1. Iron deficiency anemia
Dr . YASSER AL-AHMADI

2. Definition of Anemia
A reduction in the concentration of hemoglobin in the PB below the normal for the age and sex
WHO criteria
Adult male < 13g/dL
Adult female < 12g/dL
Pregnant female < 11g/dL

3. Body Iron Distribution and Storage
Duodenum
Dietary iron
(average, mg
Utilization
Utilization
per day)
Plasma
(TIBC)
transferrin
(3 mg)
Bone
Muscle
marrow
(myoglobin)
Circulating
(300 mg)
(300 mg)
Storage
erythrocytes
iron
(hemoglobin)
(Ferritin)
(1,800 mg)
Iron absorption in the intestine is controlled by signaling mechanisms
The liver removes and stores excess iron
Iron is transported in the plasma in a complex with transferrin
Iron is utilized by the muscles to generate myoglobin and by the bone marrow to generate hemoglobin for red blood cells
Iron released by tissue breakdown is absorbed and recycled by the body
Traces (1 to 2 mg) of iron are lost each day by sloughing of mucosal cells, loss of epithelial cells, blood loss, and menstruation
Iron can increase through greater intake of dietary iron, increased efficiency of intestinal absorption, and blood transfusion
The human body has not evolved a mechanism to clear excess iron
Reference
Andrews NC. Disorders of iron metabolism. N Engl J Med. 1999;341:
Sloughed mucosal cells
Desquamation/Menstruation
Other blood loss
(average, mg per day)
Liver
Reticuloendothelial
macrophages
(1,000 mg)
Iron loss
(600 mg)

4. GI Absorption of Iron

5. The distribution of body iron
Amount of iron Male Female %
in average adult (g) (g) of total Hb
ferritin & hemosiderin
Myoglobin
Heme enzyme
Transferrin-bound
iron

6. Estimated daily iron requirements, Units are mg/day
0.5-1
1-2
1.5-3
1.1
Adult men
Postmenopausal female
Menstruating female
Pregnant female
Children
Female (age 12-15)

7. What is iron-deficiency anemia ?
It is the lack of iron in the blood, which is necessary to make hemoglobin.

8. Causes of IDA Increased iron requirement Inadequate iron intake
Growth spurt: infants, adolescence
Menstruation
Pregnancy
Inadequate iron intake
Low iron diet
Malabsorption
Increased iron loss
GI tract
Menorrhagea
Others

9. Diagnosis of Anemia History Physical Examination
Laboratory Investigation

10. Patient History Symptoms and its duration Dietary habits/Pica
Fatigue, muscle weakness, headache, vertigo, syncope, dyspnea, palpitations, indigestion, etc
Dietary habits/Pica
Blood loss: Melena, Hematochezia, Hemorrhoid, Menstruation(Menorrhagea)
Medications
Previous record
Family history

11. Physical Examination Skin pallor Pale conjunctiva/Jaundice
Smooth tongue/Stomatitis
Splenomegaly/Hepatomegaly
Koilonychia (Nail spooning)
Esophageal Web

13. Laboratory Investigation
First Line Studies
- CBC:Hb, Hcrit, Rbc indices, Cell count, Reti count
- PB morphology examination
- Chemistry(with LDH )
Second Line Studies
- Iron/TIBC/Ferritin
- Stool occult blood(3 times)
- BM study, others

14. BLOOD AND BONE MARROW SMEAR
microcytosis, hipochromia, anulocytes, anisocytosis poikilocytosis
BONE MARROW
high cellularity
mild to moderate erythroid hyperplasia (25-35%; N 16 – 18%)
polychromatic and pyknotic cytoplasm of erythroblasts is vacuolated and irregular in outline (micronormoblastic erythropoiesis)
absence of stainable iron

15. Serum iron & iron binding capacityFe
TIBC
TRANSFERIN SATURATION
FERRITIN

16. Treatment of IDA Correct underlying cause, if present
Iron supplementation
Oral iron:
The best preperation is ferrous sulphate which contains 67mg of iron in each 200mg (anhydrous) tablet and is best given on an empty stomach in doses spaced by at least 6 hours.if side effects occur (e.g.nausea,abd pain ,costipation or diahrea) these can be reduced by giving iron with food or by using a preparation of lower iron content e.g. ferrous gluconate which contains less iron 37mg per 300mg tablet. The hb should rise at the rate of about 2g/dl every 3 weeks.

17. Parentral iron
- Iron –sorbitol-citrate (jectofer) is given as repeated i.m injections whereas ferric hydroxide-sucrose (venofer) is administered by slow i.v inj or infusion. There may be hypersensitivity or anaphylactoid reactions and parentaral iron is therefore only given when it is considered necessary to replenish body iron rapidly (late pregnancy or p.t on hemodialysis and erythropoietin therapy or when oral iron is ineffective (e.g. severe malabsorption ).the hematological response is the same as in oral therapy.

18. Q & A When do we prescribe iron for pregnant women ?
When ferritin < 8 ng/mL
Not when ferritin > 12 ng/mL
When do we expect normalization of hemoglobin in patients with IDA undergoing iron treatment (if no continued iron loss) ?
Usually in 4 – 6 weeks
Does intramuscular or intravenous iron restore hemoglobin level faster than oral iron ? No

19. Helicobacter pylori infection
H. pylori infection usually acquired by oral ingestion in childhood
Prevalence 20-50% in industrialized countries
Prevalence inversely related to socioeconomic conditions
May be inadvertently cured by antibiotics treatment for other reasons
Causes continuous gastric inflammation in all infected subjects
Well characterized at the molecular biochemical and clinical levels.
Effect of this genetic polymorphism is highly penetrant when TPMT-deficient patients are treated with std doses of thiopurine.
Dr. Barry Marshall, Nobel laureate

20. Effects of H. pylori infection
High acid output
Antral gastritis
Duodenal ulcer
Low acid output
Atrophic gastritis
Gastric ulcer
Gastric cancer
MALT lymphoma
Well characterized at the molecular biochemical and clinical levels.
Effect of this genetic polymorphism is highly penetrant when TPMT-deficient patients are treated with std doses of thiopurine.
Rugae are almost completely lacking

21. H. pylori infection and iron deficiency anemia
Epidemiologic studies show H. pylori (+) associated with decreased ferritin levels
Well characterized at the molecular biochemical and clinical levels.
Effect of this genetic polymorphism is highly penetrant when TPMT-deficient patients are treated with std doses of thiopurine.
Herschko, C Best Practice Clin Hemat :363

22. H. pylori infection: Mechanism of iron deficiency
Occult GI bleeding
Competition for dietary iron -
would expect more patients to be
iron deficient
Effect on gastric secretion
High intragastric pH
Low gastric juice ascorbic acid
Well characterized at the molecular biochemical and clinical levels.
Effect of this genetic polymorphism is highly penetrant when TPMT-deficient patients are treated with std doses of thiopurine.
Possible cause of iron deficiency in H. pylori2€ection mediated by achlorhydria
Annibale, B. et al. Gut 2003; 52:496

23. Treatment of H. pylori infection: Effect on pH and ascorbic acid
Treatment of H. pylori depends on presence of atrophy
Well characterized at the molecular biochemical and clinical levels.
Effect of this genetic polymorphism is highly penetrant when TPMT-deficient patients are treated with std doses of thiopurine.
Annibale, B. et al. Gut 2003; 52:496