What Are the Signs of a Vitamin B6 Overdose?

Vitamin B6 is a nitrogen-containing compound that exists mainly in three natural forms: pyridoxine (PN), pyridoxal (PL), pyridoxamine (PM), and their phosphate derivatives (PLP, PNP, PMP). Vitamin B6 deficiency includes two kinds of vitamin B6 deficiency and vitamin B6 dependence in the narrow sense. The former refers to the syndrome caused by insufficient vitamin B6 intake from food or inactivation or increased excretion of vitamin B6 by taking a certain drug . Vitamin B6 dependence refers to the amount of vitamin B6 that a patient consumes in a healthy person, but still suffers from a deficiency of vitamin B6, which is mostly a genetic disorder.

Vitamin B6 deficiency

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Vitamin B6 is a nitrogen-containing compound that exists mainly in three natural forms: pyridoxine (PN), pyridoxal (PL), pyridoxamine (PM), and their phosphate derivatives (PLP, PNP, PMP). Vitamin B6 deficiency includes two kinds of vitamin B6 deficiency and vitamin B6 dependence in the narrow sense. The former refers to the syndrome caused by insufficient vitamin B6 intake from food or inactivation or increased excretion of vitamin B6 by taking a certain drug . Vitamin B6 dependence refers to the amount of vitamin B6 that a patient consumes in a healthy person, but still suffers from a deficiency of vitamin B6, which is mostly a genetic disorder.

Western Medicine Name

Vitamin B6 deficiency

English name

vitamin B6 deficiency

The main symptoms

Peripheral neuropathy

Contagious

Non-contagious

Whether to enter health insurance

no

1. Peripheral neuropathy is mainly seen in patients who have been receiving large amounts of isoniazid for a long time. It is characterized by sensory loss, weakness, and reduced tendon reflexes in the distal limbs. The patient complained of acral burning and painful paresthesia.

2. Central nervous system symptoms can be expressed as emotional depression, agitation and confusion. Insufficient vitamin B6 in infants can cause seizures and seizures, and severe cases can cause mental retardation. Greenberg (1956) in monkey experiments, fed with foods without vitamin B6 for 5 to 6 months, found that many experimental animals had intimal hyperplasia, which closely resembled the changes in human atherosclerosis. Purpura.

3. Other symptoms can lead to symptoms such as pellagra-like symmetric dermatitis, angular cheilitis, urethritis, and anemia. Diarrhea, anemia, and seizures are characteristics of vitamin B6 deficiency in infants and children.

Actively treat the primary disease and supplement with an appropriate amount of vitamin B6. Usually 2 to 10 mg of vitamin B6 is taken orally every day to achieve satisfactory results, and 10 to 20 mg per day is required during pregnancy. Vitamin B6 (pyridoxine) deficiency associated with special drugs that inhibit metabolism of vitamin B6 (pyridoxine) (such as isoniazid, cycloserine, and penicillamine) requires larger doses (may be as high as 100 mg per day) to Improve peripheral neuropathy. Generally, when you start taking vitamin B6 antagonists, you should take vitamin B6 at the same time to prevent side effects. Once supplemented with vitamin B6 when damage is caused, nerve damage cannot be completely reversed.

Large doses of vitamin B6 are contraindicated in patients receiving levodopa, as large doses of vitamin B6 can affect the efficacy of levodopa. For vitamin B6 dependent syndromes, such as vitamin B6 dependent epilepsy and vitamin B6 dependent anemia, large doses of vitamin B6 are required, usually in the range of 300 to 500 mg per day.

Vitamin B6 toxicity: A large intake of vitamin B6 from food sources has no side effects, but supplementation with vitamin B6 at 2 g / d or higher can cause serious side effects, manifested as sensory neurological symptoms. When the daily dose is less than 1 g, the risk of developing sensory neurological symptoms decreases rapidly. Supplements below 250mg / d are safe for most people.

Severe vitamin B6 deficiency is relatively rare. Almost all foods contain vitamin B6. Vitamin B6 (pyridoxine) is mainly derived from plant foods, and pyridoxal and pyridoxamine are derived from animal foods, especially lean meat, liver , Vegetables and all foods are the most abundant, and should be encouraged to eat more, and infant food should be added as soon as possible.

The daily requirement of vitamin B6 is 1-2 mg. Beans, cereal seeds, chicken, citrus, tomatoes, bananas, etc. are rich in vitamin B6, so this disease is rare now.

1. Vitamin B6 inadequate intake or malabsorption Although foods have a wide range of vitamin B6 sources, occasional deficiencies due to inadequate food intake, or malabsorption caused by Crohn's disease or celiac disease can occur.

2. The most important thing for long-term application of certain drugs is isoniazid. Its complex with pyridoxal phosphate makes it ineffective. Others have cycloserine, penicillamine, oral contraceptives, levodopa, etc. can make vitamin B6 inactive or increase excretion and cause vitamin B6 deficiency.

3. Alcoholism Because ethanol can accelerate the catabolism of pyridoxal phosphate, it can cause vitamin B6 deficiency.

4. Vitamin B6 dependence syndrome is a rare metabolic abnormality and is a genetic disease.

Vitamin B6 deficiency should be distinguished from other causes of dermatitis, glossitis, stomatitis, depression, dizziness, poor growth, peripheral neuropathy and seizures, and other neurological symptoms.

Laboratory inspection:

Direct measurement

(1) Direct measurement of plasma vitamin B6 level, which is normally greater than 40nmoL / L.

(2) Determination of vitamin B6 metabolites: The most commonly used is the determination of pyridoxal 5-phosphate (PLP) in plasma. It has a good correlation with tissue vitamin B6, but it has a slow response to intake and can take about 10 days. Reached steady state. At present, it is the best indicator for assessing the nutritional status of vitamin B6. Plasma PLP is greater than 20nmol / L as normal. However, various factors that affect the concentration of PLP should be considered in the evaluation. PLP levels can be reduced when protein intake increases, alkaline phosphatase activity increases, smoking and age increase.

(3) The metabolite 4-pyridoxic acid excreted in urine is measured, and if it is excreted less than 1.0 mg per day, vitamin B6 deficiency is often indicated. The output of 4-pyridoxic acid can almost immediately respond to the intake of dietary vitamin B6, and more than 3 mol / d is an indicator of suitable nutritional status.

2. Indirect determination

(1) Determination of -Erythrocyte aspartic acid transaminase (-EAST) and alanine transaminase (-Erythrocyte alanine transaminase (-EALT)) activity coefficients of -EAST and -EALT after PLP activation It is widely used to evaluate long-term vitamin B6 nutritional status. The -EAST activity coefficient is greater than 1.6 and the -EALT activity coefficient is greater than 1.25 as indicators of vitamin B6 deficiency. This method has now replaced the tryptophan stress test.

(2) Determination of tryptophan degradation products: The main pathway for tryptophan degradation is PLP-dependent urinase. After giving an oral dose of 2g tryptophan, urinary excretion of xanuric acid was greater than 65 mol in 24 hours, considering vitamin B6 deficiency.

Other auxiliary checks:

1. EEG often has fast movements, which can have spikes or can be highly irregular. Infants with vitamin B6 dependence show periodic spikes with high amplitude and occasional spikes.

2. CT or MRI showed mild cerebral cortex atrophy.

Patients with severe vitamin B6 deficiency may develop irritability, weakness, depression, dizziness, poor growth, peripheral neuropathy, and seizures. Diarrhea, anemia, and seizures are characteristics of vitamin B6 deficiency in infants and children.

Vitamin B6 deficiency is different, the severity of the disease is different (such as anemia, epilepsy), and the prognosis is also different.

The activity of vitamin B6 is reflected by three kinds of vitamin B6 and their 5-phosphates, and the active coenzyme form is pyridoxal 5-phosphate (PLP).

Vitamin B6 is easily absorbed in the jejunum by passive absorption. The absorbed vitamin B6 is converted into its respective phosphorylated form by pyridoxine kinase in the liver, and then each 5-phosphate is converted into PLP by flavin single nucleotide oxidase. Excess vitamin B6 is metabolized to 4-pyridoxic acid and excreted from the urine with other non-phosphorylated forms.

Pyridoxal phosphate PLP is a coenzyme of more than 100 enzymes in amino acid metabolism, including transaminase, decarboxylase, racemase and dehydratase. These enzymes play an important role in protein metabolism, so their requirements are related to the total amount of amino acids metabolized. PLP is also a coenzyme of serine hydroxymethyl transine, which is involved in the metabolism of one carbon group and vitamin B12 and folic acid, which can cause megaloblastic anemia when it is lacking. At the same time, PLP plays an important role in neuronal excitability, gluconeogenesis, niacin formation, lipid metabolism, nucleic acid and immune metabolism, and hormone regulation (Figure 1).