Reference Range

Vitamin B6 is a complex of 6 vitamers: pyridoxal, pyridoxol, pyridoxamine, and their 5'-phosphate esters. Vitamin B6 deficiency causes blood, skin, and nerve changes.

The reference range for pyridoxal phosphate (PLP), the biologically active form of vitamin B6, is 5-50 µg/L.^{[1, 2, 3]}

Interpretation

Conditions associated with vitamin B6 deficiency include the following:

Atherosclerosis
Early myocardial infarction
Early stroke
Recurrent thromboembolism
Peripheral neuropathy
Depression
Generalized seizures
Anemia
Progressive nerve compression disorders (carpal tunnel syndrome, tarsal tunnel syndrome)

Factors that may increase the risk of vitamin B6 deficiency include the following:

Malabsorption
Malnutrition
Sickle cell disease
Inflammatory conditions
Rheumatoid arthritis
Hospitalization
Celiac disease
Hepatitis and extrahepatic biliary obstruction
Hepatocellular carcinoma
Chronic renal failure
Kidney transplant
Hyperoxaluria types I and II
Excessive alcohol ingestion
High serum alkaline phosphatase (eg, in cirrhosis, tissue injury)
Catabolic state
Hemodialysis
Peritoneal dialysis
Phototherapy for hyperbilirubinemia
Certain medications (cycloserine, hydralazine, isoniazid, D-penicillamine, pyrazinamide)

Marked increases in serum pyridoxal phosphate (PLP) levels are seen in hypophosphatasia.

Collection and Panels

Specifics for collection and panels are as follows:

Specimen type: Blood plasma
Container: Vacutainer, green top (heparin)
Collection method: Venipuncture
Specimen volume: 1 mL

Other instructions include the following:

Overnight fasting specimen
No vitamin supplements in preceding 24 hours
Transport in light-protective container
Centrifuge at 4°C; refrigerate immediately
Transfer plasma to dark-brown polypropylene or polyethylene transport tubes to protect from light

Panels include vitamin B complex.

Related tests include alkaline phosphatase and pyridoxic acid.

Description

Vitamin B6 is a complex of 6 vitamers: pyridoxal, pyridoxol, pyridoxamine, and their 5'-phosphate esters. Pyridoxine 5'-phosphate (PLP) is an essential cofactor in various transamination, decarboxylation, and synthesis pathways involving carbohydrates, sphingolipids, sulfur-containing amino acids, heme, and neurotransmitters. Vitamin B6 deficiency causes blood, skin, and nerve changes. This vitamin is unique in that either deficiency or excess can cause peripheral neuropathy.

Dietary sources of vitamin B6 include cereals, beans, vegetables, liver, meat, and eggs. After absorption, pyridoxine, pyridoxamine, and pyridoxal are transported into hepatic cells by facilitated diffusion. Pyridoxal kinase phosphorylates pyridoxine and pyridoxamine, after which they are converted to PLP, a coenzyme in tryptophan and methionine metabolism. PLP is the primary active pyridoxal form, and serum PLP is used as the primary index of whole-body pyridoxal levels.

In methionine deficiency, S-adenosylmethionine accumulates, resulting in the inhibition of sphingolipid and myelin synthesis. Tryptophan is a precursor to several neurotransmitters and is required for niacin production. Thus, pyridoxine deficiency can cause a syndrome indistinguishable from pellagra. The neurotransmitters dopamine, serotonin, epinephrine, norepinephrine, glycine, glutamate, and gamma aminobutyric acid (GABA) also require PLP for their production. Homocystine metabolism is dependent on pyridoxine, and high homocystine levels can result from pyridoxine deficiency.

Hypophosphatasia is a rare inborn error of metabolism caused by low activity of the tissue-nonspecific isoenzyme of alkaline phosphatase (TNSALP). Alterations in the TNSALP gene lead to rickets, osteomalacia, or both. Serum PLP levels are typically elevated and are used in determining the diagnosis.

Laboratory methods to detect deficiency are as follows:

Pyridoxine level in blood
Xanthurenic-acid level in urine
Erythrocyte glutamic oxalo-acetic transaminase
Lymphocytic growth response

Methods to make a quantitative assessment are as follows:

High-performance liquid chromatography (HPLC) method, using cyanide derivatization: Method to determine the plasma pyridoxal-5-phosphate (PLP) concentrations as an indicator of vitamin B6 adequacy
Tandem mass spectrometry

A study by Talwar et al indicated that in patients with disorders linked to low albumin levels or altered alkaline phosphatase (ALP) activity, determining the presence of true versus apparent vitamin B6 deficiency is probably more reliably achieved with red cell PLP measurements than with serum PLP concentrations. The investigators pointed out that the systemic inflammatory response induces decreased plasma levels of most vitamins, so that low plasma PLP does not necessarily signal true vitamin B6 deficiency. They also reported that albumin concentrations and ALP activity are associated not only with plasma PLP levels, but also with red cell PLP concentrations. Albumin levels between 10 and 44 g/L were found to be directly related to increased plasma PLP levels and inversely related to red cell PLP concentrations, while ALP activity was inversely correlated with plasma PLP levels and directly related to red cell PLP concentrations.^[4]