PHOSPHATE

•Phosphorus in the body exists only as inorganic

phosphate or as organic phosphate esters. About 80% of
the phosphates are incorporated into the bone together
with calcium.
•Most organic phosphates are present inside the cells as
components of molecules e.g., the DNA, phospholipids,
ATP, etc.
•In contrast, most inorganic phosphates are mostly
confined in the extracellular fluid where they act as
buffers.
•There are many sources of phosphates in the diet. Once
inside the body, the phosphates can be excreted
principally via the urine.
> Phosphates are involved in the following:
•Transfer of energy during metabolism e.g., ATP
•Maintenance of pH of body fluids e.g.,
phosphate buffers
•Constituents of bones
•Membrane structure e.g., phospholipids

➢Phosphate homeostasis is closely linked with

calcium regulation. The same hormones regulate
the levels of the two minerals.
➢PTH, for example, stimulates the kidney to
excrete phosphate while conserving calcium.
➢In addition, the growth hormone is another
hormone that increase the reabsorption of
phosphates in the kidney.

➢Usually, the relationship between calcium

and phosphorus is inverse.
•Assay Notes
*The patient must be in the fasting state. If not,
the inorganic phosphorus level increases.
*Hemolyzed samples are avoided since the red
blood cells are rich in phosphates. Commercial
heparin preparations also contains phosphates.
•Levels of phosphates have diurnal variation.
•Higher values are obtained in the morning. It is
preferable to collect fasting samples in the
morning.
•There is a reciprocal relationship between calcium
and phosphorus. Usually, patients with
hypercalcemia have hypophosphatasia.
•Hypophosphatasia is seen in hyperparathyroidism
since increased PTH favors phosphate loss via the
kidney.

•Other cases accompanied by hypophosphatasia

are avitaminosis D, rickets, and osteomalacia.

•Hyperphosphatasia is seen in
hypoparathyroidism, chronic glomerulonephritis
resulting in decreased phosphate excretion, and
uremia due to phosphate retention.
•MAGNESIUM

•Magnesium is the 4th most abundant cation in the

body. Majority of this mineral is stored in the bones
in complex with calcium and phosphates.

•It is not readily metabolized. About 70% of

magnesium is free and only 30% is bound to protein.

•Most of the magnesium in the body is located

•within the cell.
•Magnesium is an essential activator of several
enzymes e.g., phosphatases, kinases,
phosphorylases and enolases.
•In reactions where ATP is the substrate, the true
substrate is Mg2+-ATP.
•This ion is also necessary in the oxidative
phosphorylation occurring in the mitochondria.
•It is a therapeutic agent and has an anti-
convulsant, laxative and antacid effects.
> Normal values of magnesium fall within the
range of 1.3 to 2.1 mEq/L or 0.65 to 1.05
mmol/L.
•Increased magnesium (hypermagnesemia) is seen
in chronic renal disease, severe dehydration, and
adrenal insufficiency with aldosterone deficiency.

•Decrease levels (hypomagnasemia) are seen in

gastrointestinal disorders (malabsorption,
prolonged diarrhea, bowel or kidney fistulas, acute
pancreatitis), acute alcoholism, prolonged
parenteral fluid therapy without magnesium
supplementation, and the use of diuretics.
 Effects of Ethyl Alcohol on Electrolytes

Problem Major Cause(s)

Low sodium level Massive intake of solute-free fluid
(hyponatremia) beer
Low potassium level Dietary deficiency, gastric losses,
(hypokalemia) leaky membranes, shifts from
extracellular to intracellular
Low phosphorus level Dietary deficiency, malabsorption,
(hypophosphatemia) increased cellular uptake
Low magnesium level Dietary deficiency, malabsorption,
(hypomagnesemia) phosphorus deficiency
COPPER
•Normal adult body contains about 80 to 120 mg copper.
•The average daily intake is 2-5 mg. Dietary sources include
grains, shellfish, legumes, organ meats, cocoa, and water.
•In the blood, copper is seen in red blood cells or is bound
to transport proteins e.g., albumin, and ceruloplasmin.
•Ceruloplasmin is necessary for the absorption of iron by
oxidizing ferrous iron to the ferric state, a prerequisite for
binding by transferrin.
•It has a peroxidase activity. Copper is important in
erythropoiesis (hemoglobin synthesis) and catalytic activity
of several enzymes e.g., cytochrome oxidase and uricase.
•MEASUREMENT OF COPPER

•The reference ranges are as follows:

Infants: 20-70 µg/dL
Children: 80-190 µg/dL
Men: 70-140 µg/dL
Non-pregnant women: 80-155 µg/dL
Pregnant women: 120-300 µg/dL
> To convert to SI, multiply µg/dL by 0.157 to get values in
µmol/L.
> Hypocupremia is seen in anemia in infants, Menkes
kinky hair syndrome (a genetic defect of copper
absorption that leads to progressive brain disease in
infants); (cont’)
•kwashiorkor, nephrosis, sprue, celiac disease,
and Wilson’s disease (hepatolenticular
degeneration where copper accumulates in the
liver causing toxicity).

•Hypercupremia is seen in acute copper poisoning,

pregnancy, estrogen therapy, lymphomas,
leukemias, rheumatoid arthritis, systemic lupus
erythematosus, and thalassemia.
IRON

* Total body iron in humans is approximately 3-5 g with

about 70% incorporated in the red blood cells.

•About 25% is found in the reticuloendothelial system,

incorporated with ferritin and hemosiderin as stored
iron.

•The two forms of iron in the body:

•Ferrous iron: This is found in oxyhemoglobin and
reduced hemoglobin
•Ferric iron: This is found in ferritin, hemosiderin,
transferrin, and met-hemoglobin.
•The two other proteins involved in the transport
of iron:
•Haptoglobin: This binds hemoglobin and serves
to facilitate disposal of the iron from this
molecule.

•Hemopexin: This binds heme to aid its removal

from the circulation.

•The normal serum iron concentration falls

within 65 to 165 µg/dL (11.6-29.5 µmol/L) for
men and 45 to 160 µg/dL (8.1-28.6 µmol/L) for
women.
•Values obtained are higher at birth but then falls
below adult levels, where it remains during infancy
and childhood.
•Higher values are obtained in the morning due to
diurnal variations.

Total Iron Binding Capacity (TIBC) and Transferrin

Saturation.
> A known amount of ferric ions, more than
sufficient to fully saturate the serum transferrin
with iron, is added to a serum sample.
•The excess ferric ions, not bound to transferrin, is
removed by addition of a small amount of buffered
ion-exchange resin.
•The sample is diluted and centrifuged, and an
aliquot of the supernate is analyzed for iron
content of the fully saturated transferrin; this value
is the TIBC.

•The % saturation of transferrin is measured as

follows:
Serum Fe
Transferrin Saturation = ---------------------- X 100
(%saturation) TIBC
•TIBC varies from 260 to 440 µg/dL (46.5-78.8
µmol/L). Transferrin saturation ranges from 20-
50%.
•Serum iron is increased in cases of:
1. Increased red blood cell destruction
(hemolytic anemia)
2. Ineffective or decreased erythrocyte
formation (pernicious anemia in relapse,
aplastic anemia, marrow damage by toxins)
3. Blocks in heme synthesis (lead poisoning,
pyridoxine deficiency)
4. Increased release of storage iron (acute
hepatic cell necrosis)
 5. Increased intake or impaired control of iron
absorption (ingestion of large amounts of iron,
hemochromatosis, hemosiderosis)
•TIBC is increased when plasma transferrin
increases. This occurs during late pregnancy, in
iron deficiency anemia, after acute hemorrhage,
and after destruction of liver cells.

•Transferrin increases in iron overload states e.g.,

hemochromatosis and hemosiderosis, hemolytic
anemia, acute hepatitis, and pernicious anemia in
relapse.
•Decreased serum iron occurs in:
1. Decreased intake of iron (iron deficiency
anemia, malabsorption of iron)
2. Accelerated loss of iron (acute or chronic
blood loss, late pregnancy)
3. Impaired release of stored iron from
reticuloendothelial cells (infection, neoplasia,
rheumatoid arthritis)

TIBC is decreased when synthesis of transferrin is

decreased (infection, neoplasia, uremia) or loss of
transferrin in the urine (nephrosis).
 •Transferrin saturation is decreased in iron
deficiency anemia, late pregnancy, infection,
neoplasia, and after acute hemorrhage.

Zinc Protopophyrin/Heme Ratio (ZPP/H).

➢This is an excellent screening test for detecting
iron deficiency anemia and for monitoring the
course of therapy.
•The results are displayed as a ratio of µmol ZPP/mol
heme.
•It is normal in thalassemia but increased in iron
deficiency anemia.
•The ratio is elevated in all types of iron deficiency
syndromes and chronic exposure to lead.
Disease Iron TIBC / UIBC %Transferri Ferritin
Transferrin (Unsatura n Saturation (intracellular
(plasma -ted Iron protein that stores
glycoprotein Binding iron)
s) Capacity)
Iron Deficiency Low High High Low Low
Hemochromatosis High Low Low High High
Chronic Illness / Low Low Low/Norm Low Normal/High
anemia of chronic al
disease (ACD)
Hemolytic Anemia High Normal/Low Low/Norm High High
al
Sideroblastic Normal/Hig Normal/Low Low/Norm High High
Anemia h al
Iron Poisoning High Normal Low High Normal
Pregnancy or Normal High. The increased Low, as High
use of hormonal liver there is
contraception, increases excess
but without iron the transferrin
deficiency production with normal
of serum iron
transferrin, levels.
thus raising
TIBC.
HOW TO DIAGNOSE ?
ZINC

➢Zinc is an essential trace element which is

important as an activator of enzymes e.g., alkaline
phosphatase, carbonic anhydrase,
carboxypeptidase, alcohol dehydrogenase, DNA
and RNA polymerases, etc.

➢It is also involved in insulin and porphyrin

metabolism.

➢It was found out to be critical for growth and

sexual maturation.
•It is also involved in wound healing and sensory
perception especially the taste and the smell
senses.
•In plasma, zinc is bound to albumin, transferrin
and α2-macroglobulin.
•Excretion of zinc occurs via the gut.

•The reference range for plasma zinc is 70-150

µg/dL (10-23 µmol/L).
•Zinc is increased in zinc toxicity. Zinc chloride
causes tissue necrosis. Zinc oxide fumes causes
chemical pneumonitis.
•MANGANESE
•This trace element is seen mainly in grains and
cereals. It is also present in instant coffee and tea.
• Manganese is essential for lipid and
carbohydrate metabolism, bone and tissue
formation and reproductive process.
•Manganese is also a component of enzymes e.g.,
pyruvate decarboxylase, superoxide dismutase,
and some hydrolase occurs primarily via the bile.
•Toxicity occurs after inhalation of manganese
dust.
•This results in basal ganglia damage and produce
both psychological and neurological effects.
COBALT
•Vitamin B12 contains cobalt.
•Its deficiency results in pernicious anemia.
•No dietary requirement exists for cobalt because
no cobalt-containing enzymes have been found so
far.

MOLYBDENUM

•This help form the active sites of certain enzymes

e.g., xanthine oxidase, aldehyde oxidase, and
sulfite oxidase.
CHROMIUM
•It is an essential component of the glucose
tolerance factor which helps maintain the normal
insulin response to a glucose load.
•In its absence, insulin becomes less effective in
reducing hyperglycemia.

NICKEL
•This stabilizes the nucleic acid structure allowing
the synthesis of proteins.
• It is also linked to iron metabolism.
* Nickel deficiency is accompanied by iron
deficiency.
*Serum nickel can be determined by AAS (Atomic
Absorption Spectrophotometry). Its concentration
normally falls within 1 to 4 µg/dL (17-70 nmol/L).

IODIDE
* Iodine is a component of the thyroid hormones
thyroxine (T4) and triiodothyronine (T3), which
regulate the basal metabolic rate and are
necessary for proper growth and development.
•Goiter usually develops in people living in areas
where iodide is lacking in drinking water and food.
•Determination of serumT3 is the simplest test to
evaluate iodide levels.
•If the levels of T3 is below the reference range (70 to
200 ng/dL or 1.1 to 3.1 nmol/L), thyroid insufficiency
is indicated.

SELENIUM
•This is a component of the enzyme glutathione
peroxidase.
•This enzyme protects the tissues from the
damaging effects of peroxidases (hydrogen
peroxide and lipid hydroperoxide) and other
oxidants by decomposing them.
•It also prevents the formation of free radicals.

•Selenium deficiency is associated with

malnourishment, chronic bowel disease, or
hyperalimentation without selenium
supplementation.
1 Peter 5:8
8 Be sober, be vigilant; because your adversary the https://lifeteen.com/blog/why-pray-truth-prayer/

devil walks about like a roaring lion, seeking whom

he may devour.”