Chemical formula: C₁₉H₁₉N₇O₆ Molecular mass: 441.398 g/mol PubChem compound: 6037
Folic acid interacts in the following cases:
Both ethanol and acetylsalicylic acid increase folic elimination.
Chloramphenicol may interfere with folate metabolism.
Folate supplements enhance the efficacy of lithium therapy.
Folic acid may interfere with the toxic and therapeutic effects of methotrexate. Methotrexate and trimethoprim are specific anti-folates and the folate deficiency caused by their prolonged use cannot be treated by folic acid.
Nitrous oxide anaesthesia may cause an acute folic acid deficiency.
There is a specific interaction between phenytoin and folate such that chronic phenytoin use produces folate deficiency. Correction of the folate deficiency reduces plasma phenytoin with potential loss of seizure control.
There is a specific interaction between phenytoin and folate such that chronic phenytoin use produces folate deficiency. Correction of the folate deficiency reduces plasma phenytoin with potential loss of seizure control. Similar but less marked relationship exist with all anti-convulsant treatments including sodium valproate, carbamazepine and the barbiturates (including phenobarbital and primidone).
Sulphasalazine and triamterene also inhibit the absorption of e folic acid.
Patients with vitamin B12 deficiency should not be treated with folic acid unless administered with adequate amounts of hydroxocobalamin, as it can mask the condition but the subacute irreversible damage to the nervous system will continue. The deficiency can be due to undiagnosed megaloblastic anaemia including in infancy, pernicious anaemia or macrocytic anaemia of unknown aethiology or other cause of cobalamin deficiency, including lifelong vegetarians.
There are no known hazards to the use of folic acid in pregnancy, supplements of folic acid are often beneficial.
Non-drug – induced folic acid deficiency, or abnormal folate metabolism, is related to the occurrence of birth defects and some neural tube defects. Interference with folic acid metabolism or folate deficiency induced by drugs such as anticonvulsants and some antineoplastics early in pregnancy results in congenital anomalies. Lack of the vitamin or its metabolites may also be responsible for some cases of spontaneous abortion and intrauterine growth retardation.
Folic acid is actively excreted in human breast milk. Accumulation of folate in milk takes precedence over maternal folate needs. Levels of folic acid are relatively low in colostrum but as lactation proceeds, concentrations of the vitamin rise. No adverse effects have been observed in breast fed infants whose mothers were receiving folic acid.
No effect on concentration and co-ordination.
Rare (≥1/10,000 to <1/1,000): Anorexia, nausea, abdominal distension and flatulence.
Rare (≥1/10,000 to <1/1,000): Allergic reactions, comprising erythema, rash, pruritus, urticaria, dyspnoea, and anaphylactic reactions (including shock).
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