penatalaksanaan nutrisi pada anemia

8/12/2019 Penatalaksanaan Nutrisi Pada Anemia

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Nutritional management in

anemia

Deasy Irawati

Content

Nutritional anemia

Iron deficiency

Vitamin B deficiency

The role of other nutrients


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NUTRITIONAL ANEMIA


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Definition

Anaemia is a condition in which the number ofred blood cells or their oxygen-carryingcapacity is insufficient to meet physiologicneeds, which vary by age, sex, altitude,smoking, and pregnancy status

Nutritional vitamin and mineraldeficiencies

Non-nutritionalinfection andhemoglobinopathies

IRON DEFICIENCY


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Definiton

Iron deficiency: a state in which there is insufficient iron to maintainthe normal physiological function of tissues such as the blood,brain, and muscles.

Iron deficiency can exist in the absence of anaemia if it has notlasted long enough or if it has not been severe enough to cause thehaemoglobin concentration to fall below the threshold for thespecific sex and age group

Iron depletion: the state in which storage iron is absent or nearlyabsent but the tissues that need iron are able to maintain normal

physiological functions. Functional iron deficiency can develop even when iron stores are

present if the normal physiological systems for transporting iron totarget tissues are impaired cytokines due to inflammation(hepcidin)


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Source: Gibson R. Principles of Nutritional Assessment.

2nd ed. New York: Oxford University Press, 2005

Nutritional causes

Low iron intake

poor absorption of iron from diets (Low

bioavailability of iron intake = 5%

bioavailability)

Low heme iron diet

High content of iron absorption inhibitors

(phytate, calcium, tannin and oxalates)


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Nutritional treatment

In settings where iron deficiency is the mostfrequent cause

Iron supplementation continue until iron stores aresufficient 3 months after normalization of Hbconcentration

In settings where iron deficiency is not the only

cause of anaemia Combined treatment with other micronutrient folic

acid, vitamin A, vitamin B12, riboflavin, vitamin C,copper

Prevention

Foodbased approaches to increase iron intake

food fortification : milk, wheat flour, soy sauce,

salt, cereals

dietary diversification

Give iron supplementation in high risk group(low birth age baby, weaning children,

pregnancy, lactation)


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Food sources

High bioavailability iron sources: meat, fish,

egg

Medium bioavailability: beans, nut

Low bioavailability: most vegetables (spinach,

etc)

VITAMIN B DEFICIENCY


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Megaloblastic anemia

Dietary intake is the source of cobalamin and folate

Cobalamin must be bound to intrinsic factor (IF) absorbed in theterminal ileum cobalamin is bound to another protein,transcobalamin II (TCII) transported to storage sites

Considerable amounts of cobalamin are accumulated in storagesites years elapse before cobalamin deficiency develops inpatients who cannot take up dietary cobalamin.

Most often caused by folate dietary insufficiency

Very little folate is stored

can occur within months of cessation offolate ingestion

Vit B12 and folatemaintain purine and pyrimidinebiosynthesis

Vit B 12 and folate deficiencyreduction in ability to synthesizeDNA and maintain cell division affect synthesis of red cellsmacrocytic megaloblastic anemia

Other vitamin B

Improving Hb concentration riboflavin (B2),

pyridoxal (B6)

Niacin, thiamine (B1), panthothenic acid

insufficient evidence


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Food source

Mainly in meat, milk product, serealia, beans,

fruits

Treatment and prevention

Micronutrient supplementation

Food fortification

Dietary diversity


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THE ROLE OF OTHER NUTRIENTS

Anemia and vitamin A

Vitamin A deficiency may increase the risk of irondeficient-erythropoiesis and anemia iron absorption, storage, transport and delivery to

bone marrow

reduce erythrocytosis by lowering erythropoietinproduction

induce iron sequestration due to increased severity ofinfection

Vitamin A intervention that maintains a plasmaretinol increment 5 g/dL (0.175 mol/L) mightexpect to raise hemoglobin by up to 4 g/L


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van Stuijvenberg ME, Kruger M, Badenhorst CJ, Mansvelt EP, Laubscher JA.Response to an iron fortification programme in relation to vitamin A status in

6-12-year-old school children. Int J Food Sci Nutr 1997;48:419

In South Africa

vitamin A deficiency appeared to blunt serumiron and transferrin saturation responses inschool children who were given a soup fortifiedwith iron (20 mg) and vitamin C (100 mg) fornearly four months

Increased serum ferritin concentrationssuggested that iron had been absorbed andstored, but not released in children with poorervitamin A status.

0

0.2

0.4

0.6

0.8

1Odd ratio anemia

Placebo VA Fe VA+Fe

0.47

0.230.16

8 weeks of daily supplementation with vitamin A (2.4 mg), iron (60 mg) or both

vitamin A and iron relative to placebo receipt among 251 initially anemic, pregnant

Indonesian women significantly raised hemoglobin concentration by 3.7 g/L over

that of placebo recipients, an effect that explained 35% of pregnancy-related anemia

Suharno D, West CE, Muhilal, Karyadi D, HautvastJG. Supplementation with vitamin

A and iron for nutritional anaemia in pregnant women in West Java, Indonesia.

Lancet 1993;342:13258


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Anemia and vitamin E

iron deficiency anemia are more susceptible to oxidative damagein erythrocyte membranesassociated with decreased productionof hemoglobin (Hb) and other iron-containing proteins such asmyoglobin, catalase, peroxidase, and cytochromes.

Iron supplementation to deficient individuals was found to increasethe oxidative stress (i.e., increased malnodialdehyde (MDA) levelsand compromised antioxidant enzyme activities)

High levels of free iron may enhance radical production via theFenton and Haber-Weiss reactions

Treatment of iron-deficient patients with a combination of iron andvitamins A, C, and E proved effective in normalizing the oxidativestress

In the absence of vitamin E, these ROO can abstract a hydrogen from PUFA (RH) and

generate both a hydroperoxide (ROOH) and another carbon-centered radical (R),

which in the presence of oxygen (O2) will form a ROO and thus a lipid peroxidation

chain reaction occurs. If a-tocopherol (a-TOH) is present it intercepts the radical 1000

times faster than the radical reacts with PUFA, and both a ROOH and an a-TO are

formed. This a-TO radical can be detoxified and a-TOH regenerated by intracellular

antioxidants including vitamin C, glutathione, and reducing equivalents (NAD(P)H)

derivedfrom oxidative metabolism.


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Defective iron mobilization

From stores

Defective iron incorporation to

protoporphyrinIX

Decreased iron absorption

Decreased iron

availability for

heme synthesis

Decreased plasma

erythropoietin levels

Shortened erythrocyte life

span due to oxidative stress

Anemia

Potential mechanisms by which copper deficiency

can induce anemia

Anemia and Selenium

Selenium could contribute to anemia

maintenance of an optimal concentration of

glutathione peroxidase, a key antioxidant

selenoenzyme, in erythrocytes

Glutathione peroxidase protects hemoglobinagainst oxidation in erythrocytes


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Women aged 7079 years living in the community in the Womens Health and Aging

Studies (WHAS) I and II. In WHAS, the prevalence of anemia decreased from the

lowest to the highest quartile of serum selenium.

Serum selenium level

Semba RD, Ferrucci L, Cappola AR, Ricks MO, Ray AL, Xue QL, et al. Low serumselenium is associated with anemia among older women living in the community.

Biol Trace Elem Res 2006;112:97108

Reference

De Benoist B, McLean E, Egli I, Cogswell M. 2008.Worldwide prevalence of anaemia 19932005 : WHO globaldatabase on anaemia. WHO

Gibson R. Principles of Nutritional Assessment. 2nd ed.New York: Oxford University Press, 2005

Kraemer K, Zimmermann MB. 2007. Nutritional Anemia.

Sight and Life Press WHO, FAO. 2004. Vitamin and mineral requirements in

human nutrition. 2 edition

WHO, UNICEF, UNU. Iron deficiency anaemia: assessment,prevention, and control. A guide for programme managers.Geneva, World Health Organization, 2001. WHO/NHD/01.3

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