M.

Prasad Naidu
MSc Medical Biochemistry, Ph.D,.

Iron (Fe)
2 types of body iron
heme iron
hemoglobin, myoglobin, catalases, peroxidases, cytochromes (a,
b and c involved in electron transport), cytochrome P450
(involved in drug metabolism)
non-heme iron
ferritin, hemosiderin, hemofuscin, transferrin,
ferroflavoproteins, aromatic amino acid hydroxylases
food iron is also classified as heme and non-heme
Food iron
heme iron
meats
poultry
fish

20-23% of heme-iron is
absorbable
non-heme iron
vegetables
fruits
legumes
nuts
breads and cereals
only ~ 3% on non heme
iron is absorbed
Iron absorption
occurs in upper part of small intestine
about 10% of food iron is absorbed
requires gastric HCl (releases ionic iron)
also requires copper
ferrous is better absorbed than ferric form
Fe
++
forms chelates with ascobic acid, certain sugars
and amino acid
Iron distribution and storage
carried in blood stream via transferrin (a b globulin)
stored in 2 forms:
ferritin (a water soluble complex consisting of a core of ferric
hydroxide and a protein shell (apoferritin)
hemosiderin (a particulate substance consisting of aggregates
of ferric core crystals)
stored in liver, spleen, bone marrow, intestinal
mucosal cells and plasma
FOOD IRON
Fe
++
Fe+++
APOFERRITIN
FERRITIN
mucosal cell
(upper small
intestine)
gastric HCl, ascorbic acid
intestinal
secretion
1-2 mg/day
Fe
+++
- transferrin
plasma
apotransferin
Fe++ - hemoproteins
(hemoglobin, myoglobin
Fe
+++
- ferritin
Fe
+++
- hemosiderin
bone marrow
muscle
liver
unabsorbed Fe
(fecal excretion)
Iron elimination
there is no mechanism for excretion of iron
iron is normally lost by exfoliation of intestinal
mucosal cells into the stools
trace amounts are lost in bile, urine and sweat (no
more than 1 mg per day)
bleeding (vaginal, intestinal) is a more serious
mechanism of elimination
IRON DEFICIENCY
Initial symptoms are vague and ill-defined
easy fatigability
lack of appetite
headache
dizziness
palpitations

then: hypochromic-microcytic anemia
microcytosis (small RBCs)
hypochromia (poor fill of hemoglobin)
poikilocytosis (bizarre shapes)
anisocytosis (variable sizes)
IRON DEFICIENCY
Causes:
excessive blood loss (parasitic, accidental, menstrual): is
most common cause
rapid growth in children with limited intake of iron
malabsorption
gastric resection
sprue
increased metabolic requirement
pregnancy, lactation or neoplasia
Diagnosis of iron deficiency
hematology (microcytic hypochromic cells)
low serum iron
low serum ferritin( indicates low body stores)
in some conditions (inflammation, hepatitis) ferritin may be
high
low hemosiderin
high total iron binding capacity (TIBC)
Iron absorption
average diet contains 10 - 15 mg of iron perday
a normal person absorbs 5 -10% of this iron or 0.5 -
1.0 mg daily
iron absorption increases in response to low iron
stores
menstruating women: 1 - 2 mg per day
pregnant women: 3 - 4 mg per day
absorption is via active process
Different types of iron
Ferrous sulfate 20%
Exsiccated ferrous sulfate
ferrous gluconate 11.6%
ferrous fumarate 33%
ferrocholinate 12%
polysaccharide-iron complex
iron dextran (Imferon)
Treatment of iron deficiency
give 200 - 400 mg of iron per day
up to 25% of the iron preparation may be absorbed
50 - 100 mg of iron may be utilized in case of
deficiency
give on an empty stomach
enteric coated iron tablet should not be used since
we want absorption to occur in the stomach and
proximal duodenum
Treatment of iron deficiency
parenteral iron is used in patients who have had bowel
resections or in cases of inflammatory bowel disease
normally given IM (painful) Z-track minimizes tatoo
oral iron causes black stools, constipation, cramping
do not administer with antacids or metal chelators
(tetracyclines)
Acute iron toxicity
common in small children ingesting large doses of
soluble iron compounds
toxicity is usually divided into 4 phases:
1. 30 - 60 min. following ingestion
abdominal pain
nausea and vomiting
signs of acidosis and cardiovascular collapse may be seen
Acute iron toxicity
2. Period of improvement - last about 8 to 16 hours
3. Period of progressive cardiovascular collapse (about 24
hrs after ingestion)
convulsions
coma
high mortality
4. Gastrointestinal obstruction from scarring of stomach
and small intestine
Deferoxamine mesylate (DFOM)
(CH
2
)
5
H
2
N N
C
(CH
2
)
2
C
N
(CH
2
)
5
N
O O
OH H C
(CH
2
)
2
C
O
N
O
OH (CH
2
)
5
N
C
CH
3
O
OH
H
A chelating agent which reacts with ferric ion to form a
1:1 chelate known as ferrioxamine
Marketed as Desferal Injection (Ciba)
Produced by Streptomyces pilosus
Chronic iron toxicity
causes
hereditary hemochromatosis
hemosiderosis
symptoms
cirrhosis: iron deposition in the liver
diabetes: iron deposit in the pancreas (damage to beta
cells)
skin pigmentation
cardiac failure
treatment: phlebotomy ( 1 unit of blood removes about
250 mg of iron