Iron Deficiency Anemia in

Adolescent

1

Definition
 Hemoglobin concentration is abnormally low
 age, gender, sea-level altitude
 as a result of several situation
 chronic infection
 hereditary blood conditions
 deficiency :
• folic acid, B12, B6, C,
protein, iron, zinc etc.

THERE IS NO DOUBT THAT IRON DEFICIENCY IS THE
CAUSE OF MOST ANEMIA

2

Prevalenc
e
USA
o

• Infants (9 – 24 months of age)
• Adolescent girls

}

• 3 % toddlers
IDA*
• 3 % adolescent
females
• < 1% adolescent
The Indonesian National Household
Health Survey
males
in 2001
: of adolescent girls (10-19 yrs) were
 30**%
anemic (Hgb level < 120 g/L)
 smaller studies : 22 – 44%

9% toddlers
:
o 11% adolescent femalesIron def.*
o < 1% adolescent males

India : 60 – 70% adolescent females***
• * LookerAC et.al. JAMA. 1997;277:973-976
• ** Parmesih dkk. Departemen Kesehatan . 2003
• *** Collaboration between Institute for Health Management, Pune &
International Center for Research on Women, Washington, 2000-2003

3

yet iron deficiency is the most common cause of anemia.Nutritional and metabolic aspects of iron Iron is one of the most common elements in the Earth’ crust. This is because the body has a limited ability to absorb iron and excess loss of iron as a result of hemorrhage is frequent. . affecting about 500 million people worldwide.

cytochromes. Flavoproteins) 0.Nutritional and metabolic aspects of iron Daily iron cycle Distribution of body iron (%) Hb 65 Ferritin & Hemosiderin 30 Myoglobin 3. peroxidase.5 Transferrinbound iron 0.g. catalase.5 Heme-enzymes (e.1 .

The average Western diet contains 10 – 15 mg iron daily from which only 5 .Dietary iron 1. Iron is present in food as ferric hydroxides. meat-in particular liver-is a better source than vegetables.10% is normally absorbed. 2. The proportion can be increased to 20 – 30% in iron deficiency or pregnancy but even in these situations most dietary iron remain unabsorbed. 3. . ferric-protein and heme-protein complexes. eggs or diary foods. in general. Both the iron content and the proportion of iron absorbed differ from food to food.

pancreatic secretions Solubilizing agents (e. phosphates Iron deficiency Iron excess Ineffective erythropoiesis Decreased erythropoiesis Pregnancy Infection Hereditary hemochromatosis Tea Increased expression of DMT-1 and Decreased expression of DMT1 and ferroportin in the duodenal enterocytes ferroportin induodenal enterocytes Increased hepcidin ___________________________________________________________________ . amino acid) Precipitating agentsphytates.Iron absorption __________________________________________________________________________ Factors favouring absorption Factors reducing absorption __________________________________________________________________ Heme iron Inorganic iron Ferrous form (Fe2+) Ferric form (Fe3+) Acids (HCl. vitamin C) Alkalis-antacids. sugars.g.

TfR 1. transferrin receptor 1. transferrin receptor 2.A model of the pathways of iron absorption by the entrocyte Gut lumen DMT 1 Fe2+ Enterocyte Apical Fe2 + Fe Dcyt b 3+ Fe2 + Hem e Hem e Basolater al Hephaes tin Ferriti n Intracellul ar iron pool Heme oxygenase Fe2 + Bloo d Fe3+ Transferri Fe2n Fe2 + Ferroportin + FeDMT Endocyto HF transferrin 1 sis E Fetransferrin Fe2 + TfR Transferrin 1 “Heme” TfR2 recepto The figure shows uptake of ionic iron and heme iron from the gut lumen and r transfer of iron to blood. . divalent metal transporter 1. HFE. DMT1. TfR2. hemochromatosis protein.

6 *These groups are more likely to develop iron deficiency. feces Adult male 0. • Puberty: Dietary.5 – 1 1–2 1. Therefore these groups are particularly likely to develop iron deficiency if there is additional iron loss or prolonged reduced intake.1 Female (age 12–15)* 0. Increased demands (i) menstruation. Bleeding.5 – 1 0.Estimated daily iron requirements (mg/day) Urine.5 – 1 0.5 1.5 – 1 Pregnant female* 0.5 – 1 Postmenopausal female 0.5 – 1 0.5 – 1 1.5 – 1 1–2 0. Total Menses Pregnancy sweat.5 – 1 Menstruating female* 0. (ii) each 1 kg of weight gain = 80 mL blood and requires 45 mg of iron .5 – 3 Children (average)* 0.6 0.6 Growth 0.6 – 2.

Diagnosis The degrees of iron deficiency Iron sufficient Normal Iron depletion Diminishing iron stores – insufficient iron supply Iron deficiency (without anemia) Iron deficiency anemia These iron stores are depleted further and begin to impair Hb synthesis Overt anemia– the iron supply is insufficient to maintain normal levels of Hb 10 .

Clinical Aspects  The signs & symptoms depend on the degree of deficiency and the rate at which the anemia develops. if any.Fatigue -Even severe anemia .Splenomegaly incidentally! .Cardiac dilatation .Exercise intolerance may be asymptomatic . . signs or symptoms.Pallor  Iron Deficiency Anemia-.Systolic murmurs -45 % were diagnosed .Tachycardia . anorexia 11 .Irritability.  Iron deficiency or mild-to-moderate anemia may show few.

al.Consequences  systematic condition • anemia • impaired exercise capacity • functional alteration • behavior and cognitive performance • lower mental and motor (early childhood) developmental test • School-aged scores • cognitive achievement children* • adolescent* • lower standardized math scores } Halterman JS et.107:1381-1386 * 12 . Pediatrics 2001.

Mechanisms • Uncertain • Several hypothesis:  altered neurotransmitter function  diminished activity of several enzymes (monoamine oxidase. which persists into adulthood despite correction of the anemia !! 13 . aldehyde oxidase)  reduced activity of dopamine Dd2 receptor  myelination may also be  a brief period of ID during the brain growth spurt affected causes a lasting deficit in brain iron.

 Total body iron – ferritin To describe the degrees of Iron Deficiency  Transport iron – transferrin saturation  Serum iron  Hematologic markers  Biochemical markers 14 .

Look AT. hematocrit.0 40 36 83 76 5 12 – 14 12. 409 15 0 . 0 12. Nathan and Oski’s hematology of infancy 14. editors. Philadelphia: WB Saunders Company. 2003. Brugnara C.0 46 38 86 78 F M 14. Nathan DG. 12. and childhood. 15 – 0 12. 12. 14.0 42 37 90 80 18 – 15. Orkin SE. Ginsburg D. p. In: Data from Nathan DG.0 41 36 87 79 17 13. (Hct) and MCV Hb (g/dL) Hct (%) Age MCV limit (μ3) Mean Lower Mean Lower limit Mean (y) Lower limit 8 – 11 13.Normal mean values for hemoglobin (Hb).0 47 40 90 80 F: 49 female 0 M : male F M Oski FA.5 43 37 84 77 M 5 14. A diagnostic approach to the anemic patient.0 41 36 85 78 F 13.

I=increased. CHr: reticulocyte hemoglobin content.Hematologic markers for identifying iron deficiency Hematologic Normal Iron Iron deficiency Iron marker depletion without anemia deficiency Hemoglob N : ≥ 11 N : ≥ 11 N : ≥ 11 Danemia :< in 11 (g/dL) N : 70 – N : 70 – N : 70 – MCV (fL) 100 100 100 D:< 70 RDW (%) N : < 15 N : < 15 N : < 15 I : ≥ 15 CHr (pg) N : ≥ 29 N : ≥ 29 D : < 29 D:< N: 1 – 5 Reticuloc N:1–5 N:1–5 29 ytes MCV: mean corpuscular volume. N=normal. D=decreased Values for ages 6 mo to 2 y 16 . RDW: red blood cell D:<1 distribution width.

D = decreased protoporphyrin/Hem N e (mcmol/mol) < 40 17 . I = increased.Biochemical markers for identifying iron deficiency Biochemical Normal Iron Iron deficiency Iron deficiency marker Serum ferritin (mcg/dL) anemia Serum iron (mcg/dL) Total iron-binding capacity Transferrin saturation (%) Serum transferring receptor (nmol/L) N 100 ± 60 N 115 ± 50 N 330 ± 30 N 35 ± 15 N < 35 depletion D < 20 N < 115 N 360 – 390 N < 30 I ≥ 35 Dwithout anemia D ≤ 10 < 10 D D < 60 < 40 N/I I 390 – ≥ 410 410 D D < 10 < 20 I I ≥ 35 ≥ 35 N < 40 I ≥ 40 I ≥ 70 Zinc N = normal.

Making the Diagnosis : Sideroblast ic anemia Thalasse mia trait Microcytic Iron deficienc y The results of these tests diurnal variation • recent iron intake • Chronic disease: inflammatio n. infection. cancer Lead poisonin g 18 .

Detect iron deficiency  Biochemical tests are before the onset of based on iron anemia. for Generally are more readily available and less expensive. metabolism ! CHr may help diagnose iron deficiency before anemia is present 19 .Making the Diagnosis  “Gold standard” : a direct test-bone marrow biopsy with Prussian blue staining  Hematologic tests are based on RBC features Too invasive routine use.

N=normal. Hoffbrand AV et. I=increased. 1993 20 .A=abnormal Weiss G.2006. Oski FA. Chronic Lead poisoning Inflammation Combination R R R R R R I N I N R R R N/I I R N R N/I R/N I I N N/I I/N I R I I N N N I I N I I N Both N N N I N N N N N A R=reduced.al. Iron def. several tests are often Differential diagnosis of microcytosis used Marker Thalassemia Hb MCV RDW FEP Serum iron TIBC Ferritin sTfR sTfR/log ferritin Cytokine CRP Hb Electro. 2005. Goodnough LT.Because many of these tests lack specificity..

The diagnosis of moderately severe iron-deficiency anemia is easy The diagnosis of mild forms of iron deficiency anemia may present a greater challenge  MCV  Serum ferritin  Serum iron  Serum iron-binding capacity  Red-cell protoporphyrin  Red-cell distribution width  Hemoglobin after the laboratory tests the of iron mayinstitution be less reliable therapy  the values of irondeficient and ironsufficient persons overlap considerably 21 .

.In the appropriate clinical setting : The important of iron intake history • an abnormally low Hb/Ht + • a dietary history of low iron intake •an abnormally low Hb/Ht + • a normal diet history of adequate iron intake Ferriti n Strongly suggest IDA Response to a therapeutic trial To look for blood loss e.g. occult rectal bleeding 22 .

Therapeutic trial Oral iron salts (ferrous sulfate) Presumpti ve IDA Children: 3 to 6 mg/kg per day (qd or tid) Adolescents: 60 mg/dose (qd or bid) IDA nutritional The response to iron typically rapid Hb increase ≥ 1 g/dL after 1 month of therapy 23 .

Preventi on PRIMARY PREVENTIO N Sufficient dietary iron must be available from 4 months of age and through the weaning period. SECONDA RY PREVENTI ON SUPPLEMENTARY IRON FORTIFICATION OF FOODS DIETARY EDUCATION REGULAR SCREENING PROMPT DIAGNOSIS TREATMENT OF IRON DEFICIENCY 24 .

menstrual losses.Treatment of Iron Deficiency • Iron Supplementation • RBC Transfusion Determining the cause and correcting the abnormality  Growth spurts. poor dietary patterns. and benign gastrointestinal bleeding  Oral iron supplementation usually replaces stores most efficiently 25 .

Oral Supplementation  Iron salts: ferrous sulfate  inexpensive  effective therapy for iron deficiency  frequently complain of gastrointestinal discomfort. bloating. stool discoloration– making its use unacceptable to many  children: 3 to 6 mg/kg/day– threetimes-a-day dosing or single-dose daily regimen  Ascorbic  adolescents acid enhances iron (qd or : 60 mg/dose bid) absorption  on an empty stomach at night 26 . constipation.

serum ferritin. RDW.Oral Diagnose : Supplementation IDA Oral iron supplementati on for 1 month Hb measureme nt No improvement in Hb further evaluation : MCV. search for possible sources of blood loss Hb should be remeasure d An increase of 1 g/dL (10 g/L) or greater Iron therapy Hb has returned to a normal level Iron 6 therapy : m Iron 2 – 3 o months therapy: STOP 27 .

Reasons for Poor Response to Oral Iron Noncompliance  Ongoing blood loss  Insufficient duration of therapy  High gastric pH • Antacids  Inhibitors of iron absorption/utilization • Lead • Aluminum intoxication (hemodialysis patients) • Chronic inflammation • Neoplasia  Incorrect diagnosis • Thalassemia disorder • Sideroblastic anemia • Anemia of chronic inflammation 28 .

Oral iron is not tolerated Parenteral iron Erythrocyte transfusion should be used only if the anemia is causing severe cardiovascular compromise. hypervolemia and cardiac dilatation may result from rapid correction of the anemia !! 29 .

iron gluconate. erythropoietin therapy is necessary  An anaphylactic reaction (in renal dialysis patients)  Dose (mL) = 0.26 x Lean body weight) 30 .Parental Iron Replacement  iron dextran. rapid replacement of iron stores is needed 3. iron sucrose  Indication 1.0442 x (Desired Hb – Observed Hb) x Lean body weight + (0. Oral iron is poorly tolerated 2. gastrointestinal iron absorption is compromised 4.

otherwise. anemia should be screened for every 5 to 10 years 31 .Regular screening Adolescents AAP : screening all adolescents once between ages 11 and 21 years  screening menstruating females annually CDC :  annual screening of adolescent females if their risk is increased.

3. Cow’s milk should be avoided during the first year because it contains substances that chelate 32 iron and it sometimes induces occult . Infants who are not breast-fed should be nourished with an iron-supplemented formula (at least 12 mg/L) until the end of the first year of life. 2. Iron-enriched cereals should should be among the first foods introduced with a solid diet. Breast milk should be provided for at least 5 to 6 months.Iron Replacement in Infants The Committee on Nutrition of the American Academy of Pediatrics 1. Iron supplementation of 1 mg/kg/day should be provided to infants who are exclusively fed breast milk beyond 6 months of age. 5. 4.

The evidence is clear that early diagnosis and adequate treatment of IDA are critical to prevention or reversal of any negative medical or behavioral effects. Pediatricians must screen for this common nutritional deficiently actively and accurately. 33 .

Thank you and have a nice day .