Folic Acid Tablets Bp 0.4mg
SUMMARY OF PRODUCT CHARACTERISTICS
1 NAME OF THE MEDICINAL PRODUCT
Folic Acid Tablets BP 0.4 mg.
2 QUALITATIVE AND QUANTITATIVE COMPOSITION
Each tablet contains 0.40 mg Folic Acid BP (anhydrous).
Product contains lactose.
For full list of excipients, see section 6.1.
3 PHARMACEUTICAL FORM
Tablet.
Appearance: Pale yellow, circular, biconvex tablet.
4 CLINICAL PARTICULARS
4.1 Therapeutic indications
Folic acid tablets 0.4 mg are indicated for the prevention of first occurrence neural tube defects in the foetus. For use by women who are planning a pregnancy.
4.2 Posology and method of administration
Adult females: One tablet (0.4mg) daily
Supplementation should begin by taking one tablet (0.4 mg) daily prior to conception and be continued for at least the first 12 weeks of pregnancy.
Administration: Oral.
The tablets should be swallowed with a drink of water.
4.3 Contraindications
1. Hypersensitivity to folic acid or any of the ingredients in this medicine.
2. Folic acid should not be given alone in the treatment of Addisonian pernicious anaemia and other vitamin B12 deficiency states, as this may precipitate the onset of subacute combined degeneration of the spinal cord.
3. Long term folate therapy is contra-indicated in any patient with untreated cobalamin deficiency. This can be untreated pernicious anaemia or other cause of cobalamin deficiency, including life long vegetarians. In elderly people, a cobalamin absorption test should be done before long-term folate therapy. Folate given to such patients for three months or longer has precipitated cobalamin neuropathy. No harm results from short courses of folate
4. Folic acid should not be used in malignant disease unless megaloblastic anaemia owing to folate deficiency is an important complication
5. Patients with folate-dependent tumour
4.4 Special warnings and precautions for use
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.
Caution should be exercised when administering folic acid to patients who may have folate dependent tumours.
Patients with rare hereditary problems of galactose intolerance, the Lapp lactase deficiency or glucose-galactose malabsorption should not take this medicine.
4.5 Interaction with other medicinal products and other forms of interaction
Folic acid status may be affected by a number of drugs:
o Anti epileptics: Folic acid can reduce plasma concentrations of anticonvulsants, particularly phenytoin, phenobarbital and primidone and therefore patients on anti- epileptic therapy may need to have their dose adjusted at regular intervals and should be under the supervision of a physician while taking folic acid supplements o Antibacterials: chloramphenicol and co-trimoxazole may interfere with folate metabolism
o Sulfasalazine: can reduce the absorption of folic acid
o Preparations containing folic acid or its derivatives may decrease the effectiveness of methotrexate.
Patients with hypersensitivity to folic acid have been demonstrated to have antibodies that cross react with other folic acid analogues, including methotrexate, folinic acid (leucovorin) and aminopterin.
4.6 Fertility, Pregnancy and lactation
Pregnancy
There are no known hazards to the use of folic acid in pregnancy, supplements of folic acid are often beneficial.
The product is indicated for use during pregnancy. In normal use, the recommended dose of 400 pg of folic acid per day is not associated with deleterious effects during pregnancy and lactation.
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.
Lactation
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.
4.7 Effects on ability to drive and use machines
There are no known effects of this medicine on the ability to drive or use machines.
4.8 Undesirable effects
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Gastrointestinal disorders Rare (>1/10,000 til <1/1,000) |
Anorexia, nausea, abdominal distension and flatulence |
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Immune system disorders Rare (>1/10,000 til <1/1,000) |
Allergic reactions, comprising erythema, rash, pruritus, urticaria, dyspnoea, and anaphylactic reactions (including shock). |
Reporting of suspected adverse reactions
Reporting suspected adverse reactions after authorisation of the medicinal product is important. It allows continued monitoring of the benefit/risk balance of the medicinal product. Healthcare professionals are asked to report any suspected adverse reactions via the yellow card scheme at www.mhra.gov.uk/yellowcard
4.9 Overdose
No cases of this kind have been reported, but even extremely high doses are unlikely to cause harm to the patient.
5.1 Pharmacodynamic properties ATC Code BO3B B01
Folic acid is a member of the vitamin B group. Folic acid is reduced in the body to tetrahydrofolate, which is a co-enzyme for various metabolic processes including the synthesis of purine and pyrimidine nucleotides and hence in the synthesis of DNA; it is also involved in some amino- acid conversions and in the formation and utilization of formate.
5.2 Pharmacokinetic properties
Absorption: folic acid is rapidly absorbed from the gastrointestinal tract, mainly from the proximal part of the small intestines. Dietary folates are stated to have about half the bioavailability of crystalline folic acid. The naturally occurring folate polyglutamates are largely deconjugated and reduced by dihydrofolate reductase in the intestine to form 5-methyltetrahydrofolate (5MTHF). Folic acid given therapeutically enters the portal circulation largely unchanges, since it is a poor substrate for reduction by dihydrofolate reductases.
Distribution: via portal circulation. 5MTHF from naturally occurring folate is extensively plasma bound. The principle storage site of folate is in the liver; it is also actively concentrated in the CSF. Folate is distributed into the breast milk.
Metabolism: therapeutically given folic acid is converted into the metabolically active form 5MTHF in the plasma and liver. There is an enterohepatic circulation for folate.
Elimination: folate metabolites are eliminated in the urine and folate in excess of body requirements is excreted unchanged in the urine. Folic acid is removed by haemodialysis.
5.3 Preclinical safety data
Studies have shown that while it is possible to produce toxicity with very large doses of folate in rats, by precipitation of folate in renal tubules, this effect is not relevant in the proposed uses or doses.
6.1 List of excipients
Lactose PhEur Maize Starch PhEur Pregelatinised Starch BP Magnesium Stearate PhEur Purified Water PhEur (Not detected)
6.2 Incompatibilities
None stated.
6.3 Shelf life
2 years.
6.4 Special precautions for storage
Store below 25°C in a dry place. Protect from light.
6.5 Nature and contents of container
Blister packs consisting of 250 pm clear PVC and 20 pm hard temper aluminium foil contained in a carton.
Pack sizes: 28, 56, 84, 90, 98 and 100 tablets.
6.6 Special precautions for disposal
Not applicable.
7 MARKETING AUTHORISATION HOLDER
Relonchem Limited Cheshire House Gorsey Lane Widnes WA8 0RP
8 MARKETING AUTHORISATION NUMBER(S)
PL 20395/0106
9 DATE OF FIRST AUTHORISATION/RENEWAL OF THE AUTHORISATION
18/03/2009
10 DATE OF REVISION OF THE TEXT
26/03/2014