Feroglobin

Feroglobin Uses, Dosage, Side Effects, Food Interaction and all others data.

Copper is a transition metal and a trace element in the body. It is important to the function of many enzymes including cytochrome c oxidase, monoamine oxidase and superoxide dismutase . Copper is commonly used in contraceptive intrauterine devices (IUD) .

Copper is incorporated into many enzymes throughout the body as an essential part of their function . Copper ions are known to reduce fertility when released from copper-containing IUDs .

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.

Iodine is commonly used as an antiseptic for minor cuts and abrasions, preventing infections that may result from contaminated wounds. Additionally, iodine has been studied in the treatment of fibrocystic disease and breast cancer.

Pyridoxine is a water-soluble vitamin which functions in the metabolism of carbohydrates, proteins and fats. It is essential in Hb formation and GABA synthesis within the CNS. It also aids in the release of glycogen stored in the liver and muscles.

Vitamin B6 (pyridoxine) is a water-soluble vitamin used in the prophylaxis and treatment of vitamin B6 deficiency and peripheral neuropathy in those receiving isoniazid (isonicotinic acid hydrazide, INH). Vitamin B6 has been found to lower systolic and diastolic blood pressure in a small group of subjects with essential hypertension. Hypertension is another risk factor for atherosclerosis and coronary heart disease. Another study showed pyridoxine hydrochloride to inhibit ADP- or epinephrine-induced platelet aggregation and to lower total cholesterol levels and increase HDL-cholesterol levels, again in a small group of subjects. Vitamin B6, in the form of pyridoxal 5'-phosphate, was found to protect vascular endothelial cells in culture from injury by activated platelets. Endothelial injury and dysfunction are critical initiating events in the pathogenesis of atherosclerosis. Human studies have demonstrated that vitamin B6 deficiency affects cellular and humoral responses of the immune system. Vitamin B6 deficiency results in altered lymphocyte differentiation and maturation, reduced delayed-type hypersensitivity (DTH) responses, impaired antibody production, decreased lymphocyte proliferation and decreased interleukin (IL)-2 production, among other immunologic activities.

Thiamine, in the form of thiamine pyrophosphate, is the coenzyme for decarboxylation of α-ketoglutaric acid. Thiamine deficiency affects the peripheral nervous system, the gastrointestinal tract, and the cardiovascular system. This vitamin is necessary for the optimal growth of infants and children. Thiamine is not stored in the body, and is regularly lost from tissues during short periods of deficiency. In order to maintain normal health, an adequate amount of thiamine is required every day. Deficiency of thiamine leads to fatigue, anorexia, gastrointestinal disturbance, tachycardia, irritability and neurological symptoms. Beriberi, a disease due to vitamin B1 deficiency, is common in alcoholics, in pregnant women receiving an inadequate diet, and in people with malabsorption syndrome, prolonged diarrhoea and hepatic disease.

Thiamine is well absorbed from the gastrointestinal tract and widely distributed throughout the body. Thiamine is rapidly absorbed from the upper small intestine. Thiamine is not stored in the body to any appreciable extent. Excess ingested thiamine appears in urine as intact thiamine or as pyrimidine, which arises from degradation of the thiamine molecule. The plasma half life of thiamine is 24 hours.

Thiamine is a vitamin with antioxidant, erythropoietic, cognition-and mood-modulatory, antiatherosclerotic, putative ergogenic, and detoxification activities. Thiamine has been found to protect against lead-induced lipid peroxidation in rat liver and kidney. Thiamine deficiency results in selective neuronal death in animal models. The neuronal death is associated with increased free radical production, suggesting that oxidative stress may play an important early role in brain damage associated with thiamine deficiency. Thiamine plays a key role in intracellular glucose metabolism and it is thought that thiamine inhibits the effect of glucose and insulin on arterial smooth muscle cell proliferation. Inhibition of endothelial cell proliferation may also promote atherosclerosis. Endothelial cells in culture have been found to have a decreased proliferative rate and delayed migration in response to hyperglycemic conditions. Thiamine has been shown to inhibit this effect of glucose on endothelial cells.

Vitamin A plays an essential role in the function of retina and is essential for growh and differentiation of epithelial tissue.

Vitamin A is effective for the treatment of Vitamin A deficiency. Vitamin A refers to a group of fat-soluble substances that are structurally related to and possess the biological activity of the parent substance of the group called all-trans retinol or retinol. Vitamin A plays vital roles in vision, epithelial differentiation, growth, reproduction, pattern formation during embryogenesis, bone development, hematopoiesis and brain development. It is also important for the maintenance of the proper functioning of the immune system.

Vitamin D ultimately comprises a group of lipid-soluble secosteroids responsible for a variety of biological effects, some of which include increasing the intestinal absorption of calcium, magnesium, and phosphate. With reference to human use, there are 2 main forms of vitamin D - vitamin D3 (cholecalciferol) and vitamin D2 (ergocalciferol). When non-specific references are made about 'vitamin d', the references are usually about the use of vitamin D3 and/or D2.

Vitamin D3 and D2 require hydroxylation in order to become biologically active in the human body. Since vitamin D can be endogenously synthesized in adequate amounts by most mammals exposed to sufficient quantities of sunlight, vitamin D functions like a hormone on vitamin D receptors to regulate calcium in opposition to parathyroid hormone. Vitamin D plays an essential physiological role in maintaining calcium homeostasis and metabolism. There are several different vitamin D supplements that are given to treat or to prevent osteomalacia and rickets, or to meet the daily criteria of vitamin D consumption.

The in vivo synthesis of the predominant two biologically active metabolites of vitamin D occurs in two steps. The first hydroxylation of vitamin D3 or D2 occurs in the liver to yield 25-hydroxyvitamin D while the second hydroxylation happens in the kidneys to give 1, 25-dihydroxyvitamin D . These vitamin D metabolites subsequently facilitate the active absorption of calcium and phosphorus in the small intestine, serving to increase serum calcium and phosphate levels sufficiently to allow bone mineralization . Conversely, these vitamin D metabolites also assist in mobilizing calcium and phosphate from bone and likely increase the reabsorption of calcium and perhaps also of phosphate via the renal tubules . There exists a period of 10 to 24 hours between the administration of vitamin D and the initiation of its action in the body due to the necessity of synthesis of the active vitamin D metabolites in the liver and kidneys . It is parathyroid hormone that is responsible for the regulation of such metabolism at the level of the kidneys .

Feroglobin
Uses
Dosage
Side Effect
Precautions
Interactions
Uses during Pregnancy
Uses during Breastfeeding
Accute Overdose
Food Interaction
Half Life
Volume of Distribution
Clearance
Interaction With other Medicine
Contradiction
Storage

Trade Name	Feroglobin
Generic	Fe + Zn + Copper + Mg + Iodine + vitamin A + Vitamin D + Thiamine + Pyridoxine + Folic Acid + Vitamin B
Weight	2mg, 1.2mg, 100mcg, 12.5mg, 10mcg, 375iu, 3100iu, 0.35mg, 0.4mg, 30mcg, 120.4mcg., 20mg, 6mg, 40mg,
Type	Drops, Syrup
Therapeutic Class
Manufacturer	Vitabiotics Healthcare, Vitabiotics Nigeria Limited
Available Country	Indonesia, United Kindgom, Nigeria
Last Updated:	September 19, 2023 at 7:00 am

Uses

Copper is a transition metal found in a variety of supplements and vitamins, including intravenous solutions for total parenteral nutrition (TPN).

For use in the supplementation of total parenteral nutrition and in contraception with intrauterine devices .

Prophylaxis of megaloblastic anaemia in pregnancy, Supplement for women of child-bearing potential, Folate-deficient megaloblastic anaemia, Prophylaxis of neural tube defect in pregnancy

Iodine is an ingredient of nutritional supplements that is also used for disinfection.

Investigated for use/treatment in breast disorders (unspecified) and pain (acute or chronic).

Pyridoxine (vitamin B6) is used to prevent or treat low levels of vitamin B6 in people who do not get enough of the vitamin from their diets. Most people who eat a normal diet do not need extra vitamin B6. However, some conditions (such as alcoholism, liver disease, overactive thyroid, heart failure) or medications (such as isoniazid, cycloserine, hydralazine, penicillamine) can cause low levels of vitamin B6. Vitamin B6 plays an important role in the body. It is needed to maintain the health of nerves, skin, and red blood cells.

Pyridoxine has been used to prevent or treat a certain nerve disorder (peripheral neuropathy) caused by certain medications (such as isoniazid). It has also been used to treat certain hereditary disorders (such as xanthurenic aciduria, hyperoxaluria, homocystinuria).

Thiamine is specifically used in the treatment of the various manifestations of thiamine deficiency such as Beriberi and Wernick's encephalopathy, neuritis associated with pregnancy and pellagra. Supplementary Thiamine may be used prophylactically in conditions where there is low dietary intake or impaired gastro intestinal absorption of thiamine (e.g. alcohol) or where requirements are increased (pregnancy, carbohydrate rich diet).

Effective for:

Vitamin A deficiency. Taking vitamin A by mouth is effective for preventing and treating symptoms of vitamin A deficiency. Vitamin A deficiency can occur in people with protein deficiency, diabetes, over-active thyroid, fever, liver disease, cystic fibrosis, or an inherited disorder called abetalipoproteinemia.

Possibly Effective for:

Breast cancer. Premenopausal women with a family history of breast cancer who consume high levels of vitamin A in their diet seem to have reduced risk of developing breast cancer. It is not known if taking vitamin A supplements has the same benefit.
Cataracts. Research suggests that high intake of vitamin A in the diet is linked to a lower risk of developing cataracts.
Diarrhea related to HIV. Taking vitamin A along with conventional medicines seems to decrease the risk of death from diarrhea in HIV-positive children with vitamin A deficiency.
Malaria. Taking vitamin A by mouth seems to decrease malaria symptoms in children less than 3 years-old living in areas where malaria is common.
Measles. Taking vitamin A by mouth seems to reduce the risk of measles complications or death in children with measles and vitamin A deficiency.
Precancerous lesions in the mouth (oral leukoplakia). Research suggests that taking vitamin A can help treat precancerous lesions in the mouth.
Recovery from laser eye surgery (photoreactive keratectomy). Taking vitamin A by mouth along with vitamin E seems to improve healing after laser eye surgery.
Complications after pregnancy. Taking vitamin A seems to reduce the risk of diarrhea and fever after pregnancy in malnourished women.
Complications during pregnancy. Taking vitamin A by mouth seems to reduce the risk of death and night blindness during pregnancy in malnourished women.
Eye disease affecting the retina (retinitis pigmentosa). Research suggests that taking vitamin A can slow the progression of an eye disease that causes damage to the retina.

Vitamin D is an ingredient found in a variety of supplements and vitamins.

Vitamin D is indicated for use in the treatment of hypoparathyroidism, refractory rickets (also known as vitamin D resistant rickets), and familial hypophosphatemia .

Feroglobin is also used to associated treatment for these conditions: Emergency Contraception, IUD, Trace Element Deficiency, Dietary supplementationAnaemia folate deficiency, Folate deficiency, Iron Deficiency (ID), Iron Deficiency Anemia (IDA), Latent Iron Deficiency, Neural Tube Defects (NTDs), Vitamin Deficiency, Methotrexate toxicity, Nutritional supplementationInfection in minor cuts, scrapes, or burns, Antisepsis, Antimycotic, Prophylaxis of bacterial skin infectionsBackache, Dizziness, Fever, Headache, Hepatic; Functional Disturbance, Hepatitis, Iron Deficiency Anemia (IDA), Ketosis, Macrocytic anemia, Menière's Disease, Menstrual Distress (Dysmenorrhea), Metabolic Acidosis, Motion Sickness, Nausea and vomiting, Neuralgia, Sciatic, Neuritis, Neurological Conditions caused by B Vitamin Deficiency, Secondary anemia, Soreness, Muscle, Toothache, Toxinfectious state, Trigeminal Neuralgia (TN), Vitamin B1 deficiency, Vitamin B12 Deficiency, Vitamin B6 Deficiency, Vitamin Deficiency, Minor aches and pains, Minor pain, Nutritional supplementation, Supplementation, Vitamin supplementation, Wellness of the LiverAnemia, B12 Deficiency Anemia, Beriberi, Cardiovascular Heart Disease caused by Thiamine Deficiency, Folic Acid Deficiency Anemia, Infantile Beriberi, Infection, Iron Deficiency (ID), Liver disorder, Neuritis caused by Pregnancy, Secondary anemia, Thiamine Deficiency, Vitamin Deficiency, Wernicke's encephalopathy, Nutritional supplementation, Vitamin supplementation, Dietary supplementationDeficiency, Vitamin A, Deficiency, Vitamin D, Degenerative Retinal Disorders, Disorder of the Epithelium, Disorder of the Mesoderm, Inner ear disorder, Vitamin Deficiency, Vitamin E Deficiency, Nutritional supplementationDeficiency, Vitamin D

How Feroglobin works

Copper is absorbed from the gut via high affinity copper uptake protein and likely through low affinity copper uptake protein and natural resistance-associated macrophage protein-2 . It is believed that copper is reduced to the Cu1+ form prior to transport. Once inside the enterocyte, it is bound to copper transport protein ATOX1 which shuttles the ion to copper transporting ATPase-1 on the golgi membrane which take up copper into the golgi apparatus. Once copper has been secreted by enterocytes into the systemic circulation it remain largely bound by ceruloplasmin (65-90%), albumin (18%), and alpha 2-macroglobulin (12%).

Copper is an essential element in the body and is incorporated into many oxidase enzymes as a cofactor . It is also a component of zinc/copper super oxide dismutase, giving it an anti-oxidant role. Copper defiency occurs in Occipital Horn Syndrome and Menke's disease both of which are associated with impaired development of connective tissue due to the lack of copper to act as a cofactor in protein-lysine-6-oxidase. Menke's disease is also associated with progressive neurological impairment leading to death in infancy. The precise mechanisms of the effects of copper deficiency are vague due to the wide range of enzymes which use the ion as a cofactor.

Copper appears to reduce the viabilty and motility of spermatozoa . This reduces the likelihood of fertilization with a copper IUD, producing copper's contraceptive effect . The exact mechanism of copper's effect on sperm are unknown.

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.

Molecular iodine is known to inhibit the induction and promotion of N-methyl-n-nitrosourea-induced mammary carcinogenesis, to regress 7,12-dimethylbenz(a)anthracene-induced breast tumors in rats.It has also been shown to have beneficial effects in fibrocystic human breast disease.

Vitamin B6 is the collective term for a group of three related compounds, pyridoxine (PN), pyridoxal (PL) and pyridoxamine (PM), and their phosphorylated derivatives, pyridoxine 5'-phosphate (PNP), pyridoxal 5'-phosphate (PLP) and pyridoxamine 5'-phosphate (PMP). Although all six of these compounds should technically be referred to as vitamin B6, the term vitamin B6 is commonly used interchangeably with just one of them, pyridoxine. Vitamin B6, principally in its biologically active coenzyme form pyridoxal 5'-phosphate, is involved in a wide range of biochemical reactions, including the metabolism of amino acids and glycogen, the synthesis of nucleic acids, hemogloblin, sphingomyelin and other sphingolipids, and the synthesis of the neurotransmitters serotonin, dopamine, norepinephrine and gamma-aminobutyric acid (GABA).

It is thought that the mechanism of action of thiamine on endothelial cells is related to a reduction in intracellular protein glycation by redirecting the glycolytic flux. Thiamine is mainly the transport form of the vitamin, while the active forms are phosphorylated thiamine derivatives. Natural derivatives of thiamine phosphate, such as thiamine monophosphate (ThMP), thiamine diphosphate (ThDP), also sometimes called thiamine pyrophosphate (TPP), thiamine triphosphate (ThTP), and thiamine triphosphate (AThTP), that act as coenzymes in addition to their each unique biological functions.

Vision:Vitamin A (all-trans retinol) is converted in the retina to the 11-cis-isomer of retinaldehyde or 11-cis-retinal. 11-cis-retinal functions in the retina in the transduction of light into the neural signals necessary for vision. 11-cis-retinal, while attached to opsin in rhodopsin is isomerized to all-trans-retinal by light. This is the event that triggers the nerve impulse to the brain which allows for the perception of light. All-trans-retinal is then released from opsin and reduced to all-trans-retinol. All-trans-retinol is isomerized to 11-cis-retinol in the dark, and then oxidized to 11-cis-retinal. 11-cis-retinal recombines with opsin to re-form rhodopsin. Night blindness or defective vision at low illumination results from a failure to re-synthesize 11-cis retinal rapidly.
Epithelial differentiation: The role of Vitamin A in epithelial differentiation, as well as in other physiological processes, involves the binding of Vitamin A to two families of nuclear retinoid receptors (retinoic acid receptors, RARs; and retinoid-X receptors, RXRs). These receptors function as ligand-activated transcription factors that modulate gene transcription. When there is not enough Vitamin A to bind these receptors, natural cell differentiation and growth are interrupted.

Most individuals naturally generate adequate amounts of vitamin D through ordinary dietary intake of vitamin D (in some foods like eggs, fish, and cheese) and natural photochemical conversion of the vitamin D3 precursor 7-dehydrocholesterol in the skin via exposure to sunlight.

Conversely, vitamin D deficiency can often occur from a combination of insufficient exposure to sunlight, inadequate dietary intake of vitamin D, genetic defects with endogenous vitamin D receptor, or even severe liver or kidney disease . Such deficiency is known for resulting in conditions like rickets or osteomalacia, all of which reflect inadequate mineralization of bone, enhanced compensatory skeletal demineralization, resultant decreased calcium ion blood concentrations, and increases in the production and secretion of parathyroid hormone . Increases in parathyroid hormone stimulates the mobilization of skeletal calcium and the renal excretion of phosphorus . This enhanced mobilization of skeletal calcium leads towards porotic bone conditions .

Ordinarily, while vitamin D3 is made naturally via photochemical processes in the skin, both itself and vitamin D2 can be found in various food and pharmaceutical sources as dietary supplements. The principal biological function of vitamin D is the maintenance of normal levels of serum calcium and phosphorus in the bloodstream by enhancing the efficacy of the small intestine to absorb these minerals from the diet . At the liver, vitamin D3 or D2 is hydroxylated to 25-hydroxyvitamin D and then finally to the primary active metabolite 1,25-dihydroxyvitamin D in the kidney via further hydroxylation . This final metabolite binds to endogenous vitamin d receptors, which results in a variety of regulatory roles - including maintaining calcium balance, the regulation of parathyroid hormone, the promotion of the renal reabsorption of calcium, increased intestinal absorption of calcium and phosphorus, and increased calcium and phosphorus mobilization of calcium and phosphorus from bone to plasma to maintain balanced levels of each in bone and the plasma .

Dosage

Feroglobin 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.

ADULTS:

BY MOUTH:

For hereditary sideroblastic anemia: Initially, 200-600 mg of vitamin B6 is used. The dose is decreased to 30-50 mg per day after an adequate response.
For vitamin B6 deficiency: In most adults, the typical dose is 2.5-25 mg daily for three weeks then 1.5-2.5 mg per day thereafter. In women taking birth control pills, the dose is 25-30 mg per day.
For abnormally high levels of homocysteine in the blood: For reducing high levels of homocysteine in the blood after childbirth, 50-200 mg of vitamin B6 has been taken alone. Also, 100 mg of vitamin B6 has been taken in combination with 0.5 mg of folic acid.
For preventing macular degeneration: 50 mg of vitamin B6 in the form of pyridoxine has been used daily in combination with 1000 mcg of vitamin B12 (cyanocobalamin) 1000 mcg and 2500 mcg of folic acid for about 7 years.
For hardening of the arteries (atherosclerosis): A specific supplement (Kyolic, Total Heart Health, Formula 108, Wakunga) containing 250 mg of aged garlic extract, 100 mcg of vitamin B12, 300 mcg of folic acid, 12.5 mg of vitamin B6, and 100 mg of L-argininedaily for 12 months.
For kidney stones: 25-500 mg of vitamin B6 has been used daily.
For nausea during pregnancy: 10-25 mg of vitamin B6 taken three or four times per day has been used. In people who don't respond to vitamin B6 alone, a combination product containing vitamin B6 and the drug doxylamine (Diclectin, Duchesnay Inc.) is used three or four times per day. Also, another product containing 75 mg of vitamin B6, 12 mcg of vitamin B12, 1 mg of folic acid, and 200 mg of calcium (PremesisRx, KV Pharmaceuticals) is used daily.
For symptoms of premenstrual syndrome (PMS): 50-100 mg of vitamin B6 is used daily, alone or along with 200 mg of magnesium.
For treating tardive dyskinesia: 100 mg of vitamin B6 per day has been increased weekly up to 400 mg per day, given in two divided doses.

INJECTED INTO THE MUSCLE:

Hereditary sideroblastic anemia: 250 mg of vitamin B6 daily, reduced to 250 mg of vitamin B6 weekly once adequate response is achieved.

CHILDREN:

BY MOUTH:

For kidney stones: Up to 20 mg/kg daily in children aged 5 years and up.

INJECTED INTO THE VEIN OR MUSCLE:

For seizures that respond to vitamin B6 (pyridoxine-dependent seizures): 10-100 mg is recommended.

The daily recommended dietary allowances (RDAs) of vitamin B6 are:

Infants 0-6 months, 0.1 mg
Infants 7-12 months, 0.3 mg
Children 1-3 years, 0.5 mg
Children 4-8 years, 0.6 mg
Children 9-13 years, 1 mg
Males 14-50 years, 1.3 mg
Males over 50 years, 1.7 mg
Females 14-18 years, 1.2 mg
Females 19-50 years, 1.3 mg
Females over 50 years, 1.5 mg
Pregnant women, 1.9 mg
Breast-feeding women, 2 mg
Some researchers think the RDA for women 19-50 years should be increased to 1.5-1.7 mg per day.

The recommended maximum daily intake is:

Children 1-3 years, 30 mg
Children 4-8 years, 40 mg
Children 9-13 years, 60 mg

Adults, pregnant and breast-feeding women:

14-18 years, 80 mg
over 18 years, 100 mg

Prophylaxis: 3 to 10 mg daily.

Mild chronic deficiency: 10 to 25 mg daily.

Severe deficiency: 200 to 300 mg daily.

Vitamin A deficiency For severe deficiency with corneal changes: 500,000 unit/day for 3 days, followed by 50,000 unit/day for 2 wk and then 10,000-20,000 unit/day for 2 mth as follow-up therapy.

For cases without corneal changes: 10,000-25,000 unit/day until clinical improvement occurs (usually 1 -2 wk).

May be taken with or without food.

Side Effects

GI disturbances, hypersensitivity reactions; bronchospasm.

Pyridoxine usually has no side effects when used in recommended doses.

If your doctor has prescribed this medication, remember that he or she has judged that the benefit to you is greater than the risk of side effects. Many people using this medication do not have serious side effects.

Pyridoxine can cause side effects when taken in large doses for a long time. Tell your doctor right away if any of these unlikely but serious side effects occur: headache, nausea, drowsiness, numbness/tingling of arms/legs.

A very serious allergic reaction to this drug is rare. However, seek immediate medical attention if you notice any symptoms of a serious allergic reaction, including: rash, itching/swelling (especially of the face/tongue/throat), severe dizziness, trouble breathing.

This is not a complete list of possible side effects. If you notice other effects not listed above, contact your doctor or pharmacist.

Vitamin B1 does not have adverse effects when given orally, but in a few fatal cases anaphylactic reactions have occurred after intravenous administration of large doses (400 mg) in sensitive patients, especially children, and in one case following an intramuscular dose of 125 mg. The risk of such reactions increases with repeated administration of the drug by parenteral route. Transient mild soreness may occur at the site of intramuscular administration

Hypervitaminosis A characterised by fatigue, irritability, anorexia, weight loss, vomiting and other Gl disturbances, low-grade fever, hepatosplenomegaly, skin changes, alopoecia, dry hair, cracking and bleeding lips, SC swelling, nocturia, pains in bones and joints.

Toxicity

Copper toxicity is belevied to be due to fenton-type redox reactions occuring with high copper concentrations which produce damaging reactive oxygen species .

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

Oral Rat LD50 = 4 gm/kg. Toxic effects include convulsions, dyspnea, hypermotility, diarrhea, ataxia and muscle weakness.

Thiamine toxicity is uncommon; as excesses are readily excreted, although long-term supplementation of amounts larger than 3 gram have been known to cause toxicity. Oral mouse LD₅₀ = 8224 mg/kg, oral rat LD₅₀ = 3710 mg/kg.

Acute toxicity to vitamin A can occur when adults or children ingest >100x or >20x the RDA, respectively, over a period of hours or a few days. The RDA for vitamin A differs depending on age and sex and can range from 300 - 900 μg retinol activity equivalents (RAE) per day. Symptoms of acute systemic toxicity generally include mucocutaneous involvement (e.g. xerosis, cheilitis, skin peeling) and may involve mental status changes. Children are typically more susceptible to acute vitamin A toxicity - daily intakes of as little as 1500 IU/kg have been observed to result in toxicity.

Chronic vitamin A toxicity can develop following the long-term ingestion of high vitamin A doses. While there is a wide variation in the lowest toxic vitamin A dose, the ingestion of >25 000 IU daily for 6 years or 100,000 IU daily for 6 months is considered to be toxic. Chronic vitamin A toxicity can affect many organ systems and can lead to the development of osteoporosis and CNS effects (e.g. headaches).

The use of pharmacological or nutraceutical vitamin d and/or even excessive dietary intake of vitamin d is contraindicated in patients with hypercalcemia, malabsorption syndrome, abnormal sensitivity to the toxic effects of vitamin d, and hypervitaminosis D .

Hypersensitivity to vitamin d is one plausible etiologic factor in infants with idiopathic hypercalcemia - a case in which vitamin d use must be strictly restricted .

As vitamin d intake is available via fortified foods, dietary supplements, and clinical drug sources, serum concentrations and therapeutic dosages should be reviewed regularly and readjusted as soon as there is clinical improvement . Dosage levels are required to be individualized on an individual patient by patient basis as caution must be exercised to prevent the presence of too much vitamin d in the body and the various potentially serious toxic effects associated with such circumstances .

In particular, the range between therapeutic and toxic doses is quite narrow in vitamin d resistant rickets . When high therapeutic doses are used, progress should be followed with frequent blood calcium determinations .

When treating hypoparathyroidism, intravenous calcium, parathyroid hormone, and/or dihydrotachysterol may be required .

Maintenance of normal serum phosphorus levels by dietary phosphate restriction and/or administration of aluminum gels as intestinal phosphate binders in those patients with hyperphosphatemia as frequently seen in renal osteodystrophy is essential to prevent metastatic calcification .

Mineral oil interferes with the absorption of lipid-soluble vitamins, including vitamin d preparations .

The administration of thiazide diuretics to hypoparathyroid patients who are concurrently being treated with vitamin d can result in hypercalcemia .

At this time, no long term animal studies have been performed to evaluate vitamin potential for carcinogens, mutagenesis, or fertility .

As various animal reproduction studies have demonstrated fetal abnormalities in several species associated with hypervitaminosis D, the use of vitamin d in excess of the recommended dietary allowance during normal pregnancy should be avoided . The safety in excess of 400 USP units of vitamin d daily during pregnancy has not been established . The abnormalities observed are similar to the supravalvular aortic stenosis syndrome described in infants that is characterized by supravalvular aortic stenosis, elfin facies, and mental retardation .

In a nursing mother given large doses of vitamin D, 25-hydroxycholecalciferol appeared in the milk and caused hypercalcemia in her child. Caution is subsequently required when contemplating the use of vitamin d in a nursing woman, and the necessity of monitoring infants' serum calcium concentration if vitamin d is administered to a breastfeeding woman .

Adverse reactions associated with the use of vitamin d are primarily linked to having hypervitaminosis D occurring [FDA Lanel]. In particular, hypervitaminosis D is characterized by effects specific effects on specific organ systems. At the renal system, hypervitaminosis D can cause impairment of renal function with polyuria, nocturne, polydipsia, hypercalciuria, reversible asotemia, hypertension, nephrocalcinosis, generalized vascular calcification, or even irreversible renal insufficiency which may result in death . Elsewhere, hypervitaminosis D can also cause CNS mental retardation . At the level of soft tissues, it can widespread calcification of the soft tissues, including the heart, blood vessels, renal tubules, and lungs . In the skeletal system, bone demineralization (osteoporosis) in adults can occur while a decline in the average rate of linear growth and increased mineralization of bones, dwarfism, vague aches, stiffness, and weakness can occur in infants and children . Finally, hypervitaminosis D can also lead to nausea, anorexia, and constipation at the gastrointestinal level as well as mild acidosis, anemia, or weight loss via metabolic processes .

The LD(50) in animals is unknown .

Precaution

Treatment resistance may occur in patients with depressed haematopoiesis, alcoholism, deficiencies of other vitamins. Neonates.

Before taking pyridoxine, tell your doctor or pharmacist if you are allergic to it; or if you have any other allergies. This product may contain inactive ingredients, which can cause allergic reactions or other problems. Talk to your pharmacist for more details.

During pregnancy, this vitamin has been found to be safe when used in recommended doses.

This vitamin passes into breast milk and is considered to be safe during breast-feeding when used in recommended doses. Consult your doctor for more information.

Cholestatic jaundice; fat-malabsorption conditions. Monitor patients closely for toxicity. Liver impairment and children.

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.

The effects of some drugs can change if you take other drugs or herbal products at the same time. This can increase your risk for serious side effects or may cause your medications not to work correctly. These drug interactions are possible, but do not always occur. Your doctor or pharmacist can often prevent or manage interactions by changing how you use your medications or by close monitoring.

To help your doctor and pharmacist give you the best care, be sure to tell your doctor and pharmacist about all the products you use (including prescription drugs, nonprescription drugs, and herbal products) before starting treatment with this product. While using this product, do not start, stop, or change the dosage of any other medicines you are using without your doctor's approval.

Some products that may interact with this vitamin include: altretamine, cisplatin, phenytoin.

This vitamin may interfere with certain laboratory tests (including urine test for urobilinogen), possibly causing false test results. Make sure laboratory personnel and all your doctors know you use this vitamin.

No hazardous drug interactions have been reported. Vitamin B1 acts synergistically with other vitamins of the B-complex group and its potential for causing adverse effects is considerably reduced.

Decreased absorption with neomycin. Increased risk of hypervitaminosis A with synthetic retinoids eg, acitretin, isotretinoin and tretinoin. Increased risk of toxicity when used with alcohol.

Volume of Distribution

Tetrahydrofolic acid derivatives are distributed to all body tissues but are stored primarily in the liver.

Pyridoxine main active metabolite, pyridoxal 5’-phosphate, is released into the circulation (accounting for at least 60% of circulating vitamin B6) and is highly protein bound, primarily to albumin.

Elimination Route

Copper absorption varies inversely with intake. Absorption range is 12-65%.

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.

The B vitamins are readily absorbed from the gastrointestinal tract, except in malabsorption syndromes. Pyridoxine is absorbed mainly in the jejunum. The Cmax of pyridoxine is achieved within 5.5 hours.

Absorbed mainly from duodenum, by both active and passive processes

Readily absorbed from the normal gastrointestinal tract

Vitamin D3 and D2 are readily absorbed from the small intestine (proximal or distal) .

Half Life

The total adult body pool consists of 16 to 25 mg of pyridoxine. Its half-life appears to be 15 to 20 days.

1.9 hours

Although certain studies suggest the half-life of 1,25-hydroxyvitamin D3 may be approximately 15 hours, the half-life of 25-hydroxyvitamin D3 appears to have a half-life of about 15 days . Intriguingly however, the half-lives of any particular administration of vitamin d can vary and in general the half-lives of vitamin D2 metabolites have been demonstrated to be shorter overall than vitamin D3 half-lives with this being affected by vitamin d binding protein concentrations and genotype in particular individuals .

Clearance

Some studies propose an estimated clearance rate for 1,25-dihydroxyvitamin D as 31 +/- 4 ml/min in healthy adults .

Elimination Route

Copper appears to be eliminated primarily through bile .

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.

The major metabolite of pyridoxine, 4-pyridoxic acid, is inactive and is excreted in urine

The primary excretion route of vitamin D is via the bile into the feces .

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).

Category A: Controlled studies in women fail to demonstrate a risk to the foetus in the 1st trimester (and there is no evidence of a risk in later trimesters), and the possibility of foetal harm remains remote.

The drug may be given safely to neonates, children, pregnant and lactating women and elderly patients.

Contraindication

Undiagnosed megaloblastic anaemia; pernicious, aplastic or normocytic anaemias.

There is no absolute contraindication but the risk of anaphylaxis is increased by repeated parenteral administration. Mild allergic phenomena, such as sneezing or mild asthma are warning signs that further may give rise to anaphylactic shock. To avoid this possibility it is advisable to start a second course of injection with a dose considerably lower than that previously used. Because of the above, vitamin B1 injection should not be given intravenously except in the case of comatose patients. Once thiamine deficiency is corrected there is no need for parenteral administration or for the administration of amounts in excess of daily requirement.

Hypervitaminosis A; pregnancy (dose exceeding RDA).