TRACE ELEMENTS IRON

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TRACE ELEMENTS IRON
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IRON METABOLISM

• DISTRIBUTION OF IRON IN THE BODY
• Between 50 to 70 mmol (3 to 4 g) of iron are
  distributed between body compartments.
• In normal subjects it is all protein-bound in
  plasma it is bound to Transferrin, in the stores
  to protein in ferritin and haemosiderin, and in
  erythrocytes it is incorporated into hemoglobin.

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Distribution of Iron in a 70 kg Adult Male
Transferrin 3-4 mg
Hemoglobin in red blood cell 2600 mg
Myoglobin and various enzymes 300 mg
Stores (Ferritin and Hemosiderin) 1000 mg
Absorption 1 mg / day
Losses 1 mg/ day
In an adult female of similar weight, the amount
in stores would be generally be less (100-400 mg)
and the losses would be greater (1.5 - 2 mg/d).
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IRON METABOLISM

• About 70 per cent of the total iron is
  circulating in erythrocyte hemoglobin.
• Up to 25 per cent of the body iron is stored in
  the reticuloendothelial system, in the liver,
  spleen and bone marrow bone marrow iron is drawn
  on for hemoglobin synthesis. Iron is stored as
  protein complexes, ferritin and haemosiderin.
  Ferritin iron is more easily released from
  protein than that in haemosiderin.
  Haemosiderin, probably an aggregate of ferritin,
  can be seen by light microscopy in unstained
  tissue preparations.

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RECOMMENDED DAILY DIETARY ALLOWANCES OF IRON
Category Iron (mg ) WHO recommendations
Infants 5-10
Children 5-10
Males 9-18 (5-10)
Females 14-18
Pregnant females 18-28
Lactating females 18-28
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IRON ABSORPTION

• The control of body iron content depends upon
  control of absorption by an active process in the
  upper small intestine. Within the intestinal cell
  some of the iron combines with the protein
  apoferritin to form ferritin, which, as elsewhere
  in the body, is a storage compound.

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IRON ABSORPTION

• Normally about 18 umol (1 mg) of iron is absorbed
  each day and this just replaces loss. This
  amounts to about 10 per cent of that taken in the
  diet,
• Iron absorption seems to be influenced by any or
  all of the following factors
• oxygen tension in the intestinal cells
• marrow erythropoietic activity
• the size of the body iron stores.

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IRON ABSORPTION

• Iron absorption is also increased in many
  non-iron deficiency anaemias.
• Most normal women taking an adequate diet
  probably absorb slightly more iron than men and
  so replace their higher losses in menstrual blood
  and during pregnancy.
• Iron requirements for growth during childhood and
  adolescence are similar to, or slightly higher
  than, those of menstruating women and can be met
  by increased absorption from a normal diet.

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Body Iron Compartments
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IRON TRANSPORT IN PLASMA

• Iron is transported in the plasma in the ferric
  form, attached to the specific binding protein,
  transferrin(2molecules/transferrin), at a
  concentration of about 18 umol/L (100 mg/dl).
• Transferrin is normally capable of binding about
  54 umol/L (300 mg/dl) of iron and is therefore
  about a third saturated.
• Transferrin-bound iron is carried to stores and
  to bone marrow cells and in the latter some iron
  passes directly into developing erythrocytes
  to form hemoglobin.

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Factors Affecting Plasma IronConcentration

• Sex and age differences
• Pregnancy and oral contraceptives
• Variation within in individual
• Random variation
• Circadian (diurnal ) rhythm
• Monthly variation in women

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IRON EXCRETION

• There is probably no control of iron excretion
  loss from the body may depend on the ferritin
  iron content of cells lost by desquamation,
  mostly into the intestinal tract and from the
  skin. The total daily loss by these routes is
  about 18 umol (1 mg). Urinary loss is negligible,
  reflecting the fact that all circulating iron is
  protein-bound.

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COMPARISON OF IRON LOSSES IN MEN AND
MENSTRUATING/ PREGNANT WOMEN
Source of loss Extra loss Daily extra loss Daily total loss
Men and non menstruating women Desquamation - - 18 umol (1 mg)
Menstruating women (mean value) Desquamation menstruation 290 umol (1 6 mg)/month 9 umol (0.5 mg) 27 umol (1.5 mg)
Pregnancy Desquamation loss to fetus and in placenta 7000 umol (380 mg)/9 months 27 umol (1.5 mg) 45 umol (2.5 mg)
Male blood donors Desquamation 1 unit of blood 4500 umol (250 mg)/4 months 36 umol (2.0 mg) 54 umol (3.0 mg)
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PATHOLOGICAL FACTORS AFFECTING PLASMA IRON
CONCENTRATION

• Iron deficiency and iron overload usually cause
  low and high plasma iron concentrations
  respectively.
• Iron deficiency is associated with a hypochromic,
  microcytic anemia and with reduced amounts of
  stainable bone marrow iron. Plasma ferritin
  concentrations are usually, but not always, low.
• Iron overload is associated with increased
  amounts of stainable iron in liver biopsy
  specimens and plasma ferritin conc are high.

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PATHOLOGICAL FACTORSAFFECTING PLASMA
IRONCONCENTRATION

• Other pathological factors
• Any acute or chronic illness, even a bad cold
• Disorders in which the marrow cannot use iron,
  either because it is hypoplastic, or because some
  other essential erythropoietic factor, such as
  vitamin B12 or folate, is deficient
• Hemolytic anemia.
• Acute liver disease.

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Transferrin and Total Iron-binding Capacity (TIBC)

• Plasma iron concentrations alone give no
  information about the state of iron stores.
• Diagnostic precision may sometimes be improved by
  measuring both the plasma transferrin and iron
  concentrations.
• The total iron-binding capacity (TIBC). Is
  usually a valid measure of the transferrin
  concentration.

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PHYSIOLOGICAL CHANGES IN THE PLASMA TRANSFERRIN
CONCENTRATION

• The plasma transferrin concentration is less
  labile than that of iron. However, it rises
• After about the 28th week of pregnancy even if
  iron stores are normal
• In women taking some oral contraceptive
  preparations
• In any patient treated with estrogens.

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THE PLASMA TRANSFERRIN PATHOLOGICAL CHANGES IN
CONCENTRATION

• Plasma transferrin concentration and TIBC
• Rise in iron deficiency and fall in iron overload
• Fall in those chronic illnesses associated with
  low plasma iron concentrations
• are unchanged in acute illness
• May be very low in the nephrotic syndrome

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SYNDROMES OF IRON OVERLOAD

• IDIOPATHIC HAEMOCHROMATOSIS
• ANAEMIA AND IRON OVERLOAD
• DIETARY IRON OVERLOAD
• INAPPROPIATE ORAL THERAPY

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IRON OVERLOAD

• CAUSES OF IRON OVERLOAD
• Increased intestinal absorption
• idiopathic haemochromatosis
• anemia with increased, but ineffective,
  erythropoiesis
• liver disease (rare cause)
• dietary excess
• inappropriate oral therapy.

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CONSEQUENCES OF IRONOVERLOAD

• Parenchymal iron overload occurs in idiopathic
  haemochromatosis and in patients with
  ineffective erythropoiesis. Iron accumulates in
  the parenchymal cells of the liver, pancreas,
  heart and other organs resulting in impairment of
  these organs diabetes mellitus, hepatic
  carcinoma.
• Reticuloendothelial iron overload is seen after
  excessive parenteral administration of iron or
  multiple blood transfusions. The iron accumulates
  initially in the R.E cells of the liver, spleen
  and bone marrow.

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CONSEQUENCES OF IRONOVERLOAD

• Haemosiderosis is a histological definition. An
  increase in iron stores as haemosiderin can be
  seen. It does not necessarily mean that there is
  an increase in total body iron for example, in
  many types of anemia there is reduced hemoglobin
  iron (less hemoglobin) but increased storage
  iron.
• Haemochromatosis describes the clinical disorder
  due to parenchymal iron-induced damage.

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TRACE ELEMENTS

• CHROMIUM

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CHROMIUM
RDA Functions Metabolism Deficiency disease Toxicity disease
50 200 ug (1-4 u mol ) Trivalent chromium, a constituent of Glucose Tolerance Factor, helps in binding of Insulin to target tissue Not well defined Impaired tolerance secondary to parenteral nutrition, decrease sensitivity of tissues to insulin Not known