Flexible Spending Accounts will reimburse you for incurred expenses during your FSA plan year (period of coverage).
“Incurred” refers to expenses that happen after a service or product is provided – not when you are billed or pay for the service.You cannot be reimbursed in advance for any services.
Because FSA funds are available to you on the first day of your plan year, you must be able to receive full reimbursement for your contribution.
So, if you opted in for $1,200 a year for your FSA, you could use that amount on the first day (if you wanted to).
You can submit for FSA reimbursement in two ways:
1. Your FSA Administrator might provide you with an FSA Debit Card to use toward FSA eligible expenses.
You’ll be able to use the card at approved stores or pharmacies (we accept FSA Debit Cards and all major credit cards at FSAstore.com!)
By using the FSA debit card, your expenses are auto-adjudicated (electronically approved or disapproved) from the card and you may not need to submit additional receipts to your FSA Administrator.
Some FSA Administrators could still require a receipt to substantiate a claim. Check with your FSA Administrator about reimbursement procedures for your plan.The FSA Debit Card would not be charged if something is not considered FSA eligible under your plan.
2. You’ll have to typically submit a reimbursement claims form with:
- your personal details,
- product/service details(provider information)
- amount owed
- date of service provided.
FSAstore.com can provide you with an itemized receipt after you make your order to submit to your FSA Administrator for FSA reimbursement.
Pyridoxine is used to prevent and to treat vitamin B6 deficiency. Deficiency of the vitamin has rarely been identified in humans except in conjunction with deficiency of other B complex vitamins or when drug-induced. Whenever possible, poor dietary habits should be corrected, and many clinicians recommend administration of multivitamin preparations containing pyridoxine in patients with vitamin deficiencies since poor dietary habits often result in concurrent deficiencies.
Although an adequate amount of pyridoxine is usually obtained from dietary sources, pyridoxine deficiency may occur in patients with uremia, alcoholism, cirrhosis, hyperthyroidism, malabsorption syndromes, and congestive heart failure and in those receiving isoniazid, cycloserine, ethionamide, hydralazine, penicillamine, or pyrazinamide. Although increased pyridoxine requirements may occur in geriatric patients, clinical signs of deficiency are rare in these patients. Biochemical evidence suggestive of, but not conclusive for, pyridoxine deficiency may occur in women receiving oral contraceptives and can be corrected with pyridoxine administration. Angular stomatitis, glossitis, and abnormal glucose tolerance during pregnancy are sometimes associated with biochemical evidence of pyridoxine deficiency and may be improved by administration of pyridoxine.
The National Academy of Sciences (NAS) has issued a comprehensive set of Recommended Dietary Allowances (RDAs) as reference values for dietary nutrient intakes since 1941. In 1997, the NAS Food and Nutrition Board (part of the Institute of Medicine [IOM]) announced that they would begin issuing revised nutrient recommendations that would replace RDAs with Dietary Reference Intakes (DRIs). DRIs are reference values that can be used for planning and assessing diets for healthy populations and for many other purposes and that encompass the Estimated Average Requirement (EAR), the Recommended Dietary Allowance (RDA), the Adequate Intake (AI), and the Tolerable Upper Intake Level (UL).
The NAS has established an EAR and RDA for vitamin B6 for adults based principally on a plasma pyridoxal phosphate concentration of 5 ng/mL. Because evidence currently available on the role of vitamin B6 in reducing the risk of vascular disease (by reducing plasma homocysteine concentrations) is limited, the NAS did not use risk reduction as a basis for setting the EAR and RDA. Because vitamin B6 is involved in amino acid metabolism, vitamin B6 requirements are considered to parallel protein intake. However, not all studies support this relationship, and NAS concluded that expressing vitamin B6 requirements in terms of protein intake does not add to the precision of the requirement. The EAR and RDA for children and adolescents 1-18 years of age was established based on data in adults, since only limited data in children and adolescents are available. An AI has been set for infants up to 6 months of age based on the observed mean vitamin B6 intake of infants fed principally human milk. An AI for infants 6-12 months of age has been set based on the AI for younger infants and data from adults.
The principal goal of maintaining an adequate intake of vitamin B6 in the US and Canada is to prevent vitamin B6 deficiency. In the US, vitamin B6 principally has been obtained from fortified ready-to-eat cereals; mixed dishes containing substantial portions of meat, fish, or poultry; white potatoes and other starchy vegetables; and noncitrus fruits.
For specific information on currently recommended AIs and RDAs of vitamin B6 for various life-stage and gender groups, see Dosage: Dietary and Replacement Requirements, under Dosage and Administration: Dosage.
Pyridoxine has been used in neonates and infants to treat seizures that are unresponsive to usual therapy. Pyridoxine-dependent seizures occur in infants with an inborn pyridoxine dependency rather than a deficiency of the vitamin.
Xanthurenic aciduria, primary cystathioninuria, primary hyperoxaluria, and primary homocystinuria resulting from genetic abnormalities may respond to pyridoxine (generally in high doses). Homocystinuria is usually caused by diminished activity of cystathionine β-synthase; pyridoxal-5-phosphate is a cofactor for the enzyme and about 50% of these patients respond to pyridoxine therapy, which may completely reverse abnormal amino acid (i.e., homocysteine, methionine, cysteine-homocysteine, cysteine) concentrations.
Prevention or Treatment of Drug-induced Neurotoxicity
Pyridoxine has been used to prevent or treat neurotoxic adverse effects (e.g., peripheral neuropathy) associated with drugs such as isoniazid, ethionamide, or capecitabine. Since patients with HIV infection may be more likely to experience isoniazid-related peripheral neuropathy, the CDC recommends that pyridoxine hydrochloride (25-50 mg daily or 50-100 mg twice weekly) be administered to all HIV-infected patients receiving antituberculosis therapy with isoniazid to reduce the occurrence of isoniazid-induced adverse nervous system effects.
Pyridoxine is used as an adjunct to other measures for the treatment of acute toxicity resulting from isoniazid, cycloserine, or hydrazine overdosage. Pyridoxine is used to treat isoniazid-induced seizures and/or coma, usually in conjunction with other anticonvulsants. Isoniazid-induced seizures are thought to be associated with decreased γ-aminobutyric acid (GABA) concentrations within the CNS, possibly resulting from inhibition by isoniazid of brain pyridoxal-5-phosphate activity. Pyridoxine has also had a beneficial effect in correcting acidosis in some patients following isoniazid overdosage, possibly by controlling seizures and resulting lactic acidosis. Following acute hydrazine overdosage in one patient, IV pyridoxine therapy reversed CNS dysfunction (e.g., confusion, lethargy) and improved hepatic function within 24 hours. Although pyridoxine also has been used as an adjunct in the treatment of levodopa overdosage, its usefulness is not well established.
Pyridoxine has been used as an adjunct to other measures for the treatment of acute toxicity caused by mushrooms of the genus Gyromitra. Pyridoxine has been used to treat marked neurologic effects (e.g., seizures, coma) induced by methylhydrazine, which results from hydrolysis of the toxins gyromitrins contained in these mushrooms.
Pyridoxine has been used for the treatment of sideroblastic anemia associated with high serum iron concentration.
Although pyridoxine has not been shown by well-controlled trials to have any therapeutic value, the vitamin has been used for the management of acne, various dermatoses, appetite stimulation, hyperlipidemia, radiation sickness, hyperemesis gravidarum, vertigo, motion sickness, psychosis, depression associated with pregnancy and oral contraceptive use, hyperkinesis, acute chorea, chronic progressive hereditary chorea, tardive dyskinesia, asthma, absence (petit mal) seizures, amenorrhea-galactorrhea syndrome, gyrate atrophy of the choroid and retina, idiopathic nephrolithiasis, alcohol intoxication, and for the suppression of postpartum lactation, prevention of leukopenia secondary to mitomycin, and reversal of procarbazine neurotoxicity. There is conflicting evidence regarding the efficacy of pyridoxine in the management of premenstrual syndrome (PMS), and additional study is necessary to determine whether the vitamin is of any value in the management of this condition.
Dosage and Administration
Pyridoxine hydrochloride is usually administered orally; however, the drug may be given by IM, IV, or subcutaneous injection when oral administration is not feasible. In infants with seizures, pyridoxine hydrochloride should be administered by IM or IV injection.
Although pyridoxine was previously considered nontoxic even at high dosages, current evidence indicates that chronic administration of large dosages (e.g., 2 g daily) for the management of various conditions can cause severe adverse neurologic effects, and the risk to benefit of such dosages must be carefully weighed.(See Chronic Toxicity.)
Dietary and Replacement Requirements
The Adequate Intake (AI) (see Uses: Dietary Requirements) of vitamin B6 currently recommended by the National Academy of Sciences (NAS) for healthy infants up to 6 months of age is 0.1 mg (0.01 mg/kg) daily and for those 6-12 months of age is 0.3 mg (0.03 mg/kg) daily. The Recommended Dietary Allowance (RDA) of vitamin B6 currently recommended by NAS for healthy children 1-3, 4-8, or 9-13 years of age is 0.5, 0.6, or 1 mg of vitamin B6 daily, respectively. The RDA of vitamin B6 for boys 14 up to 19 years of age is 1.3 mg of vitamin B6 daily, and the RDA for girls 14 up to 19 years of age is 1.2 mg of vitamin B6 daily. The RDA for healthy men and women 19-50 years of age is 1.3 mg of vitamin6 daily. The RDA of vitamin B6 for men 51 years of age or older is 1.7 mg daily, and the RDA for women 51 years of age or older is 1.5 mg daily.
For the treatment of pyridoxine deficiency in adults, the usual oral dosage of pyridoxine hydrochloride is 2.5-10 mg daily. After the clinical signs of deficiency are corrected, a multivitamin preparation containing 2-5 mg of pyridoxine hydrochloride should be given daily for several weeks. For the treatment of drug-induced deficiency anemia or neuritis, the usual oral dosage of pyridoxine hydrochloride is 100-200 mg daily for 3 weeks followed by the prophylactic oral administration of 25-100 mg daily. To correct biochemical evidence suggestive of pyridoxine deficiency in women taking oral contraceptives, the usual oral dosage of pyridoxine hydrochloride is 25-30 mg daily.
For the treatment of pyridoxine-dependent seizures in neonates or infants, IM or IV pyridoxine hydrochloride doses of 10-100 mg have been recommended. Seizures generally stop within 2-3 minutes following administration of the drug. Some clinicians recommend administration of pyridoxine hydrochloride in any neonate with seizures for which no apparent cause can be found. Infants who have had pyridoxine-responsive seizures often require lifelong oral administration of pyridoxine hydrochloride dosages of 2-100 mg daily.
The RDA of vitamin B6 recommended by the NAS for pregnant women is 1.9 mg of vitamin B6 daily. To ensure a vitamin B6 concentration in milk of 130 ng/mL, the NAS recommends a RDA of 2 mg of vitamin B6 daily for lactating women.
For the treatment of hereditary, sideroblastic anemia, the usual oral dosage of pyridoxine hydrochloride is 200-600 mg daily. If a therapeutic response does not occur after 1-2 months of pyridoxine therapy, other therapy should be considered. If an adequate response occurs, dosage of pyridoxine hydrochloride may be decreased to 30-50 mg daily; lifelong therapy with the vitamin may be required to prevent anemia in patients with this condition.
For the treatment of primary hyperoxaluria, primary homocystinuria, primary cystathioninuria, or xanthurenic aciduria, an oral pyridoxine hydrochloride dosage of 100-500 mg daily can generally overcome the metabolic defect. If an adequate response occurs, the same dosage should generally be continued indefinitely. Some patients with type I primary hyperoxaluria may be adequately treated with lower dosages (e.g., physiologic dosages or dosages less than 100 mg daily) than have usually been administered for this disorder. Consequently, some clinicians suggest that high dosages be used initially to attain a maximum reduction in urinary oxalate excretion in patients with type I primary hyperoxaluria and that dosage then be reduced in a stepwise fashion at not less than 3-month intervals to determine the minimum dosage required to maintain the initial effect of the drug.However, some patients with severe type I primary hyperoxaluria may require relatively high, potentially neurotoxic pyridoxine dosages to prevent irreversible renal damage associated with this condition, and careful monitoring for adverse effects of the drug is necessary if such dosages are used.
Drug-Induced Pyridoxine Deficiency and Acute Intoxication
To prevent pyridoxine-deficiency anemia or neuritis in patients receiving isoniazid or penicillamine, an oral pyridoxine hydrochloride dosage of 10-50 mg daily has been recommended. To prevent seizures in patients receiving cycloserine, an oral pyridoxine hydrochloride dosage of 100-300 mg daily, given in divided doses, has been recommended.
For the treatment of seizures and/or coma resulting from acute isoniazid toxicity, a dose of pyridoxine hydrochloride equal to the amount of isoniazid ingested is usually given along with other anticonvulsants as needed. Generally, 1-4 g of pyridoxine hydrochloride is given IV followed by 1 g IM every 30 minutes until the entire dose has been given. For the treatment of cycloserine overdosage, a pyridoxine hydrochloride dose of 300 mg daily has been recommended. For the treatment of acute hydrazine toxicity, a pyridoxine hydrochloride dose of 25 mg/kg has been recommended; one-third of this dose is given IM and the rest is given by IV infusion over 3 hours. For the treatment of neurologic effects induced by ingestion of mushrooms of the genus Gyromitra (secondary to methylhydrazine), an IV pyridoxine hydrochloride dose of 25 mg/kg infused over 15-30 minutes and repeated as necessary to control such effects up to a maximum cumulative dose of 15-20 g daily has been suggested. Lower pyridoxine doses may be effective for the management of seizures associated with poisoning from these mushrooms when diazepam is used concomitantly.
Pyridoxine is usually nontoxic; however, chronic administration of large dosages has been associated with adverse neurologic effects. (See Chronic Toxicity.) Nausea, headache, paresthesia, somnolence, and increased serum AST (SGOT) and decreased serum folic acid concentrations have been reported. Burning or stinging at the injection site may occur following IM or subcutaneous injection of pyridoxine. Seizures have occurred following IV administration of very large doses. Allergic reactions have been reported occasionally in patients receiving the vitamin.
Precautions and Contraindications
Pyridoxine should not be used in patients with a history of sensitivity to the vitamin. According to one manufacturer, pyridoxine should not be administered IV to patients with heart disease.
Pyridoxine hydrochloride reverses the therapeutic effects of levodopa by accelerating peripheral metabolism of levodopa. Concomitant administration of carbidopa with levodopa prevents the reversal by pyridoxine of levodopa's effects. Pyridoxine hydrochloride should not be administered in dosages greater than 5 mg daily to patients receiving levodopa alone.
In one study, 200 mg of pyridoxine hydrochloride daily for 1 month resulted in a 50% decrease in serum concentrations of phenobarbital and phenytoin.
Although isoniazid interferes with pyridoxine metabolism, the American Academy of Pediatrics (AAP) states that children receiving isoniazid do not need pyridoxine supplements unless they have or are likely to have nutritional deficiencies. The AAP currently recommends that children and adolescents receiving meat- and milk-deficient diets, those with nutritional deficiencies (including symptomatic children with human immunodeficiency virus [HIV] infection), infants who are breast-feeding and their mothers, and pregnant women receive pyridoxine supplements.
Pyridoxine, pyridoxal, and pyridoxamine are readily absorbed from the GI tract following oral administration; however, GI absorption may be diminished in patients with malabsorption syndromes or following gastric resection. Normal serum concentrations of pyridoxine are 30-80 ng/mL.
Vitamin B6 is stored mainly in the liver with lesser amounts in muscle and brain. The total body store of vitamin B6 is estimated to be about 167 mg. Pyridoxal and pyridoxal phosphate, the principal forms of the vitamin present in blood, are highly protein bound. Pyridoxal crosses the placenta, and plasma concentrations in the fetus are 5 times greater than maternal plasma concentrations. The concentration of vitamin B6 in milk is about 150-240 ng/mL following maternal intake of 2.5-5 mg of vitamin B6 daily. Following maternal intake of less than 2.5 mg of vitamin B6 daily, vitamin B6 concentration in milk averages 130 ng/mL.
In erythrocytes, pyridoxine is converted to pyridoxal phosphate and pyridoxamine is converted to pyridoxamine phosphate. In the liver, pyridoxine is phosphorylated to pyridoxine phosphate and transaminated to pyridoxal and pyridoxamine which are rapidly phosphorylated. Riboflavin is required for the conversion of pyridoxine phosphate to pyridoxal phosphate. The principal forms of the vitamin in the blood are pyridoxal and pyridoxal phosphate.
The biologic half-life of pyridoxine appears to be 15-20 days. In the liver, pyridoxal is oxidized to 4-pyridoxic acid which is excreted in urine. In cirrhosis, the rate of degradation may be increased. Pyridoxal is removed by hemodialysis.