TIBC (Iron bind capacity & iron & % saturation)

Order Code

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2118

Preferred Specimen

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Collect 3 mL of serum using an SST tube. Allow the sample to clot upright for a minimum of 30 minutes, then centrifuge within 2 hours of collection. Store the specimen refrigerated.

ContainerType

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Serum separator tube

Minimum Volume

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3 mL serum

Transport Temperature

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Refrigerated

Specimen Stability

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5 days room temperature; 1 week refrigerated

Methodology

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Roche COBAS automated methodology or other
automated chemistry method.

Rejection Criteria

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• Moderate or greater hemolysis
• Moderate or greater lipemia

Overview

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Disruptions in iron regulation are among the most prevalent disorders encountered clinically. These conditions may involve iron deficiency—resulting from inadequate absorption or excessive loss—or iron overload, where iron accumulates due to normal erythropoiesis exceeding transferrin’s binding capacity or increased red cell breakdown. Serum iron concentrations can vary widely in response to both physiological and pathological factors, necessitating additional tests to accurately evaluate a patient’s iron status. Measurement of serum iron, total iron-binding capacity (TIBC), and ferritin levels together provides a comprehensive assessment.

Iron circulates in the bloodstream primarily bound to transferrin. Total iron-binding capacity reflects the maximum amount of iron required to fully saturate transferrin, serving as an indirect measure of transferrin concentration. The serum iron test quantifies the amount of iron currently bound to transferrin in the blood.

Clinical Significance

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• Support a diagnosis of iron deficiency
  • Due to inadequate intake, malabsorption, or altered metabolism
  • Due to blood loss
• Support a diagnosis of iron overload
  • Primary: Hereditary hemochromatosis (HH) where overload is caused by increased gastrointestinal iron absorption (erythropoiesis is normal); excessive iron is deposited in the liver and other organs causing fibrosis if untreated
  • Secondary: Hemosiderosis where iron overload is caused by a variety of conditions including anemias due to ineffective erythropoiesis (eg, thalassemias), repeated blood transfusion, excessive parenteral or oral replacement, etc
• Aid in distinguishing iron deficiency from chronic disease when the serum iron is low
• Monitor iron replacement therapy (transferrin saturation)
• Confirm diagnosis of iron toxicity (child overdose via vitamin ingestion) and monitor levels
• Monitor iron levels in patients undergoing dialysis
• To follow treatment for iron overload with deferoxamine or with regimen of recombinant human erythropoietin and phlebotomy

Interpretative Information

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Increased serum (plasma) iron:

• Iron is increased in hemosiderosis, hemolytic anemias (especially thalassemia), sideroblastic anemias, hepatitis, acute hepatic necrosis, hemochromatosis, and with inappropriate iron therapy.
• Some patients who receive multiple transfusions (eg, some hemolytic anemias, thalassemia, renal dialysis patients) will have increased serum iron levels.
• Iron may reach high levels with iron poisoning, which presents with emesis and severe abdominal pain. Metabolic acidosis with increased anion gap, leukocytosis, and hyperglycemia may be found with increased bilirubin, AST, ALT, and LD.

Decreased serum (plasma) iron:

• Serum (plasma) iron is decreased with insufficient dietary iron, chronic blood loss (including the hemolytic anemias, paroxysmal nocturnal hemoglobinuria), inadequate absorption of iron; and impaired release of iron stores as in inflammation, infection, and chronic diseases.
• In recovery from pernicious anemia, especially just after B₁₂ dose, iron levels are low.
• Serum iron is reported to drop with acute infarct of myocardium.

Increased TIBC:

• Iron-deficiency, oral contraceptives, late pregnancy

Decreased TIBC:

• Hypoproteinemia from many causes, including kwashiorkor, inflammation, hemochromatosis, hemosiderosis, thalassemia, hyperthyroidism, nephrotic syndrome, anemia of chronic disease, hemolytic anemia

Limitations

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• Although serum iron, TIBC, and % saturation are widely used for the diagnosis of iron deficiency, serum ferritin is a much more sensitive and reliable means of demonstration of this disorder.
• Gross hemolysis may interfere with serum (plasma) iron.
• Serum (plasma) iron levels do not always correlate with the severity or the clinical phase of iron toxicity (as in overdose). This is because testing is measuring free iron circulating in the blood. It is the intracellular iron that causes the toxic damage (Liebelt, 2013).
• Deferoxamine, used in therapy of iron toxicity, interferes with TIBC. TIBC may be overestimated in the presence of excessive free iron (ie, iron toxicity); thus, the IBC has only limited value in acute iron overdose (Siff, 1999).
• In overdose situation a specimen collected after 8 hours from ingestion may yield a deceivingly low result as iron is rapidly cleared from the blood.
• Low iron level may not indicate iron deficiency in acute infection with leukocytosis.
• Low iron concentrations may be misleading in chronic infection, inflammation, and malignancy; high ferritin levels occur in many such states.
• TIBC and transferrin are increased in patients on oral contraceptives, with normal saturation.

References

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Diagnostic Role

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Iron Status Indicators in Various Disease States

Disease	Ferritin	Transferrin / TIBC	Serum Iron	Iron Saturation
Uncomplicated iron deficiency	↓	↑	↓	N/↓
Anemia of chronic disease	N/↑	N/↓	↓	N/↓
Sideroblastic anemias	↑	N/↓	N/↑	↑
Hemolytic anemias	↑	N/↓	↑	↑
Hemochromatosis	↑	Slight ↓	↑	↑↑
Protein depletion		N/↓	N/↓	N/↓
Acute liver disease	↑	Var	↑	↑
↑ = increase; ↓ = decrease; N = normal; Var = variable.

Uncomplicated iron deficiency: Serum transferrin (and TIBC) high, serum iron low, saturation low. Usual causes of depleted iron stores are due to blood loss and inadequate dietary iron. RBCs in moderately severe iron deficiency are hypochromic and microcytic. The red cell distribution width increases and MCV decreases. Stainable marrow iron is absent. Serum ferritin decrease is the earliest indicator of iron deficiency if inflammation is absent.

Anemia of chronic disease: Serum transferrin (and TIBC) low to normal, serum iron low, saturation low or normal, ferritin increased. Transferrin decreases with many inflammatory diseases. With chronic disease there is a block in movement to and utilization of iron by marrow. This leads to low serum iron and decreased erythropoiesis. Examples include acute and chronic infections, malignancy, and renal failure.

Sideroblastic anemia: Serum transferrin (and TIBC) normal to low, serum iron normal to high, saturation high.

Hemolytic anemias: Serum transferrin (and TIBC) normal to low, serum iron high, saturation high.

Hemochromatosis: Serum transferrin (and TIBC) slightly low, serum iron high, saturation very high. Genetic tests for detecting hemochromatosis mutations (C282Y and H63D) are available. Homozygosity for C282Y mutation is responsible for up to 90% of hemochromatosis patients; see HFE Gene, Whole Blood.

Protein depletion: Serum transferrin (and TIBC) may be low, serum iron normal or low (if patient also is iron deficient). This may occur as a result of malnutrition, liver disease, renal disease (eg, nephrosis), or other entities.

Liver disease: Serum transferrin variable; with acute viral hepatitis, high along with serum iron and ferritin. With chronic liver disease (eg, cirrhosis), transferrin may be low. Patients who have cirrhosis and portacaval shunting have saturated TIBC/transferrin as well as high ferritin.

Test Setup Days

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Monday through Friday

CPT

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83550, 83540 Limited Coverage Test For Medicare.
Advance Beneficiary Notice Of Non-Coverage (ABN)
Required If Diagnosis Not Covered.
Medicaid Will Only Pay For Iron When Ordered On
The Same Day As Ferritin.