4. Intestinal iron absorption
• non-heme iron
• plants source: beans,
– dark green leafy vegetables
(spinach, kangkung)
– Fortified cereals, rice, enriched
whole-grain
– phytates /tannin, high gastric pH:
absorption
– Ascorbic acid: absorption
• heme iron >>
– Animal source: beef,
chicken, fish, cow’s milk
– More readily absorbed
5. Iron transport
Regulation of iron absorption and exportation by enterocytes.
Both heme and non-heme iron are absorbed by specific pathways, including
divalent metal transporter-1 (DMT-1) and heme carrier protein (HCP1), in
association with the ferrireductase, duodenal cytochrome B (Dcytb).
www.servier.fr/servier-medical-art).
6. Iron Requirements
• Infants & children
– <6 mo: 0.27 mg/day
– 7 mo - 1 year: 11 mg/day
– 1 - 3 years: 7 mg/day
– 4 - 8 years: 10 mg/day
Food and Nutrition Board at the Institute of Medicine
• Males
– 9 to 13 years: 8 mg/day
– 14 to 18 years: 11 mg/day
• Females
– 9 to 13 years: 8 mg/day
– 4 to 18 years: 15 mg/day
7. Epidemiology - IDA
SKRT 2001
• Infant 0-6 mo: 61,3%
• Infant 6-12 mo: 64,8%
• Toddler <5 yr: 48,1%.
SKRT 2007
• Toddler: 40-45%
USA, 2000
• Age 1-2 yr: 7 %
• Age 3-4 yr: 5%
Age %
12-59 mo 28,1
5-14 year 26,4
15-24 year 18,4
Riskesdas 2013
8. Etiology
Increased demands
o Growth during infancy & childhood
o Treatment with erythropoiesis-stimulating agents
Limited external supply
o Poor intake
o Inappropriate diet with deficit in bioavailable iron &/or ascorbic acid
o Malabsorption
Gastric resection
Helicobacter pylori infection (even without significant bleeding)
Malabsorption syndromes (Crohn disease and coeliac disease)
o Drug interference (gastric anti-acid agents & antisecretory drugs)
Increased losses
o Phlebotomy
o Haemorrhage: surgery, trauma, GIT /respiratory tract bleeding
Munoz, M.et al. (2011).. Journal of Clinical Pathology, 64, 287
19. Labs
• Iron status
– serum iron
– transferrin saturation
– TIBC
– Ferritin
– sTfr
Low erythropoiesis
• Reticulocyte
• CHr
https://courses.washington.edu/conj/bess/iron/ironfig.png
20. Algorithm diagnosis
(modified from Weiss and Goodnough
(2005)
soluble form of transferrin
receptor (sTfR): total amount of
cell surface transferrin receptors
: IDA
: low erythroid progenitor
22. Treatment
Iron therapy
1. Elemental iron 4-6 mg/kg/day
– Empty stomach
– High iron dietary uptake
– Avoid tea, coffee, antacid, H2 antihistamine
blocker, proton pump inhibitor
2. Ascorbic acid supplementation
3. Folic acid supplementation (female teenager)
4. Treat the primary illness
23. • Iron preparation
– Ferrous sulfate (20% elemental iron)
– Ferrous gluconate (15% elemental iron)
– Elemental iron
• Continue therapy 2 months after anemia
resolved : iron storage
24. Parenteral iron therapy
Indications:
• oral iron is poorly tolerated;
• rapid replacement of iron stores is needed;
• gastrointestinal iron absorption is
compromised;
• erythropoietin therapy is necessary,
particularly in renal dialysis patients.
27. REKOMENDASI IDAI
tentang Suplementasi Besi untuk Bayi dan Anak
Suplementasi besi diberikan kepada semua
anak, dengan prioritas usia balita (0-5 tahun),
terutama usia 0-2 tahun.
28. REKOMENDASI IDAI
–BBLR (<2500 g): 3 mg/kgBB/hari untuk usia 1
bl-2 th (dosis max 15 mg/hari, dosis tunggal).
–Bayi cukup bulan: 2 mg/kgBB/hari usia 4 bl-2 th
–Usia 2-12 tahun (usia sekolah): 1
mg/kgBB/hari, 2x/minggu selama 3 bl
berturut-turut/thn
–Usia 12-18 th (remaja): 60 mg/hari atau 1
mg/kgBB/hari, 2x/mgg selama 3 bl berturut-
turut/th (remaja perempuan + 400 µg asam
folat).
29. Take home messages
• Check any risk of iron deficiency
– Diet history, risk factors
– Good clinical exams
• Supplementation (rekomendasi IDAI)
Editor's Notes
Regulation of iron absorption and exportation by enterocytes. Both heme and non-heme iron are absorbed by specific pathways, including divalent metal transporter-1 (DMT-1) and heme carrier protein (HCP1), in association with the ferrireductase, duodenal cytochrome B (Dcytb). Within the cell, iron can be stored within the ferritin molecule. The metal is exported by the protein ferroportin (FPN1), and transported into the blood by transferrin. In presence of hepcidin, ferroportin is internalized and degradated. Thus, iron exportation is blocked. Inversely, in the absence of hepcidin, ferroportin is maintained on the cell membrane, and iron transportation is facilitated (illustrations used elements from Servier Medical Art: www.servier.fr/servier-medical-art).