Elements found in the body in low-concentration circulating in the body
Have specific in vivo metabolic functions and other similar elements cannot effectively do it
Consists of metals except for selenium, halogens, fluoride, and iodine
Essential Trace Elements
Iron
Iron
Common metallic element
Reduced form is the biologic form
Responsible for converting ferric to ferrous
Responsible for converting ferric to ferrous
Ferric Reductase - an enzyme responsible for converting ferric form to ferrous form of iron in the intestinal epithelium
Iron is a Prooxidant, contributing to lipid peroxidation, atherosclerosis, DNA damage, and neurodegenerative diseases
Iron is a Prooxidant
Contributes to lipid peroxidation, atherosclerosis, DNA damage, and neurodegenerative diseases
Non-Essential Trace Elements
It does not contribute to biochemical or functional process
Medically significant due to toxicity
Trace elements
Iron, Copper, and Zinc
Ultratrace elements
Selenium, Chromium, and Manganese
Two classifications of trace elements
According to Contribution/ Function to Biochemical Process
According to Concentration in Plasma/ Serum
Enzyme responsible for converting ferric form to ferrous form of iron in the intestinalepithelium
ferric reductase
We need Anti-oxidants instead of prooxidants in the free form
Iron in the plasma/serum can be a prooxidant
Iron is mainly present in the red blood cell
Amount of Iron in different locations
2-2.5g in HEMOGLOBIN
3-5mg in PLASMA (FREE & BOUND TYPE)
130mg in MYOGLOBIN
8mg in TISSUE
Iron is stored in the Liver, Spleen, and Bone Marrow as Ferritin and Hemosiderin
Apoferritin
Binds to the ferrous form of iron in the intestinal mucosa
Ferritin
Stores the ferrous form of iron
A low ferritin level is used as a diagnostic tool for determining individuals with iron deficiency
Apotransferrin
Binds the ferric form of iron for transport throughout the body
Transferrin
Transporter for the ferric form of iron
Ferroportin
Regulates/promotes the exportation of iron from cells
Hepcidin
Regulates iron absorption in the upper GIT by modulating the activity of ferroportin
Serum iron levels are falsely elevated by hemolysis and affected by diurnal variation
Diurnal Variation: Iron levels are highest in the morning and lowest at night
Nocturnal Variation: Iron levels are high in the evening and low in the morning
Conditions with Increased Iron Levels
Iron Poisoning (Overdose)
Hemochromatosis
Viral Hepatitis
Non-Iron Deficiency Anemias
Thalassemia
Aplastic anemia
Megaloblastic anemia
Sideroblastic anemia
Hemolytic anemia
Pernicious anemia
Conditions with Decreased Iron Levels
Iron Deficiency Anemia (IDA)
When insulin supply is low
Can cause diabetes mellitus
Non-Iron Deficiency Anemias
Thalassemia
Aplastic anemia
Megaloblastic anemia
Sideroblastic anemia
Hemolytic anemia
Pernicious anemia
Iron Deficiency Anemia (IDA)
Most common anemia; especially among children/pediatrics
Common in impoverished communities
DECREASE LEVEL OF IRON
IDA
Malnutrition - low intake of iron-rich food or no iron supplement
Malignancy (e.g. cancer, malignant conditions)
Chronic Infection
Nephrotic Syndrome
Most trace elements, including iron, are derived from the diet. A low iron level in the diet results in a decrease in iron level
Total Iron Binding Capacity
The amount of iron that could be bound by saturating transferrin and other minor-iron binding proteins present in the serum or plasma sample
In patients with Iron Deficiency Anemia (IDA), they have high Total Iron Binding Capacity (TIBC) because they have no/low iron in the plasma or serum, resulting in no binding of iron in the transferrin (no saturated transferrin)
In patients with Non-IDA such as hemolytic, megaloblastic, sideroblastic types of anemia, they have low Total Iron Binding Capacity (TIBC) because they have high iron levels; more transferrin will be saturated
Increased Total Iron Binding Capacity (TIBC)
Occurs in IDA, hepatitis, iron-supplemented pregnancy