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Iron is an essential trace mineral element which forms an important component of hemoglobin,
metallocompounds and Vitamin A. Deficiency of iron, leads to microcytic hypochromic anemia. The toxic
effects of iron are deposition of iron in various organs of the body and hemochromatosis.
Total Iron Binding capacity (TIBC) is a direct measure of the protein Transferrin which transports iron from
the gut to storage sites in the bone marrow. In iron deficiency anemia, serum iron is reduced and TIBC
increases.
Transferrin Saturation occurs in Idiopathic hemochromatosis and Transfusional hemosiderosis where no
unsaturated iron binding capacity is available for iron mobilization. Similar condition is seen in congenital
deficiency of Transferrin.
Note
1. TSH levels are subject to circadian variation, reaching peak levels between 2 - 4.a.m. and at a
minimum between 6-10 pm. The variation is of the order of 50%. hence time of the day has influence
on the measured serum TSH concentrations.
2. TSH Values <0.03 uIU/mL need to be clinically correlated due to presence of a rare TSH variant in
some individuals
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Lipoprotein Electrophoresis .
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| REMARKS | CHOLESTEROL:HDL Ratio |
| | |
|----------------|------------------------|
| Low risk | 3.3 - 4.4 |
|----------------|------------------------|
| Average risk | 4.5 - 7.1 |
|----------------|------------------------|
| Moderate risk | 7.2 - 11.0 |
|----------------|------------------------|
| High risk | >11.0 |
-----------------------------------------
Note
1. Measurements in the same patient can show physiological& analytical variations. Three serial samples
1 week apart are recommended for Total Cholesterol, Triglycerides, HDL& LDL Cholesterol.
2. NLA-2014 identifies Non HDL Cholesterol(an indicator of all atherogenic lipoproteins such as LDL ,
VLDL, IDL, Lpa, Chylomicron remnants)along with LDL-cholesterol as co- primary target for cholesterol
lowering therapy. Note that major risk factors can modify treatment goals for LDL &Non HDL.
3. Apolipoprotein B is an optional, secondary lipid target for treatment once LDL & Non HDL goals have
been achieved.
4. Additional testing for Apolipoprotein B, hsCRP, Lp(a ) & LP-PLA2 should be considered among patients
with moderate risk for ASCVD for risk refinement
Comment
A variety of genetic conditions are associated with accumulation in plasma of specific class of lipoprotein
particles. The critical first step in managing lipid disorder is to determine the class or classes of lipoprotein that
are increased or decreased in a patient. Frederickson classification can be helpful in this regard. The
hyperlipidemic status should be evaluated to determine if it is a primary lipoprotein disorder or secondary to
metabolic disease. The diagnosis of primary hyperlipidemia is made after secondary causes have been ruled
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| FREDRICKSON CLASSIFICATION |
|------------------------------------------------------------------------------------------------|
| Type of |Molecular |Estimated |Lipoprotein |Cholesterol,|Triglyceride|Serum |
|Hyperlipoproteinemia|defect |incidence |elevated |Total(mg/dL)|(mg/dL) |Appearance |
|--------------------|-----------|-----------|------------|------------|------------|------------|
| I |Lipoprotien|1 in |Chylomicrons|+ to ++ | ++++ |Milky |
|Familial |lipase |1,000,000 | |200-400 |>3000 | |
|Chylomicronemia |deficiency;| | | | | |
|Syndrome |Apo C II | | | | | |
| |deficiency | | | | | |
|--------------------|-----------|-----------|------------|------------|------------|------------|
| IIa |Mutation in|1 in 500 | LDL | +++ |Normal |Clear |
|Familial |LDL | | |300-1000 | | |
|Hypercholesterolemia|receptor, | | | | | |
| |Apo B 100 | | | | | |
|--------------------|-----------|-----------|------------|------------|------------|------------|
| II b |Unknown |1 in 200 |LDL & VLDL |++ to +++ | ++ |Clear to |
|Familial Combined | | | |280-350 |200-500 |slightly |
|Hyperlipidemia | | | | | |turbid |
|--------------------|-----------|-----------|------------|------------|------------|------------|
| III |Genetic |1 in 10,000|Chylomicron |++ to +++ |++ to +++ |Clear to |
|Familial Dysbeta |variation | |and VLDL |300- 500 |200- 900 |slightly |
|lipoproteinemia or |in APO E | |remnant | | |turbid |
|Familial broadbeta | | | (IDL) | | | |
|disease | | | | | | |
|--------------------|-----------|-----------|------------|------------|------------|------------|
| IV |Unknown |1 in 500 | VLDL |Usually | ++ |Turbid |
|Familial | | | |<270 |200-1000 | |
|hypertriglyceridemia| | | | | | |
|--------------------|-----------|-----------|------------|------------|------------|------------|
| V |Unknown |1 in 500 |Chylomicron |++ to +++ | ++++ |Milky |
|Familial | | |& VLDL |<500 |<3000 | |
|hypertriglyceridemia| | | | | | |
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