IRON DEFICIENCY ANEMIA in PREGNANCY

Nyoman Arya Adi Wangsa 030.09.171

FAC !"Y OF MEDICINE "RI#A$"I NI%ER#I"Y &A$AR"A D'('m)'r *+ ,01,

Pr'-a(' 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 Prof. Muzief (????) as my supervisor. With his guidance, this paper has been done. In this paper, I would present a discussion about Iron Deficiency that this paper can provide 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 improve in the future. nemia in !regnancy. I hope

&a.ar/a+ D'('m)'r *+ ,01,

Nyoman Arya Adi Wangsa

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A)s/ra(/ nemia is one of the four ma8or problem in Indonesia that e9perienced by appro9imately 3': of pregnant women. ccording to WH(, anemia in pregnancy is the cause of /7: 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. bout ;3: of anemia in pregnancy caused by iron deficiency.

WH( reported the prevalence of pregnant mothers who e9perience iron deficiency appro9imately -3<;3: and increases as you age pregnancy. *his is really unfortunate, given the importance of ade"uate nutrition, especially iron for growth and development of the fetus is getting more comple9 as you age pregnancy. (f the 57 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, / people in the second trimester and +' people in the third trimester. Iron deficiency anemia in pregnancy is a risk factor for preterm delivery and subse"uent 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 subse"uent pregnancy. $'y Words ? weight nemia, iron deficiency anemia, pregnancy, trimester, preterm delivery, birth

C0AP"ER I In/rod1(/ion Iron deficiency anemia @ID A is a type of anemia that affects most people in developing countries, including in Indonesia. s many as '><37: of men suffer from ID in Indonesia with

the most common cause of hookworm infection @3/:A and haemorrhoids @+;:A. +3</5: of adult women in Indonesia suffer menorraghia ID with the most common cause @--:A, hemorrhoids

@';:A and hookworm infection @';:A. /><B+: of pregnant women in Indonesia suffer from ID woman loses about 377 mg of iron with each pregnancy. 0enstrual losses are highly variable, ranging from '7 to +37 m1 @/<'77 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 severe iron deficiency upon learning capability, growth, and development. $ace probably has no significant effect upon the occurrence of iron deficiency anemiaC however, because diet and socioeconomic factors play a role in the prevalence of iron deficiency, it more fre"uently is observed in people of various racial backgrounds living in poorer areas of the world. @+A *he limitation of the problem of this paper is about Iron Deficiency nemia, pregnancy, and their relation. *he 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. *he method that the writer uses is literature review. *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 Iron Deficiency chapter II and III. nemia in !regnancy. *hese all will be written in

C0AP"ER II IRON ME"A2O!I#M 0ost of the iron within the body is found in hemoglobin within erythrocytes @about '577 mg of ironA. Iron is stored in macrophages @and to a lesser e9tent in hepatocytesA, which represents the storage pool of iron @about '>77 mg of ironA. Small amounts of iron are found in myoglobin and in plasma @bound to transferrin. Iron is conserved within the body. *he typical adult human body contains about -777</777 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 ma8ority of iron re"uired by the body is ac"uired by recycling iron from senescent red cells. Iron A)sor3/ion in Gas/roin/'s/ina4 "ra(/
Pic 1. Iron Absorption in Intestine

Dietary iron is obtained either from inorganic sources or animal sources @in heme from breakdown of hemoglobin or myoglobinA. Dietary iron enters intestinal cells via 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 activityA 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
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diet cannot be transferred to plasmaA. Hepcidin, a main iron regulating protein, decreases ferroportin and thus decreases iron absorption. Iron "rans-'r5r'(y(4ing Iron is not free in the circulation but e9ists as transferrin @bound to apotransferrinA. 0ost of the iron used for red blood cell hemoglobin production is obtained from
Pic 2. Iron Transfer

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, liver, bone marrowA. Hydrolytic en#ymes in macrophages degrade the ingested $,&s and release hemoglobin. !roteolytic digestion of hemoglobin liberates heme and globins. 6lobins are broken down to amino acids which can be used for protein production. *he iron is released from heme, leaving a porphyrin ring which is converted 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 @via ferroportinA, or stored as ferritin @like enterocytes < see above 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. 1ike enterocytes, hepcidin downregulates ferroportin causing iron se"uestration in macrophages.

Iron 3/a.' )y Ey/6roid Prog'ni/ors *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 levels are regulated primarily at the level of absorption by enterocytes, there is no regulated pathway for active 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 preventing macrophages from releasing iron @causing iron se"uestrationA. Hepcidin is regulated by iron levels and erythropoiesis. Increased iron will upregulate hepcidin which then decreases iron and vice versa. ctive

erythropoiesis inhibits hepcidin @allowing iron to be absorbed=released for hemoglobin synthesisA. Hepcidin is increased by inflammatory cytokines, particularly I1<>, and reduces available 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. @'A

*able '. )ormal Distribution of Iron &omponent in 0en and Women @mg=kgA

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
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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.@+A Ca1s's Iron deficiency anemia occurs when your body doesnEt 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 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 eventually develop. &auses of iron deficiency anemia include? ,lood loss, a lack of iron in diet, an inability to absorb iron, pregnancy. #ym3/oms 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 !ale skin Weakness Shortness of breath Headache Di##iness or lightheadedness &old hands and feet
*able -. Iron Deficiency nemia Symptoms

Irritability Inflammation or soreness of your tongue ,rittle nails Fast heartbeat .nusual cravings for non<nutritive substances, such as ice, dirt or starch !oor appetite, especially in infants and children with iron deficiency anemia n uncomfortable tingling or crawling feeling in your legs @restless legs syndromeA

Pa/6o36ysio4ogy Iron is re"uired for the formation of the haem moiety in haemoglobin, myoglobin, and haem

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en#ymes, also known as cytochromes.

dults lose appro9imately ' mg @menA to '.3 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 8e8unum, 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 level, and dyspnoea on e9ertion.@-A "'s/ and Diagnosis 0any tests and procedures are used to diagnose iron<deficiency anemia. *hey can help confirm a diagnosis, look for a cause, and find out how severe the condition is. Com34'/' 24ood Co1n/ 7 (ften, the first test used to diagnose anemia is a (om34'/' )4ood

(o1n/ @&,&A. *he &,& measures many parts of your blood. *his test checks your
hemoglobin and hematocrit levels. low level 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 volume @0&FA and the mean corpuscular hemoglobin concentration @0&H&A have values below the normal range for the laboratory performing the test. $eference range values for 0&F and 0&H& are 5-<B; f1 and -+<-> g=d1, respectively. R'/i(14o(y/' (o1n/ 7 *his test measures the number of reticulocytes in your blood. $eticulocytes are young, immature red blood cells. (ver time, reticulocytes become mature red blood cells that
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carry o9ygen throughout your body.

reticulocyte count shows whether your bone marrow is

making red blood cells at the correct rate. P'ri36'ra4 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. "'s/s /o m'as1r' iron 4'8'4s. *hese tests can show how much iron has been used from your bodyGs stored iron. *ests to measure iron levels include?

Serum iron. *his test measures the amount of iron in your blood. *he 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.

measure of this

protein helps your doctor find out how much of your bodyGs stored iron has been used.

*ransferrin level, 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 have iron<deficiency anemia, youGll have a high level of transferrin that has no iron.@+,-A

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Table 4. Normal Hemoglobin Consentration (WHO)

C0AP"ER III IRON DEFICIENCY ANEMIA in PREGNANCY P6ysio4ogy o- Pr'gnan(y !regnancy causes physiologic changes in all maternal organ systems such as cardiovascular,

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hematologic, respiratory, endocrine, urinary, dermatology, and othersC most return to normal after delivery. In general, the changes are more dramatic in multifetal than in single pregnancies. 0'ma/o4ogi(7 *otal blood volume increases proportionally with &(, but the increase in plasma volume is greater @close to 37:, usually by about '>77 m1 for a total of 3+77 m1A than that in $,& mass @about +3:AC thus, Hb is lowered by dilution, from about '-.- to '+.' g=d1. *his dilutional anemia decreases blood viscosity. With twins, total maternal blood volume increases more @closer to >7:A. W,& count increases slightly to B,777 to '+,777=H1. 0arked leukocytosis @I +7,777=H1A 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 -77 mg of iron, and the increased maternal $,& mass re"uires an additional 377 mg. %9cretion accounts for +77 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 -77 to 377 mgA is usually insufficient to meet the demands of pregnancy. @/,'7A R'g14a/ion o- Iron "rans-'r /o "6' F'/1s *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 +3 week of gestation, probably as a result of iron utili#ation for e9pansion of the maternal red blood cell mass. 0ost iron transfer to the fetus occurs after week -7 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
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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. %9cessive iron transport to the fetus may be prevented by the placental synthesis of ferritin. s discussed

later in this review, evidence 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.@3A Pa/6og'n'sis 0'mog4o)in Con('n/ra/ion C6ang's in Pr'gnan(y nemia in pregnancy is a condition with elevated maternal hemoglobin values below '' g in first trimester and third trimester, or levels of hemoglobin values of less than '7.3 g: in trimester two @&enters for Disease &ontrol, 'BB5A. 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. !lasma volume rises 37:, but red blood cells increase only about -7:, 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 +5<-7 weeks of pregnancy in the healthy, well<nourished mother and is an e9cellent indicator of how well the blood volume is or is not e9panding. falling hemoglobin and a healthy well<grown fetus often go together. fter +5

weeks, the hemoglobin values begin to rise again as the plasma stops e9panding and red blood cells continue to increase.

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n e9panded plasma volume decrease hemoglobin hematocrit, concentration blood 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<;<5 to the pregnancy, and continued until week '> to ++ when the balance point is reached. hemoglobin of '' g=dl of whole blood or more at 5 weeks of pregnancy is a good starting point. gradual +<gram drop by +5<-7 weeks is normal and may be even greater for women value below '' g=dl at 5 weeks merits treatment, since that +<gram drop is

carrying twins.

anticipated. We did not want to arrive at the end of pregnancy with a hemoglobin of '7 or less. It often takes ;<'+ days for hemoglobin levels to start to respond to therapy. *herefore, if the plasma volume e9pansion 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. !regnant women are generally considered to be anemic if hemoglobin levels below '' g = dl or hematocrit less than --:. *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 averages close to 577 < '777 mg @elemental ironA, of which about -77 mg is for the fetus and the placenta, -77</77 mg for increasing red blood cells @peaks at week -+A, and about 'B7 mg is lost during delivery. @>A
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E--'(/s o- Iron D'-i(i'n(y An'mia in Pr'gnan(y '. )egative %ffects on the 0other 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 377,777 maternal deaths ascribed to childbirth or early post< partum occur every year, the vast ma8ority taking place in the developing countries. 0ortality decreased as Hb concentration rose. It is important to reali#e that severe anaemia is associated with very poor overall socioeconomic and health conditions in certain countries and regions of the developing world. s a rule malaria, other infections, and multiple nutritional deficiencies, are also endemic in these populations. Iron deficiency, however, is

including folate and vitamin

responsible for, or contributes significantly to, the ma8ority of anaemia cases during pregnancy.*he risk of complications during birth, including fetal mortality, is higher among stunted populations who also e9hibit poor pelvic development. 6eneral undernutrition and specifically iron and folate deficiencies during childhood and adolescence impair physical growth. ,oth iron and folate supplementation can result in improved growth in children and in pregnant teenage girls. b) Performance !"ring pregnanc$ an! !eli%er$. Iron deficient anemic women have shorter pregnancies than non<anemic, or even anemic but not iron deficient pregnant women. Several studies showed that all anemic pregnant women had a higher risk of pre<term delivery in relation to non<anemic women. *he iron<deficient, anemic group had twice the risk of those with anemia in general. Several studies showed that better nutrition, including lesser prevalence of anemia, was associated with better newborn weights and
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lower rates of pre<term deliveries *he more severe the anemia the greater the risk of low<birth weight. c) Imm"nit$ stat"s. *wo 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. n important control variable lacking in these studies is documentation of folate nutrition. +. )egative %ffects on the Infant. aA Healt& an! !e%elopment. *here is mounting evidence that in infants iron deficiency anaemia may produce long<lasting defects in mental development and performance that my further impair the childEs learning capacity.@;,BA "'s/ and Diagnosis9:; *he ..S. !reventive Services *ask Force @.S!S*FA and the &enters for Disease &ontrol and !revention @&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 volume. *herefore, it is recommended anemia criteria for the specific stage of pregnancy be used ? "rim's/'r First Second *hird M'' M'7,3 M'' 0'mog4o)in 9g5d4; M-M-+ M-0'ma/o(ri/ 9<;

*able 3. Iron Deficiency nemia &riteria in !regnancy @&D&A

Param'/'r MC%

Iron Deficiency nemia M57 f1

)ormal level 5+ N B+ f1

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MC0C #'r1m Iron 9#I; "I2C &'n16 "rans-'rin #'r1m F'ri/in

M -' : M 37 ugr: O /77 ugr: M '3 : M '+ ugr=l

-+ N -3 : 57 N '>7 ugr: +37 N /77 ugr: -7 N -3 : '+ N +77 ugr=l

*able >. Iron Deficiency nemia &riteria

"r'a/m'n/ and Pr'8'n/ion9=; *he iron re"uirement increases from a 7.5 mg=day in the first trimester to > to ; mg=day in the second half of pregnancy. (verall, a pregnant woman needs about + to /.5 mg of iron per day. *he woman must consume +7 to /5 mg of dietary iron to absorb this "uantity of iron daily. n

average vegetarian diet does not provide more than '7 to '3 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 even though the bioavailability of iron from the gastrointestinal @6IA tract is moderately increased during pregnancy and menstrual iron loss ceases. *herefore, iron supplementation during pregnancy is recommended universally even in nonanemic women.

Table '. (electe! ecommen!e! )ail$ Inta*es for Iron+ b$ ,stimate! )ietar$ Iron -ioa%ailabilit$

Children (13 years) 15 % 10 % 5% 3.9 5.8 11.6

Children (46 years) 4.2 6.3 12.6

Women (1950 years) 19.6 29.4 58.8

Women during pregnancy (second trimester) > 50.0 > 50.0 > 50.0

Women during breast eeding (03 months lactation) 10.0 15.0 30.0

!en (1950 years) 9.1 13.7 27.4

)umbers are mg per day.

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*here are - main strategies for correcting iron deficiency in populations, which can be used alone or in combination? '. %ducation combined with dietary modification or diversification to improve iron intake and bioavailability.
2. Iron supplementation @provision of iron, usually in higher doses, without foodA? 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 womenA and can be cost<effective, but the logistics of distribution and compliance issues are ma8or limitations. For oral supplementation, ferrous iron salts @ferrous sulphate and ferrous gluconateA are preferred because of their low cost and high bioavailability. Standard therapy for iron<deficiency anemia in adults is a -77<mg tablet of ferrous sulphate @>7 mg of ironA - or / times per day. In studies supported by WH( in southeast sia, iron and folic acid supplementation every week to women of childbearing age improved iron nutrition and reduced iron<deficiency anemia. Iron supplementation during pregnancy is advisable in developing countries, where women often enter pregnancy with low iron stores. -. Food<based pproaches and Iron fortification of foods ? Food<based approaches can

broadly be categori#ed into + interventions? dietary improvement and food fortification. %fforts to reduce iron deficiency should be directed toward promoting the availability of and access to iron<rich foods. ,ioavailability of iron<containing foods is strongly influenced by enhancers in the diet and inhibitors. %9amples of simple alterations in food habits that may improve iron bioavailability include?

Including fresh fruits or fruit 8uices and other sources of vitamin & such as tomatoes, spinach, cabbage, cauliflower, potatoes, and other green leafy vegetables and tubers in the
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mealC

&onsuming milk, cheese, and other dairy products as between<meal snacks rather than at mealtimesC

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, cornflakesA.

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 in cooking

oil. *he 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 fat o9idation or both. *hus, 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. /. !regnant women should receive ' adult tablet per day for '77 days. %ach tablet contains '77 mg of elemental iron and 377 mcg of folic acid. *hese tablets should be provided to women after the first trimester of pregnancy.

Con(41sion

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nemia is one of the four ma8or problem in Indonesia that e9perienced by appro9imately 3': of pregnant women. bout ;3: 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. nemia in pregnancy adversely 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.

R'-'r'n('s '. HD&. ,asic Iron 0etabolism. vailable at?

http?==ahdc.vet.cornell.edu=clinpath=modules=chem=femetb.htm. ccessed on 0ay '+, +7'+. +. 0edscape. Iron Deficiency nemia. vailable at?

http?==emedicine.medscape.com=article=+7+---<overview. ccessed on 0ay '+, +7'+.

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-. ,0P.

!athophysiology

Iron

Deficiency

nemia.

vailable

at?

http?==bestpractice.bm8.com=best<practice=monograph=B/=basics=pathophysiology.html. ccessed on 0ay '/, +7'+. /. 0erck 0anuals. !hysiology of !regnancy. vailable at?

http?==www.merckmanuals.com=professional=gynecologyQandQobstetrics=normalQpregnancyla borQandQdelivery=physiologyQofQpregnancy.html. ccessed on 0ay '/, +7'+. 3. Scholl *(, Hediger 01. nemia and Ion Deficiency nemia? &ompilation of Data on

!regnancy (utcome. merican Pournal of &linical )utritionC+77>Cvol. 3BCp. /B+ >. 6autam &S, Saha 1, Sekhri R, Saha !R. Iron Deficiency in !regnancy and the $ationality of Iron Supplements !rescribed During !regnancy. 0edscape Pournal of 0edicineC+775Cvol. '7Cp. +5-. ;. Fiteri F%. *he &onse"uences of Iron Deficiency and Health, the Foetus and the naemia in !regnancy on 0aternal Infant. vailable at?

http?==www.unsystem.org=S&)=archives=scnnews''=ch7;.htm. ccessed on 0ay '+, +7'+. 5. (bfocus. Diagnosis of Iron Deficiency nemia @ID A in !regnancy. vailable at?

http?==www.obfocus.com=nutrition=Iron=Diagnosis:+7of:+7iron:+7Deficiency.htm. ccessed on 0ay '3, +7'+. B. llen 1H. nemia and Iron Deficiency? %ffects on !regnancy (utcome. merican Pournal of &linical )utritionC+777CFol. ;', no. 3Cp. '+57</. '7. Silversides &R, &olman P0. !hysiological &hanges in !regnancy. vailable at?

http?==www.blackwellpublishing.com=content=,!1QImages=&ontentQstore=SampleQchapter=B;

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5'/73'-/557=B;5'/73'-/557.pdf. ccessed on 0ay ';, +7'+. ''. Fivante 0idwifery. Increasing Iron During !regnancy. vailable at?

http?==vivantemidwifery.com=sitebuildercontent=sitebuilderfiles=IncreasingIronDuring!regnan cy.pdf. ccessed on 0ay '5, +7'+. '+. Sinurat *S. Hubungan III. .niversity nemia Defisiensi ,esi dengan .sia Rehamilan *rimester I, II, dan of Sumatra .tara. vailable at?

http?==repository.usu.ac.id=handle='+-/3>;5B=+'3;B. ccessed on 0ay '5, +7'+. 33/ 7 6//3755>>>./rans-1siong1id'4in's.org.1.5do(s53d-s5r/(?>mids@'d1@3r's@'44io//.3d-

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