Laboratory Tests for the Determination of Vitamin Status

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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 <1.3
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