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Vitamin B6 Deficiency and Dependency

(Pyridoxine Deficiency and Dependency)

By

Larry E. Johnson

, MD, PhD, University of Arkansas for Medical Sciences

Last full review/revision Aug 2019| Content last modified Aug 2019
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Because vitamin B6 is present in most foods, dietary deficiency is rare. Secondary deficiency may result from various conditions. Symptoms can include peripheral neuropathy, a pellagra-like syndrome, anemia, and seizures, which, particularly in infants, may not resolve when treated with antiseizure drugs. Impaired metabolism (dependency) is rare; it causes various symptoms, including seizures, intellectual disability, and anemia. Diagnosis is usually clinical; no laboratory test readily assesses vitamin B6 status. Treatment consists of giving oral vitamin B6 and, when possible, treating the cause.

Vitamin B6 includes a group of closely related compounds: pyridoxine, pyridoxal, and pyridoxamine. They are metabolized in the body to pyridoxal phosphate, which acts as a coenzyme in many important reactions in blood, central nervous system, and skin metabolism. Vitamin B6 is important in heme and nucleic acid biosynthesis and in lipid, carbohydrate, and amino acid metabolism (see table Sources, Functions, and Effects of Vitamins).

Dietary sources of vitamin B6 include organ meats (eg, liver), whole-grain cereals, fish, and legumes. (See also Overview of Vitamins.)

Etiology

Dietary vitamin B6 deficiency, though rare, can develop because extensive processing can deplete foods of vitamin B6.

Secondary vitamin B6 deficiency most often results from

Rarely, secondary deficiency results from increased metabolic demand (eg, in hyperthyroidism).

Rare inborn errors of metabolism can affect pyridoxine metabolism.

Symptoms and Signs

Vitamin B6 deficiency causes peripheral neuropathy and a pellagra-like syndrome, with seborrheic dermatitis, glossitis, and cheilosis, and, in adults, can cause depression, confusion, electroencephalogram abnormalities, and seizures.

Rarely, deficiency or dependency causes seizures in infants. Seizures, particularly in infants, may be refractory to treatment with antiseizure drugs.

Normocytic, microcytic, or sideroblastic anemia can also develop.

Diagnosis

  • Clinical evaluation

Vitamin B6 deficiency should be considered in

  • Any infant who has seizures

  • Any patient who has seizures refractory to treatment with antiseizure drugs

  • Any patient with deficiencies of other B vitamins, particularly in patients with alcoholism or protein-energy undernutrition

Diagnosis of vitamin B6 deficiency is usually clinical. There is no single accepted laboratory test of vitamin B6 status; measurement of serum pyridoxal phosphate is most common.

Pearls & Pitfalls

  • If antiseizure drugs do not stop seizures in infants, consider giving pyridoxine to treat possible vitamin B6 deficiency.

Treatment

  • Pyridoxine

  • Elimination of risk factors when possible

For secondary vitamin B6 deficiency, causes (eg, use of pyridoxine-inactivating drugs, malabsorption) should be corrected if possible.

Usually, pyridoxine 50 to 100 mg orally once a day corrects the deficiency in adults. Most people taking isoniazid should also be given pyridoxine 30 to 50 mg orally once a day. For deficiency due to increased metabolic demand, amounts larger than the daily recommended intake may be required. For most cases of inborn errors of metabolism, high doses of pyridoxine may be effective.

Key Points

  • Vitamin B6 deficiency is usually caused by pyridoxine-inactivating drugs (eg, isoniazid), protein-energy undernutrition, malabsorption, alcoholism, or excessive loss.

  • Deficiency can cause peripheral neuropathy, seborrheic dermatitis, glossitis, and cheilosis, and, in adults, depression, confusion, and seizures.

  • Suspect and diagnose based on clinical findings.

  • Correct secondary causes, or give supplemental pyridoxine.

Drugs Mentioned In This Article

Drug Name Select Trade
CUPRIMINE
SEROMYCIN
No US brand name
LANIAZID
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