Laboratory Tests for the Determination of Vitamin Status

Chapter 21 Laboratory Tests for the Determination of Vitamin Status

image Assessment of Vitamin Status

See Table 21-1 for laboratory tests and optimal ranges for common vitamins.15

TABLE 21-1 Laboratory Tests and Optimal Ranges for Common Vitamins

Ascorbic acid Serum
Load test
>0.3 mg/dL
30 mcg/108 WBCs
0.3-2.0 mg/h in control
24-49 mg/h after 500 mg
Biotin 3-hydroxyisovalerate <20 mcg/mg creatinine (overnight urine)
Folate Erythrocyte folate >160-650 ng/mL (~350 nmol/L)
Serum homocysteine <10 mcmol/L
Niacin Urinary N-methylnicotinamide
2-pyridone 5-carboxamide (2-PYR)
>1.6 mg/g creatinine

>1.6 mg/g creatinine
Pantothenic acid Urinary pantothenic acid >1 mg/day
Pyridoxine Serum level >50 ng/mL
Tryptophan load <35 mg/24 h xanthurenic acid
AST <1.5 (ratio)
ALT <1.25
Plasma pyridoxal 5-phosphate >30 nmol/L
Urinary 4-PASerum homocysteine >3.0 mol/d<10 µmol/L
Riboflavin EGRAC
Thiamine RBC transketolase
Whole blood thiamine (HPLC)
<15% increas
Vitamin B12 Serum B12
Urinary methylmalonic acid
Serum merhylmalonic acid
Serum homocysteine
>150 pg/mL
<5 mcg/mg creatinine

<0.45 mcmol/L

<0.10 mcmol/L
>30 pmol/L
Vitamin A Plasma retinol: 15-60 mcg/dL:
0-5 mo >20
6 mo-17 yr >30
Adult >20
Vitamin D 25 (OH) vitamin D 40-80 ng/mL
Vitamin E Plasma α-tocopherol >16.2 mcmol/L
α-tocopherol:cholestrol >5.2 mcmol/L
Vitamin K % serum uncarboxylated osteocalcin <20 ? (optimal not yet determined)

ALT, alanine aminotranferase; AST, aspartate aminotransferase; EGOT, erythrocyte glutamic oxaloacetic transaminase; EGPT, erythrocyte glutamic pyruvic transaminase: FAD, flavin adenine dinucleotide; H2O2, hydrogen perioxide; NAD, nicotinamide adenine dinucleotide; NADP, nicotinamide adenine dinucleotide phosphate; RBC, red blood cell; WBC white blood cell.

Data from references 1-5.

Water-Soluble Vitamins

Ascorbic Acid (Vitamin C)

Assessment of vitamin C is particularly difficult because ascorbate readily oxidizes in assay samples. In addition, serum levels reflect recent dietary uptake rather than actual tissue levels. Recent research in an animal model of vitamin C deficiency (the Gulo mouse) clearly demonstrated that a dietary intake that does not lead to serum saturation of vitamin C results in tissue deficits.6 Serum saturation of vitamin C was required to achieve tissue concentrations similar to wild-type animals, which can synthesize ascorbate. In humans, maximum serum saturation from oral dosing was predicted to be roughly 1/60th of that achieved with intravenous administration, highlighting the inability of serum levels to predict optimal physiologic function.7,8 Leukocyte levels are not as susceptible to dietary intake but are also readily affected by infection, hypoglycemia, and many common prescription and over-the-counter drugs. The popular lingual ascorbate test does not appear to be reliable because it does not correlate well with leukocyte or serum levels. The loading test, if carefully controlled, is probably most accurate, although good standard ranges have yet to be determined. Finally, discovery of ascorbate-dependent enzymes involved in cell signaling pathways and epigenetic modulation offer the possibility for more functional analysis in the future, although unfortunately no definitive analysis is currently available.9


Several procedures are available for assessing vitamin B6 status. Unfortunately, substantial agreement on the best methodology has not been established, because variations in phenotypes significantly alter the results of functional and loading tests. The active form of pyridoxine (pyridoxal 5′-phosphate [P5P]) is involved in some 60 enzymes, so deficient activity of these enzymes can be measured as a functional assessment of pyridoxine. Plasma levels of P5P appear to be a better functional indicator than erythrocyte levels, at least in patients with rheumatoid arthritis.17 Plasma levels below 30 nmol/L (considered borderline deficient) have independently been associated with an increased risk for coronary artery disease, with a particularly high risk when combined with high-sensitivity C-reactive protein.18,19 Although suitable for most circumstances, plasma P5P does not appear to be reliable during pregnancy or the acute phase of myocardial infarction, and alternatives should be used. Urinary 4-pyridoxic acid is a useful marker of recent intake only, whereas erythrocyte aminotransferase (EAST) and erythrocyte alanine aminotransferase (EALT) activation by pyridoxal phosphate may be a better indicator of long-term status.20 Elevated homocysteine may also be a sign of deficiency, at least in some populations.21

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Sep 12, 2016 | Posted by in MANUAL THERAPIST | Comments Off on Laboratory Tests for the Determination of Vitamin Status

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