[Skip to Content]

Folate (FOLA)

Send to a FriendPrint Page

EPIC Test Name

FOLATE

EPIC Code

LAB69

Specimen Requirements

serum
Minimum Volume:0.5 mL
Collection:Collect using standard laboratory procedures
Transport:Room Temperature ASAP
Stability:Room Temperature: 2 hours at 20-25 degrees C
Refrigerated: 2 days at 4-8 degrees C
Frozen: 4 weeks at -20 degrees C
Container:GOLD
Processing/Storage:Centrifuge pour off and freeze.
Rejection Causes:Hemolysis,
Insufficient Sample Volume, lipemic samples

Methods

Electrochemiluminescence

Turnaround Time

SpecimenTurnaround TimeFrequency
serumRoutine: 4 hours24/7

Reference Ranges

Electrochemiluminescence
All RangeUnit
>4.77 ng/mLng/mL

Clinical Indications

Folic acid, also known as folate, pteroylglutamic acid, or vitamin B9, functions as a carrier of one-carbon groups for the interconversion reactions of amino acids, e.g., homocysteine to methionine, and for the biosynthesis of purines and pyrimidines, which are required for DNA synthesis.
Multiple forms of folic acid exist in the body. They vary in the number of glutamic acid residues and the functional group, such as methyl, formyl, methylene, hydroxymethyl, in the pteroic acid residue. The principal form in the circulation or serum/plasma samples is 5-methyl-tetrahydro-folate (5-MTHF, or N5-Methyl FH4).
Folate is absorbed from dietary sources. The bioavailability of folic acid in vitamin supplement is greater than that of food sources. Polyglutamate forms of folate present in food are first converted to monoglutamates by pteroylpolyglutamate hydrolase in the intestinal mucosa. In low concentration, monoglutamyl folates are absorbed via a saturable transport process with an acidic pH optimum (pH ≈ 5); when intestinal folate concentrations exceed 5 to 10 µmol/L, absorption occurs via a nonsaturable absorption mechanism. Once being uptaken, most of the folate is reduced and methylated, and enters the circulation as tetrahyro-folate (THF), circulating loosely bound to albumin or to a lesser degree to a high-affinity folate-binding protein. Uptake by certain cells (kidney, placenta, and choroid plexus) occurs by membrane-associated folate-binding proteins that act as folate receptors, and the reduced folate carrier, a member of the SLC19 family, facilitates uptake by most tissue. Intracellularly, THF is demethylated and converted by folylpolyglutamate synthase to the polyglutamyl form which retain folate inside the cells. For release into the circulation, the polyglutamates are reconverted to monoglutamates by polyglutamate hydrolase.
In conditions the dietary folate intake is reduced, folate levels in serum/plasma samples typically fall within a few days. However, folate levels in red blood cells (RBC folate) are less subject to short-term dietary changes.
Folic acid and vitamin B12 metabolism are coupled by the reaction that transfers a methyl group from 5-MTHF to cobalamin. In cases of cobalamin (VB12) deficiency, folate is “trapped” as 5-MTHF which cannot be recycled to the active form, i.e.,THF and back into the folate pool to serve as the main one-carbon unit acceptor for many biochemical reactions, eventually causing a reduction in purine and pyrimidine synthesis and hence DNA, which results in megaloblastic anemia and neuropathies.
Significant folate deficiency is characteristically associated with macrocytosis and megaloblastic anemia. Lower than normal serum folate also has been reported in patients with neuropsychiatric disorders, in pregnant women whose fetuses have neural tube defects, and in women who have recently had spontaneous abortions. Folate deficiency is most commonly due to insufficient dietary intake and is most frequently encountered in pregnant women or in alcoholics.
Reduced levels of folate concentration may also be caused by excessive utilization, e.g,, liver disease, hemolytic disorders, and malignancies) or rare inborn errors of metabolism, e.g,, dihydrofolate reductase deficiency, formiminotransferase deficiency, 5,10-methylenetetrahydrofolate reductase deficiency, and tetrahydrofolate methyltransferase deficiency.

Additional Information

• Avoid expose samples to light.
• Patients with combined folate and iron deficiencies may not demonstrate the erythrocyte macrocytosis, a typical of folate deficiency anemia. However, these patients’ red cell distribution width (RDW) may typically be elevated.
• Nonfasting specimens yield falsely elevated results. Recent folic acid administration or dietary folate intake could result in normal or elevated values and possibly mask an underlying folate deficiency.
• Hemolyzed samples should not be tested for serum/plasma folic acid, or cause significantly increase folate values due to high concentrations of folate in red blood cells..
• It is contraindicated to measure samples from patients receiving therapy with certain pharmaceuticals, e.g. methotrexate or leucovorin, because of the cross reactivity of folate binding protein with these chemicals.

Common Synonyms

Folic Acid FOLIC ACID

Performed

Lab
Chemistry - Downtown

Interpretative Information

• Results below the low limit of reference range are suggestive of folate deficiency. Abnormal levels of serum/plasma folate are nonspecific to a disease condition. Clinical diagnosis should always be given in a combination of clinical observations and results of other diagnostic procedures.
• For evaluation of macrocytic anemias, measurements for both vitamin B12 and folate in the same sample or samples collected in the same sample drawing should be ordered. Additional serum testing for homocysteine and methylmalonic acid (MMA) helps to distinguish vitamin B12 from folate deficiency. In folate deficiency, homocysteine levels are elevated, while MMA levels are normal.
• Serum folate measurement is preferred over RBC folate measurement due to high analytic variability (coefficient of variation) of the existing assays for RBC folate. RBC folate quantitation is not recommended.

CPT

82746

LOINC

2284-8

References

1. Scott JM, Weir DG: The methyl folate trap. A physiological response in man to prevent methyl group deficiency in kwashiorkor (methionine deficiency) and an explanation for folic-acid induced exacerbation of subacute combined degeneration in pernicious anaemia. Lancet 1981;2:337-40. PMID 6115113
2. Roberts NB, Taylor A, Sodi R. Vitamins and Trace elements. In: Rifai N, Horvath AR, Wittwer CT, eds. Tietz Textbook of Clinical Chemistry and Molecular Diagnostics. 6th ed. Elsevier;2018: 639-718.
3. George L, Mills JL, Johansson AL, et al: Plasma folate levels and risk of spontaneous abortion. JAMA 2002;16;288:1867-3.
4. Klee GG: Cobalamin and folate evaluation: measurement of methylmalonic acid and homocysteine vs vitamin B12 and folate. Clin Chem. 2000;46(8 Pt 2):1277-83.
5. Benoist BD: Conclusions of a WHO Technical Consultation on folate and vitamin B12 deficiencies. Food and Nutrition Bulletin 2008 (volume 29, number 2) S238-S244

Contact Information

Chemistry - Downtown: (315)464-4460
Top