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Indications/Uses
For the treatment and prevention of folate deficiency.
For the treatment of megaloblastic anemia due to folate deficiency.
For the prevention of neural tube defects in the offspring of women planning a pregnancy and known to be at risk.
For the treatment of megaloblastic anemia due to folate deficiency.
For the prevention of neural tube defects in the offspring of women planning a pregnancy and known to be at risk.
Dosage/Direction for Use
For Oral Administration.
Adults and elderly: Folate deficient megaloblastic anemia: 5 mg daily for 4 months.
Chronic hemolytic states: 5 mg every 1 to 7 days depending on underlying disease.
Children: Consider using a more suitable dosage form for children aged 12 year and below.
Pregnancy: 5 mg daily continued to term and 3 months after delivery.
Adults and elderly: Folate deficient megaloblastic anemia: 5 mg daily for 4 months.
Chronic hemolytic states: 5 mg every 1 to 7 days depending on underlying disease.
Children: Consider using a more suitable dosage form for children aged 12 year and below.
Pregnancy: 5 mg daily continued to term and 3 months after delivery.
Overdosage
There is no known case of acute overdose and it is unlikely to cause harm to patients even with extremely high doses. No special procedures or antidote are likely to be needed.
Administration
May be taken with or without food.
Contraindications
Long-term folate therapy is contraindicated among patients with untreated cobalamin deficiency including untreated pernicious anemia. Folate administration for 3 months or more among cobalamin deficient patients may precipitate cobalamin neuropathy.
Known hypersensitivity to folic acid or any of the excipients.
Known hypersensitivity to folic acid or any of the excipients.
Special Precautions
Folic acid should never be given alone or in conjunction with inadequate amounts of vitamin B12 for the treatment of pernicious anemia, undiagnosed megaloblastic anemia or other vitamin B12 deficiency states. Folic acid may produce hematopoietic response in patients with megaloblastic anemia due to vitamin B12 deficiency without preventing aggravation of neurological symptoms, which may lead to subacute combined degeneration of the spinal cord. This product should never be used to treat anemia without a full investigation of the cause.
Administering folic acid to patients with folate dependent tumors should be done with caution.
Administering folic acid to patients with folate dependent tumors should be done with caution.
Use In Pregnancy & Lactation
Pregnancy: No harmful effects are known with the use of folic acid in pregnancy.
Lactation: Folic acid is actively excreted in human breast milk. No harmful effects have been observed in infants breastfed by mothers taking folic acid.
Lactation: Folic acid is actively excreted in human breast milk. No harmful effects have been observed in infants breastfed by mothers taking folic acid.
Adverse Reactions
The following adverse drug reactions, listed in the table, have been accumulated for folic acid capsules: Adverse drug reactions are ranked under heading of frequency, the most frequent first, using the following convention: very common (≥1/10); common (≥1/100, <1/10); uncommon (≥1/1,000, <1/100); rare (≥1/10,000, <1/1,000); very rare (<1/10,000), including isolated reports; and not known (cannot be estimated from the available data). Within each frequency grouping, adverse reactions are ranked in order of decreasing seriousness. (See table.)
Drug Interactions
Folic acid decreases phenytoin and barbiturate anti-epileptic plasma concentrations. Correction of folate deficiency may result in potential loss of seizure control.
Prolonged phenytoin use induces folate deficiency. A similar mechanism may occur with other anti-seizure drugs including sodium valproate, carbamazepine and barbiturate.
Folic acid absorption may be inhibited by sulphasalazine.
The antibacterial co-trimoxazole (i.e. trimethoprim, sulfamethoxazole) may interfere with folate metabolism.
Folate may enhance the efficacy of lithium therapy.
Methotrexate is a folic acid antagonist. It inhibits the enzyme dihydrofolate reductase resulting to suppression of purine and pyrimidine production during DNA synthesis. Folate deficiency may result from prolonged use of methotrexate.
Folic acid supplementation may decrease methotrexate plasma concentration.
Nitrous oxide anesthetics may induce acute folic acid deficiency. This is likely due to failure of intracellular transport and enhanced excretion of folate.
Prolonged phenytoin use induces folate deficiency. A similar mechanism may occur with other anti-seizure drugs including sodium valproate, carbamazepine and barbiturate.
Folic acid absorption may be inhibited by sulphasalazine.
The antibacterial co-trimoxazole (i.e. trimethoprim, sulfamethoxazole) may interfere with folate metabolism.
Folate may enhance the efficacy of lithium therapy.
Methotrexate is a folic acid antagonist. It inhibits the enzyme dihydrofolate reductase resulting to suppression of purine and pyrimidine production during DNA synthesis. Folate deficiency may result from prolonged use of methotrexate.
Folic acid supplementation may decrease methotrexate plasma concentration.
Nitrous oxide anesthetics may induce acute folic acid deficiency. This is likely due to failure of intracellular transport and enhanced excretion of folate.
Storage
Store at temperatures not exceeding 30°C.
Action
Pharmacology: Pharmacodynamics: Folic acid is a collective term for pteroylglutamic acids and their oligoglutamic acid conjugates. As a natural water-soluble substance, folic acid is involved in carbon transfer reactions of amino acid metabolism, in addition to purine and pyrimidine synthesis, and is essential for hematopoiesis and red blood cell production.
Pharmacokinetics: Absorption: Folic acid is rapidly absorbed from the gastrointestinal tract, mainly from the duodenum and jejunum.
Distribution: Folic acid is rapidly transported to tissues after intestinal absorption. Certain plasma proteins bind with folate derivatives but affinity is greater with non-methylated analogs. The role of plasma binding proteins in folate homeostasis is poorly understood.
Metabolism: Therapeutically administered folic acid enters the portal circulation mostly unchanged. Conversion to the active form 5-methyltetrahydrofolate occurs in the liver. The liver serves as the main storage site for folate. It is also actively concentrated in the cerebrospinal fluid.
Excretion: Folate undergoes enterohepatic circulation. Folate metabolites are excreted in the urine.
Folate in excess of body requirements is eliminated unchanged in the urine.
Folate is expressed in the breast milk.
Folic acid is removed by hemodialysis.
Pharmacokinetics: Absorption: Folic acid is rapidly absorbed from the gastrointestinal tract, mainly from the duodenum and jejunum.
Distribution: Folic acid is rapidly transported to tissues after intestinal absorption. Certain plasma proteins bind with folate derivatives but affinity is greater with non-methylated analogs. The role of plasma binding proteins in folate homeostasis is poorly understood.
Metabolism: Therapeutically administered folic acid enters the portal circulation mostly unchanged. Conversion to the active form 5-methyltetrahydrofolate occurs in the liver. The liver serves as the main storage site for folate. It is also actively concentrated in the cerebrospinal fluid.
Excretion: Folate undergoes enterohepatic circulation. Folate metabolites are excreted in the urine.
Folate in excess of body requirements is eliminated unchanged in the urine.
Folate is expressed in the breast milk.
Folic acid is removed by hemodialysis.
MedsGo Class
Vitamins & Minerals (Pre & Post Natal) / Antianemics
Features
Brand
Folidyn
Full Details
Dosage Strength
5mg
Drug Ingredients
- Vit. B9 (Folic Acid)
Drug Packaging
Tablet 1's
Generic Name
Vit. B9 (Folic Acid)
Dosage Form
Tablet
Registration Number
DR-XY46177
Drug Classification
Prescription Drug (RX)