Medically reviewed by Militian Inessa Mesropovna, PharmD. Last updated on 2020-04-06
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Top 20 medicines with the same components:
1. Folate deficient megaloblastic anaemia
2. Folate deficient megaloblastic anaemia in infants
3. Treatment of folate deficiency in malabsorption syndromes (parenteral administration of Folic Acid-Tsiteli A may need to be considered if oral treatment is not effective)
3.1 Tropical sprue. Tropical sprue responds to folate supplements in the early stages of the disease but cobalamin status must also be checked, particularly later.
3.2 Coeliac disease. The necessity of supplementation with folate ceases once a gluten free diet is introduced.
3.3 Non-tropical sprue. In congenital folate malabsorption, oral treatment may not be effective and parental folate may therefore be required.
4. Megaloblastic anaemia in pregnancy
5. Megaloblastic anaemia associated with alcoholism
6. Megaloblastic anaemia associated with anti-convulsant therapy
7. Folic Acid-Tsiteli A deficiency/megaloblastic anaemia associated with haemolytic anaemia e.g. Sickle Cell Anaemia
For oral administration only.
Children (persons aged 12 years and younger):
May be given 5 mg to 15 mg daily, in divided doses, according to the severity of the deficiency state.
Initial dose of 10 mg to 20 mg daily, in divided doses, for 14 days or until a haemopotoietic response has been obtained.
Maintenance dose is 2.5 mg to 10 mg daily.
Prophylactic dose in pregnancy 0.5 mg (1ml) daily.
As for adults.
Known hypersensitivity to Folic Acid-Tsiteli A.
Known hypersensitivity to hydroxybenzoate esters.
Patients with malignant disease, unless megaloblastic anaemia due to Folic Acid-Tsiteli A deficiency.
Folic Acid-Tsiteli A should not be administered for treatment of pernicious anaemia or undiagnosed megaloblastic anaemia without sufficient amounts of cyanocobalamin (vitamin B12) as Folic Acid-Tsiteli A alone will not prevent and may precipitate development of subacute combined degeneration of the spinal cord. Therefore a full clinical diagnosis should be made before initiating treatment.
Folate should not be routinely used in patients receiving coronary stents.
Caution should be exercised when administering Folic Acid-Tsiteli A to patients who may have folate dependent tumours.
Folic Acid-Tsiteli A is removed by haemodialysis.
Contains methyl- ethyl- and propyl- p-hydroxybenzoates; may cause allergic reactions (possibly delayed).
Contains 0.75 mmol (or 17.4mg) sodium per 20 ml dose, and is therefore essentially 'sodium-free'.
Contains phenylalanine. May be harmful for people with phenylketonuria.
There are no known effects of this preparation on the ability to drive or use machines.
Folic Acid-Tsiteli A is generally well tolerated, although the following side effects have been reported:
Blood and lymphatic system disorders:
Folic Acid-Tsiteli A may worsen the symptoms of co-existing vitamin B12 deficiency and should never be used to treat anaemia without a full investigation of the cause.
Immune system disorders:
Allergic reactions to Folic Acid-Tsiteli A have been reported.
Abdominal distension, flatulence, anorexia and nausea.
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.
No cases of acute overdosage appear to have been reported, but even extremely high doses are unlikely to cause harm to patients. No special procedures or antidote are likely to be needed.
ATC Code: B03B B
After conversion into co-enzyme forms it is concerned in single carbon unit transfers in the synthesis of purines, pyrimidines and methionine.
About 70 - 80 % of a 2 mg oral solution of Folic Acid-Tsiteli A is absorbed. Larger doses are probably equally well absorbed. It is distributed into plasma and extracellular fluid. In plasma, folate is bound weakly to albumin (70 %). There is a further high affinity binder for folate but this has a very low capacity and is barely detectable in normal sera. About 70 % of small doses of folate (about 1 mg) are retained and the rest excreted into the urine. With larger doses most is excreted into the urine. With a 5 mg dose of folate, urinary excretion will be complete in about five hours. There is an enterohepatic circulation of folate. The retained folate is taken into cells and reduced by dihydrofolate to tetrahydrofolate. Folic Acid-Tsiteli A is a relatively poor substrate for folate reduction, the normal substrate being dihydrofolate.
Folic Acid-Tsiteli A itself does not occur in natural materials, it is entirely a pharmacological form of the compound. Once reduced, folate has additional glutamic acid residues added, a folate pentaglutamate being the dominant intracellular analogue. These polyglutamates are the active co-enzymes.
Folic Acid-Tsiteli A is a drug on which extensive clinical experience has been obtained. Relevant information for the prescriber is provided elsewhere in the Summary of Product Characteristics.
However, we will provide data for each active ingredient