrophages @results in increased iron storesA. $his
contributes to the anemia of inflammatory disease.
$able ,. .ormal Distribution of Iron +omponent in "en and Women @mg=kgA
$able /. +omparison stage of negati#e iron balance
Iron deficiency is defined as a decreased total iron body content. Iron deficiency anemia occurs
when iron deficiency is se#ere enough to diminish erythropoiesis and cause the de#elopment of
anemia. Iron deficiency is the most pre#alent single deficiency state on a worldwide basis. It is
important economically because it diminishes the capability of indi#iduals who are affected to
perform physical labor, and it diminishes both growth and learning in children.
Iron deficiency anemia occurs when your body doesnEt ha#e enough iron to produce hemoglobin.
Hemoglobin is the part of red blood cells that gi#es blood its red color and enables the red blood
cells to carry o9ygenated blood throughout your body. If you arenEt consuming enough iron, or if
youEre losing too much iron, your body canEt produce enough hemoglobin, and iron deficiency
anemia will e#entually de#elop. +auses of iron deficiency anemia include? &lood loss, a lack of
iron in diet, an inability to absorb iron, pregnancy.
Initially, iron deficiency anemia can be so mild that it goes unnoticed. &ut as the body becomes
more deficient in iron and anemia worsens, the signs and symptoms intensify. Iron deficiency
anemia symptoms may include?
*9treme fatigue Irritability
'ale skin Inflammation or soreness of your tongue
Weakness &rittle nails
Shortness of breath Fast heartbeat
Headache 1nusual cra#ings for non<nutriti#e substances,
such as ice, dirt or starch
Di))iness or lightheadedness 'oor appetite, especially in infants and children
with iron deficiency anemia
+old hands and feet n uncomfortable tingling or crawling feeling in
your legs @restless legs syndromeA
Iron is re(uired for the formation of the haem moiety in haemoglobin, myoglobin, and haem
en)ymes, also known as cytochromes. dults lose appro9imately , mg @menA to ,.5 mg
@premenopausal womenA a day in faeces and des(uamated mucosal and skin cells. $he haem from
destroyed or senescent red blood cells is recycled back into new %&+s. 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. 'oor iron stores result in impaired haemoglobin synthesis and a
hypochromic, microcytic anaemia. naemia then results in decreased o9ygen<carrying capacity
and the resultant symptoms of fatigue, low energy le#el, and dyspnoea on e9ertion.
T+st an0 Dia5nosis
"any tests and procedures are used to diagnose iron<deficiency anemia. $hey can help confirm a
diagnosis, look for a cause, and find out how se#ere the condition is.
Com23+t+ B3oo0 Co1nt 6 -ften, the first test used to diagnose anemia is a -om23+t+ /3oo0 -o1nt
@+&+A. $he +&+ measures many parts of your blood. $his test checks your hemoglobin
and hematocrit le#els. low le#el of hemoglobin or hematocrit is a sign of anemia. $he
+&+ also checks the number of red blood cells, white blood cells, and platelets in your
blood. bnormal results may be a sign of infection, a blood disorder, or another
condition. Finally, the +&+ looks at mean corpuscular #olume @"+FA and the mean
corpuscular hemoglobin concentration @"+H+A ha#e #alues below the normal range for
$able 0. Iron Deficiency nemia Symptoms
the laboratory performing the test. %eference range #alues for "+F and "+H+ are 70<B;
f3 and 0/<0> g=d3, respecti#ely.
R+ti-13o-yt+ -o1nt 6 $his test measures the number of reticulocytes in your blood. %eticulocytes
are young, immature red blood cells. -#er time, reticulocytes become mature red blood cells that
carry o9ygen throughout your body. reticulocyte count shows whether your bone marrow is
making red blood cells at the correct rate.
P+ri2h+ra3 sm+ar! For this test, a sample of your blood is e9amined under a microscope. $he
characteri)e of Iron Deficiency nemia is microcytic hypochrom.
T+sts to m+as1r+ iron 3+7+3s! $hese tests can show how much iron has been used from your
bodyGs stored iron. $ests to measure iron le#els include?
Serum iron. $his test measures the amount of iron in your blood. $he le#el of iron in your
blood may be normal e#en 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. measure of this
protein helps your doctor find out how much of your bodyGs stored iron has been used.
$ransferrin le#el, or total iron<binding capacity. $ransferrin is a protein that carries iron in
your blood. $otal iron<binding capacity measures how much of the transferrin in your
blood isnGt carrying iron. If
you ha#e iron<deficiency anemia, youGll ha#e a high le#el of transferrin that has no iron.
Table 4. Normal Hemoglobin Consentration (WHO)
Physio3o5y o, Pr+5nan-y
'regnancy causes physiologic changes in all maternal organ systems such as cardio#ascular,
hematologic, respiratory, endocrine, urinary, dermatology, and othersC most return to normal after
deli#ery. In general, the changes are more dramatic in multifetal than in single pregnancies.
H+mato3o5i-6 $otal blood #olume increases proportionally with +-, but the increase in plasma
#olume is greater @close to 58:, usually by about ,>88 m3 for a total of 5/88 m3A than that in
%&+ mass @about /5:AC thus, Hb is lowered by dilution, from about ,0.0 to ,/., g=d3. $his
dilutional anemia decreases blood #iscosity. With twins, total maternal blood #olume increases
more @closer to >8:A. W&+ count increases slightly to B,888 to ,/,888=H3. "arked leukocytosis
@I /8,888=H3A occurs during labor and the first few days postpartum.
Iron re(uirements increase by a total of about , g during the entire pregnancy and are higher
during the /nd half of pregnancyJ> to ; mg=day. $he fetus and placenta use about 088 mg of
iron, and the increased maternal %&+ mass re(uires an additional 588 mg. *9cretion accounts for
/88 mg. Iron supplements are needed to pre#ent a further decrease in Hb le#els because the
amount absorbed from the diet and recruited from iron stores @a#erage total of 088 to 588 mgA is
usually insufficient to meet the demands of pregnancy.
R+513ation o, Iron Trans,+r to Th+ F+t1s
$ransfer 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
markedly between ,/ and /5 week of gestation, probably as a result of iron utili)ation for
e9pansion of the maternal red blood cell mass. "ost iron transfer to the fetus occurs after week
08 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. $he 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 e9its as holotransferrin into the fetal circulation. $his 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. *9cessi#e
iron transport to the fetus may be pre#ented by the placental synthesis of ferritin. s discussed
later in this re#iew, e#idence is accumulating that the capacity of this system may be inade(uate
to maintain iron transfer to the fetus when the mother is iron deficient.
Patho5+n+sis H+mo53o/in Con-+ntration Chan5+s in Pr+5nan-y
nemia in pregnancy is a condition with ele#ated maternal hemoglobin #alues below ,, g: in
first trimester and third trimester, or le#els of hemoglobin #alues of less than ,8.5 g: in trimester
two @+enters for Disease +ontrol, ,BB7A. Difference abo#e the limit #alue associated with the
incidence of hemodilution
During pregnancy, blood #olume increases dramatically in order to nourish and grow of the baby.
'lasma #olume rises 58:, but red blood cells increase only about 08:, resulting in a physiologic
dilution of red blood cells called Khemodilution of pregnancyL that can look a lot like anemia.
$his is a normal process that occurs throughout the first /7<08 weeks of pregnancy in the healthy,
well<nourished mother and is an e9cellent indicator of how well the blood #olume is or is not
e9panding. falling hemoglobin and a healthy well<grown fetus often go together. fter /7
weeks, the hemoglobin #alues
begin to rise again as the plasma
stops e9panding and red blood
cells continue to increase.
n e9panded plasma #olume
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 to
the pregnancy, and continued until week ,> to // when the balance point is reached.
hemoglobin of ,, g=dl of whole blood or more at 7 weeks of pregnancy is a good starting
point. gradual /<gram drop by /7<08 weeks is normal and may be e#en greater for women
carrying twins. #alue below ,, g=dl at 7 weeks merits treatment, since that /<gram drop is
anticipated. We did not want to arri#e at the end of pregnancy with a hemoglobin of ,8 or less. It
often takes ;<,/ days for hemoglobin le#els to start to respond to therapy.
$herefore, if the plasma #olume e9pansion constant is not followed by increased production of
erythropoietin, this will be resulting in lower le#els of hematocrit, hemoglobin concentration,
erythrocyte count below the normal le#els, then anemia occurs. 'regnant women are generally
considered to be anemic if hemoglobin le#els below ,, g = dl or hematocrit less than 00:.
$he 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
mother and the fetus increases during pregnancy. $his increased demand cannot be met without
iron supplementation. During pregnancy the total maternal need for e9tra iron a#erages close to
788 < ,888 mg @elemental ironA, of which about 088 mg is for the fetus and the placenta, 088<288
mg for increasing red blood cells @peaks at week 0/A, and about ,B8 mg is lost during deli#ery.
E,,+-ts o, Iron D+,i-i+n-y An+mia in Pr+5nan-y
,. .egati#e *ffects on the "other During 'regnancy and the 'erinatal 'eriod.
a) epro!"ction#relate! mortalit$.
It has been clearly demonstrated that the anemic pregnant woman is at greater risk of death
during the perinatal period. +lose to 588,888 maternal deaths ascribed to childbirth or early post<
partum occur e#ery year, the #ast majority taking place in the de#eloping countries. "ortality
decreased as Hb concentration rose. It is important to reali)e that se#ere anaemia is associated
with #ery poor o#erall socioeconomic and health conditions in certain countries and regions of
the de#eloping world. s a rule malaria, other infections, and multiple nutritional deficiencies,
including folate and #itamin are also endemic in these populations. Iron deficiency, howe#er, is
responsible for, or contributes significantly to, the majority of anaemia cases during
pregnancy.$he risk of complications during birth, including fetal mortality, is higher among
stunted populations who also e9hibit poor pel#ic de#elopment. !eneral undernutrition and
specifically iron and folate deficiencies during childhood and adolescence impair physical
growth. &oth iron and folate supplementation can result in impro#ed growth in children and in
pregnant teenage girls.
b) Performance !"ring pregnanc$ an! !eli%er$.
Iron deficient anemic women ha#e shorter pregnancies than non<anemic, or e#en anemic but not
iron deficient pregnant women. Se#eral studies showed that all anemic pregnant women had a
higher risk of pre<term deli#ery in relation to non<anemic women. $he iron<deficient, anemic
group had twice the risk of those with anemia in general. Se#eral studies showed that better
nutrition, including lesser pre#alence of anemia, was associated with better newborn weights and
lower rates of pre<term deli#eries $he more se#ere the anemia the greater the risk of low<birth
c) Imm"nit$ stat"s.
$wo studies in India demonstrate that se#erely anemic as well as iron deficient pregnant women
ha#e impaired cell mediated immunity that is re#ersible with iron treatment. n important control
#ariable lacking in these studies is documentation of folate nutrition.
/. .egati#e *ffects on the Infant.
aA Healt& an! !e%elopment.
$here is mounting e#idence that in infants iron deficiency anaemia may produce long<lasting
defects in mental de#elopment and performance that my further impair the childEs learning
T+st an0 Dia5nosis
$he 1.S. 're#enti#e Ser#ices $ask Force @1S'S$FA and the +enters for Disease +ontrol and
're#ention @+D+A recommend routine screening for iron deficiency anemia in pregnant women.
During pregnancy the hemoglobin concentration declines during the first and second trimesters
because of an increase in blood #olume. $herefore, it is recommended anemia criteria for the
specific stage of pregnancy be used ?
Trim+st+r H+mo53o/in 85403: H+mato-rit 8;:
First M,, M00
Second M,8,5 M0/
$hird M,, M00
$able 5. Iron Deficiency nemia +riteria in 'regnancy @+D+A
Param+t+r Iron Deficiency nemia .ormal le#el
MC' M78 f3 7/ N B/ f3
MCHC M 0, : 0/ N 05 :
S+r1m Iron 8SI: M 58 ugr: 78 N ,>8 ugr:
TIBC O 288 ugr: /58 N 288 ugr:
(+n1h Trans,+rin M ,5 : 08 N 05 :
S+r1m F+ritin M ,/ ugr=l ,/ N /88 ugr=l
Tr+atm+nt an0 Pr+7+ntion
$he iron re(uirement increases from a 8.7 mg=day in the first trimester to > to ; mg=day in the
second half of pregnancy. -#erall, a pregnant woman needs about / to 2.7 mg of iron per day.
$he woman must consume /8 to 27 mg of dietary iron to absorb this (uantity of iron daily. n
a#erage #egetarian diet does not pro#ide more than ,8 to ,5 mg of iron per day. $hus, the amount
of iron absorbed from diet, coupled with that mobili)ed from body iron stores, is usually
insufficient to meet the demands imposed by pregnancy. $his is true e#en though the
bioa#ailability of iron from the gastrointestinal @!IA tract is moderately increased during
pregnancy and menstrual iron loss ceases. $herefore, iron supplementation during pregnancy is
recommended uni#ersally e#en in nonanemic women.
Women during
Women during
breasteeding (03
months lactation)
3.9 4.2 19.6 > 50.0 10.0 9.1
$able >. Iron Deficiency nemia +riteria
Table '. (electe! ecommen!e! )ail$ Inta*es for Iron+ b$ ,stimate! )ietar$ Iron -ioa%ailabilit$
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
$here are 0 main strategies for correcting iron deficiency in populations, which can be used alone
or in combination?
,. *ducation combined with dietary modification or di#ersification to impro#e iron intake
and bioa#ailability.
2. Iron supplementation @pro#ision of iron, usually in higher doses, without foodA? Iron
supplementation is the most common strategy currently used to address iron deficiency in
de#eloping countries. Iron supplementation can be targeted to high<risk groups @eg,
pregnant womenA and can be cost<effecti#e, but the logistics of distribution and
compliance issues are major limitations. For oral supplementation, ferrous iron salts
@ferrous sulphate and ferrous gluconateA are preferred because of their low cost and high
bioa#ailability. Standard therapy for iron<deficiency anemia in adults is a 088<mg tablet of
ferrous sulphate @>8 mg of ironA 0 or 2 times per day. In studies supported by WH- in
southeast sia, iron and folic acid supplementation e#ery week to women of childbearing
age impro#ed iron nutrition and reduced iron<deficiency anemia. Iron supplementation
during pregnancy is ad#isable in de#eloping countries, where women often enter
pregnancy with low iron stores.
0. Food<based pproaches and Iron fortification of foods ? Food<based approaches can
broadly be categori)ed into / inter#entions? dietary impro#ement and food fortification.
*fforts to reduce iron deficiency should be directed toward promoting the a#ailability of
and access to iron<rich foods. &ioa#ailability of iron<containing foods is strongly
.umbers are mg per day.
influenced by enhancers in the diet and inhibitors. *9amples of simple alterations in food
habits that may impro#e iron bioa#ailability include?
Including fresh fruits or fruit juices and other sources of #itamin + such as tomatoes,
spinach, cabbage, cauliflower, potatoes, and other green leafy #egetables and tubers in the
+onsuming milk, cheese, and other dairy products as between<meal snacks rather than at
Separating tea drinking from mealtime by at least / hoursC and
+onsuming 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,
Iron fortification is probably the most practical sustainable and cost<effecti#e long<term
solution to control iron deficiency at the national le#el. Fortification of foods with iron is
more difficult than it is with other nutrients, such as iodine in salt and #itamin in cooking
oil. $he most bioa#ailable iron compounds are soluble in water or diluted acid, but these
compounds often react with other food components to cause off fla#ors and color changes or
fat o9idation or both. $hus, less<soluble forms of iron, although less well absorbed, are often
chosen for fortification to a#oid unwanted sensory changes. Fortification with low iron doses
is more similar to the physiologic en#ironment than is supplementation and might be the
safest inter#ention.
2. 'regnant women should recei#e , adult tablet per day for ,88 days. *ach tablet contains ,88
mg of elemental iron and 588 mcg of folic acid. $hese tablets should be pro#ided to women
after the first trimester of pregnancy.
nemia is one of the four major problem in Indonesia that e9perienced by appro9imately 5,: of
pregnant women. bout ;5: of anemia in pregnancy caused by iron deficiency. Iron is #ery
important in formation of red blood cells. If someone has iron deficiency, they will suffer anemia.
nemia in pregnancy ad#ersely affects to the mother and to the fetus. Iron deficiency anemia is
diagnosed by clinical history, e9amination, and laboratory test. $he treatment of iron deficiency
anemia in pregnancy include education, iron supplementation, food<based approaches,
fortification, and folic acid supplementation.
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