Neutrofer
Neutrofer Uses, Dosage, Side Effects, Food Interaction and all others data.
Folic acid is essential for the production of certain coenzymes in many metabolic systems such as purine and pyrimidine synthesis. It is also essential in the synthesis and maintenance of nucleoprotein in erythropoesis. It also promotes WBC and platelet production in folate-deficiency anaemia.
Folic acid is a water-soluble B-complex vitamin found in foods such as liver, kidney, yeast, and leafy, green vegetables. Also known as folate or Vitamin B9, folic acid is an essential cofactor for enzymes involved in DNA and RNA synthesis. More specifically, folic acid is required by the body for the synthesis of purines, pyrimidines, and methionine before incorporation into DNA or protein. Folic acid is the precursor of tetrahydrofolic acid, which is involved as a cofactor for transformylation reactions in the biosynthesis of purines and thymidylates of nucleic acids. Impairment of thymidylate synthesis in patients with folic acid deficiency is thought to account for the defective deoxyribonucleic acid (DNA) synthesis that leads to megaloblast formation and megaloblastic and macrocytic anemias. Folic acid is particularly important during phases of rapid cell division, such as infancy, pregnancy, and erythropoiesis, and plays a protective factor in the development of cancer. As humans are unable to synthesize folic acid endogenously, diet and supplementation is necessary to prevent deficiencies. In order to function properly within the body, folic acid must first be reduced by the enzyme dihydrofolate reductase (DHFR) into the cofactors dihydrofolate (DHF) and tetrahydrofolate (THF). This important pathway, which is required for de novo synthesis of nucleic acids and amino acids, is disrupted by anti-metabolite therapies such as Methotrexate as they function as DHFR inhibitors to prevent DNA synthesis in rapidly dividing cells, and therefore prevent the formation of DHF and THF.
In general, folate serum levels below 5 ng/mL indicate folate deficiency, and levels below 2 ng/mL usually result in megaloblastic anemia.
Vitamin B12 with hydroxyl group complexed to cobalt which can be displaced by cyanide resulting in cyanocobaiamin that is renally excreted.
Hydroxocobalamin is a synthetic, injectable form of Vitamin B12. Hydroxocobalamin is actually a precursor of two cofactors or vitamins (Vitamin B12 and Methylcobalamin) which are involved in various biological systems in man. Vitamin B12 is required for the conversion of methylmalonate to succinate. Deficiency of this enzyme could therefore interfere with the production of lipoprotein in myelin sheath tissue and so give rise to neurological lesions. The second cofactor, Methylcobalamin, is necessary for the conversion of homocysteine to methionine which is essential for the metabolism of folic acid. Deficiency of tetrahydrafolate leads to reduced synthesis of thymidylate resulting in reduced synthesis of DNA which is essential for cell maturation. Vitamin B12 is also concerned in the maintenance of sulphydryl groups in reduced form, deficiency leading to decreased amounts of reduced SH content of erythrocytes and liver cells. Overall, vitamin B12 acts as a coenzyme for various metabolic functions, including fat and carbohydrate metabolism and protein synthesis. It is necessary for growth, cell replication, hematopoiesis, and nucleoprotein as well as myelin synthesis. This is largely due to its effects on metabolism of methionine folic acid, and malonic acid.
| Trade Name | Neutrofer |
| Generic | Folic Acid + Hydroxocobalamin + Iron Salts |
| Weight | 750mcg/1.5ml, 75mcg/1.5ml, 75mg/1.5ml |
| Type | Injection |
| Therapeutic Class | |
| Manufacturer | Neutro Pharma (pvt) Ltd, |
| Available Country | Pakistan |
| Last Updated: | September 19, 2023 at 7:00 am |
Uses
Prophylaxis of megaloblastic anaemia in pregnancy, Supplement for women of child-bearing potential, Folate-deficient megaloblastic anaemia, Prophylaxis of neural tube defect in pregnancy
Hydroxocobalamin is used for the treatment of known or suspected cyanide poisoning.
Identifying Patients with Cyanide Poisoning: Cyanide poisoning may result from inhalation, ingestion, or dermal exposure to various cyanide-containing compounds, including smoke from closed-space fires. Sources of cyanide poisoning include hydrogen cyanide and its salts, cyanogenic plants, aliphatic nitriles, and prolonged exposure to sodium nitroprusside.
The presence and extent of cyanide poisoning are often initially unknown. There is no widely available, rapid, confirmatory cyanide blood test. Treatment decisions must be made on the basis of clinical history and signs and symptoms of cyanide intoxication. If clinical suspicion of cyanide poisoning is high, Hydroxocobalamin should be administered without delay.
In some settings, panic symptoms including tachypnea and vomiting may mimic early cyanide poisoning signs. The presence of altered mental status (e.g., confusion and disorientation) and/or mydriasis is suggestive of true cyanide poisoning although these signs can occur with other toxic exposures as well.
Smoke Inhalation: Not all smoke inhalation victims will have cyanide poisoning and may present with burns, trauma, and exposure to other toxic substances making a diagnosis of cyanide poisoning particularly difficult. Prior to administration of Hydroxocobalamin, smoke-inhalation victims should be assessed for the following:
- Exposure to fire or smoke in an enclosed area
- Presence of soot around the mouth, nose or oropharynx
- Altered mental status
Although hypotension is highly suggestive of cyanide poisoning, it is only present in a small percentage of cyanide-poisoned smoke inhalation victims. Also indicative of cyanide poisoning is a plasma lactate concentration ≥ 10 mmol/L (a value higher than that typically listed in the table of signs and symptoms of isolated cyanide poisoning because carbon monoxide associated with smoke inhalation also contributes to lactic acidemia). If cyanide poisoning is suspected, treatment should not be delayed to obtain a plasma lactate concentration.
Use with Other Cyanide Antidotes: Caution should be exercised when administering other cyanide antidotes simultaneously with Hydroxocobalamin, as the safety of co-administration has not been established. If a decision is made to administer another cyanide antidote with Hydroxocobalamin, these drugs should not be administered concurrently in the same intravenous line.
Neutrofer is also used to associated treatment for these conditions: Anaemia folate deficiency, Folate deficiency, Iron Deficiency (ID), Iron Deficiency Anemia (IDA), Latent Iron Deficiency, Neural Tube Defects (NTDs), Vitamin Deficiency, Methotrexate toxicity, Nutritional supplementationAnemia, Pernicious, B Vitamin Deficiency, Toxic effect of hydrocyanic acid and cyanides, Vitamin B12 Deficiency
How Neutrofer works
Folic acid, as it is biochemically inactive, is converted to tetrahydrofolic acid and methyltetrahydrofolate by dihydrofolate reductase (DHFR). These folic acid congeners are transported across cells by receptor-mediated endocytosis where they are needed to maintain normal erythropoiesis, synthesize purine and thymidylate nucleic acids, interconvert amino acids, methylate tRNA, and generate and use formate. Using vitamin B12 as a cofactor, folic acid can normalize high homocysteine levels by remethylation of homocysteine to methionine via methionine synthetase.
Vitamin B12 exists in four major forms referred to collectively as cobalamins; deoxyadenosylcobalamin, methylcobalamin, hydroxocobalamin, and cyanocobalamin. Two of these, methylcobalamin and 5-deoxyadenosyl cobalamin, are primarily used by the body. Methionine synthase needs methylcobalamin as a cofactor. This enzyme is involved in the conversion of the amino acid homocysteine into methionine. Methionine in turn is required for DNA methylation. 5-Deoxyadenosyl cobalamin is a cofactor needed by the enzyme that converts L-methylmalonyl-CoA to succinyl-CoA. This conversion is an important step in the extraction of energy from proteins and fats. Furthermore, succinyl CoA is necessary for the production of hemoglobin, the substances that carries oxygen in red blood cells.
Dosage
Neutrofer dosage
Supplement for women of child-bearing potential: 0.4 mg daily.
Folate-deficient megaloblastic anaemia: 5 mg daily for 4 mth, up to 15 mg daily in malabsorption states. Continued dosing at 5 mg every 1-7 days may be needed in chronic haemolytic states, depending on the diet and rate of haemolysis.
Prophylaxis of neural tube defect in pregnancy: 4 or 5 mg daily starting before pregnancy and continued through the 1st trimester.
Prophylaxis of megaloblastic anaemia in pregnancy: 0.2-0.5 mg daily.
Thirty mcg daily for 5 to 10 days followed by 100 to 200 mcg monthly injected intramuscularly. If the patient is critically ill, or has neurologic disease, an infectious disease or hyperthyroidism, considerably higher doses may be indicated. However, current data indicate that the optimum obtainable neurologic response may be expected with a dosage of vitamin B12 sufficient to produce good hematologic response. Children may be given a total of 1 to 5 mg over a period of 2 or more weeks in doses of 100 mcg, then 30 to 50 mcg every 4 weeks for maintenance.
May be taken with or without food.
Side Effects
GI disturbances, hypersensitivity reactions; bronchospasm.
Mild transient diarrhea, itching, transitory exanthema, feeling of swelling of entire body, and anaphylaxis. A few patients may experience pain after injection of hydroxocobalamin.
Toxicity
IPR-MUS LD50 85 mg/kg,IVN-GPG LD50 120 mg/kg, IVN-MUS LD50 239 mg/kg, IVN-RAT LD50 500 mg/kg, IVN-RBT LD50 410 mg/kg
Precaution
Treatment resistance may occur in patients with depressed haematopoiesis, alcoholism, deficiencies of other vitamins. Neonates.
The validity of diagnostic vitamin B12 or folic acid blood assays could be compromised by medications, and this should be considered before relying on such tests for therapy.
Vitamin B12 is not a substitute for folic acid and since it might improve folic acid deficient megaloblastic anemia, indiscriminate use of vitamin B12 could mask the true diagnosis.
Hypokalemia and thrombocytosis could occur upon conversion of severe megaloblastic to normal erythropoiesis with B12 therapy. Therefore, serum potassium levels and the platelet count should be monitored carefully during therapy.
Vitamin B12 deficiency may suppress the signs of polycythemia vera. Treatment with vitamin B12 may unmask this condition.
Interaction
Antiepileptics, oral contraceptives, anti-TB drugs, alcohol, aminopterin, methotrexate, pyrimethamine, trimethoprim and sulphonamides may result to decrease in serum folate contrations. Decreases serum phenytoin concentrations.
- history of interaction with ARI Sodium Iodide (II23) 1 -12 MBq (sodium iodide i-123)
- ARI Sodium Iodide (1123) 100-750 MBq (sodium iodide i-123) arsenic trioxide
- Chloracol (chloramphenicol) chloramphenicol
- Chloromycetin (chloramphenicol)
- Chloromycetin Sodium Succinate (chloramphenicol)
- Hicon (sodium iodide-i-131) lodotope (sodium iodide-i-131) sodium iodide i-123 sodium iodide-i-131 Trisenox (arsenic trioxide)
Volume of Distribution
Tetrahydrofolic acid derivatives are distributed to all body tissues but are stored primarily in the liver.
Elimination Route
Folic acid is absorbed rapidly from the small intestine, primarily from the proximal portion. Naturally occurring conjugated folates are reduced enzymatically to folic acid in the gastrointestinal tract prior to absorption. Folic acid appears in the plasma approximately 15 to 30 minutes after an oral dose; peak levels are generally reached within 1 hour.
Readily absorbed from the gastrointestinal tract, except in malabsorption syndromes. Vitamin B12 is absorbed in the lower half of the ileum.
Half Life
Approximately 6 days (peak plasma concentration after 8-12 hours from oral administration)
Elimination Route
After a single oral dose of 100 mcg of folic acid in a limited number of normal adults, only a trace amount of the drug appeared in the urine. An oral dose of 5 mg in 1 study and a dose of 40 mcg/kg of body weight in another study resulted in approximately 50% of the dose appearing in the urine. After a single oral dose of 15 mg, up to 90% of the dose was recovered in the urine. A majority of the metabolic products appeared in the urine after 6 hours; excretion was generally complete within 24 hours. Small amounts of orally administered folic acid have also been recovered in the feces. Folic acid is also excreted in the milk of lactating mothers.
Each hydroxocobalamin molecule can bind one cyanide ion by substituting it for the hydroxo ligand linked to the trivalent cobalt ion, to form cyanocobalamin, which is then excreted in the urine.
Pregnancy & Breastfeeding use
Pregnancy Category A. Adequate and well-controlled human studies have failed to demonstrate a risk to the fetus in the first trimester of pregnancy (and there is no evidence of risk in later trimesters).
Pregnancy Category C. Animal reproduction studies have shown an adverse effect on the fetus and there are no adequate and well-controlled studies in humans, but potential benefits may warrant use of the drug in pregnant women despite potential risks
Contraindication
Undiagnosed megaloblastic anaemia; pernicious, aplastic or normocytic anaemias.
Hypersensitivity to any component of this medication.
Storage Condition
Store at 15-30° C.
Should be stored in cool and dry place
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