FERRIMED

Indications

• Vitamin B12

Mechanism of action

Cyanocobalamin serves as a cofactor for methionine synthase and L-methylmalonyl-CoA mutase enzymes. Methionine synthase is vital for the synthesis of purines and pyrimidines necessary for DNA, while L-methylmalonyl-CoA mutase converts L-methylmalonyl-CoA to succinyl-CoA, a key step in fat and protein metabolism. The lack of vitamin B12 leads to the accumulation of methylmalonyl CoA, which is associated with neurological symptoms of deficiency. Additionally, vitamin B12 is required for synthesizing methionine from homocysteine, which is crucial for many biological processes.

Pharmacodynamics

Cyanocobalamin corrects vitamin B12 deficiency and alleviates symptoms and laboratory abnormalities linked to pernicious anemia, such as megaloblastic indices and neurological damage. It supports growth, cell reproduction, hematopoiesis, nucleoprotein, and myelin synthesis. This vitamin also plays a significant role in the metabolism of fats, carbohydrates, and proteins. Rapidly dividing cells, including epithelial and bone marrow cells, have a high demand for vitamin B12. Parenteral administration effectively reverses megaloblastic anemia and gastrointestinal symptoms, while intranasal routes can maintain serum vitamin B12 levels in stabilized patients.

Pharmacokinetics

Cyanocobalamin is well-absorbed when administered parenterally and can be stored in the liver, where it is released as needed. The pharmacokinetics can vary based on the route of administration, with parenteral forms providing rapid increases in serum concentrations. After absorption, it is transported in the bloodstream bound to transcobalamin II. The half-life of vitamin B12 can be several days, depending on the individual's status and the presence of deficiency.

Adverse effects

• Hypokalemia
• Allergic reactions
• Rash
• Itching
• Diarrhea

Interactions

• Chloramphenicol may inhibit the therapeutic effects of vitamin B12
• Anticonvulsants may affect vitamin B12 metabolism

Precautions

• Monitor potassium levels in patients with severe deficiency
• Use with caution in patients with Leber's disease
• Assess for potential allergies to cobalt or vitamin B12

Pregnancy

Cyanocobalamin is generally considered safe in pregnancy, but caution is advised. Adequate vitamin B12 levels are important for fetal development.

Breast-feeding

Cyanocobalamin is safe for use during breastfeeding, as it is excreted in breast milk in small amounts.

Storage

Store in a cool, dry place away from light. Once opened, use within a specified period as recommended by the manufacturer.

Formulations

• Intramuscular injection
• Oral tablets
• Nasal spray

Indications

• Nutritional supplementation
• Management of blood glucose levels in diabetes
• Energy source for athletes or individuals with increased energy demands
• Support for gut health as a prebiotic

Dosage

Children: Refer to specific product guidelines for dosing, as it may vary based on formulation and indication.

Adults: Refer to specific product guidelines for dosing, as it may vary based on formulation and indication.

Mechanism of action

Polymaltose is metabolized into glucose, which serves as a source of energy for the body. It is characterized by its slow digestion and absorption, which helps maintain steady blood glucose levels. The slow-release characteristic is attributed to its polysaccharide structure, which requires enzymatic breakdown in the gastrointestinal tract before absorption occurs.

Pharmacodynamics

The pharmacodynamics of polymaltose involve its role in providing a sustained release of glucose into the bloodstream, which can prevent spikes in blood sugar levels. This gradual release is particularly advantageous in managing energy levels for individuals with diabetes or those needing controlled carbohydrate intake. Additionally, polymaltose may exhibit prebiotic effects, enhancing the growth of beneficial intestinal microbiota, thus contributing to improved gastrointestinal health.

Pharmacokinetics

Polymaltose is not directly absorbed in the gastrointestinal tract due to its complex structure. Instead, it undergoes enzymatic hydrolysis primarily in the small intestine, where it is broken down into glucose units. The absorption of these glucose units occurs through the intestinal mucosa into the bloodstream. The rate of absorption is slower compared to simple sugars, resulting in a gradual increase in blood glucose levels. The elimination of glucose from the bloodstream is mediated by insulin, which facilitates its uptake by tissues for energy production.

Adverse effects

• Gastrointestinal discomfort
• Nausea
• Diarrhea
• Allergic reactions (rare)

Precautions

• Use with caution in patients with diabetes mellitus due to potential carbohydrate content
• Monitor for gastrointestinal side effects, especially in patients with pre-existing gastrointestinal disorders

Pregnancy

Polymaltose is generally considered safe during pregnancy, but medical advice should be sought before use.

Breast-feeding

Polymaltose is likely safe during breastfeeding, but it is advisable to consult with a healthcare provider.

Storage

Store in a cool, dry place away from direct sunlight. Keep out of reach of children.

Formulations

• Oral syrup
• Oral solution
• Granules

Indications

• Vitamin B6 deficiency
• Pyridoxine-responsive seizures
• Certain types of anemia
• Peripheral neuropathy
• Homocystinuria

Dosage

Children: Refer to the BNF for Children for specific dosing

Adults: Refer to established clinical guidelines or the British National Formulary for specific dosing information.

Mechanism of action

Pyridoxime functions primarily as a coenzyme for over 100 enzymes involved in amino acid metabolism, including amino acid decarboxylases, transaminases, and racemases. It participates in the conversion of homocysteine to cysteine and aids in the synthesis of neurotransmitters such as serotonin, dopamine, and gamma-aminobutyric acid (GABA). This coenzyme action is critical in regulating numerous physiological processes, including neurotransmission and the synthesis of hemoglobin.

Pharmacodynamics

Pyridoxime's pharmacodynamic effects are linked to its role in enzymatic reactions vital for amino acid metabolism and neurotransmitter production. By facilitating the conversion of amino acids, it helps regulate levels of neurotransmitters which have profound effects on mood, cognition, and overall brain function. Deficiency in pyridoxime can lead to neurological symptoms, anemia, and impaired immune function due to its involvement in heme synthesis.

Pharmacokinetics

Pyridoxime is absorbed in the intestine after oral administration and is transported in the bloodstream primarily bound to albumin. It is metabolized in the liver to its active forms and excreted in urine as pyridoxylate and other metabolites. The half-life of pyridoxime is relatively short, necessitating sufficient dietary intake for maintaining adequate physiological levels. The body stores small amounts of pyridoxime, but prolonged deficiency can rapidly lead to depletion.

Pregnancy

Pyridoxine is generally considered safe during pregnancy when used in recommended amounts. High doses should be avoided unless specifically prescribed.

Breast-feeding

Pyridoxine is excreted in breast milk. It is considered safe during breastfeeding when used in recommended amounts.

Storage

Store in a cool, dry place away from light. Keep out of reach of children.

Formulations

• Tablets
• Injectable solution

Mechanism of action

Vitamin B12 serves as a cofactor for _methionine synthase_ and _L-methylmalonyl-CoA mutase_ enzymes. Methionine synthase is essential for the synthesis of purines and pyrimidines that form DNA. L-methylmalonyl-CoA mutase converts L-methylmalonyl-CoA to _succinyl-CoA_ in the degradation of propionate, an important reaction required for both fat and protein metabolism. It is a lack of vitamin B12 cofactor in the above reaction and the resulting accumulation of methylmalonyl CoA that is believed to be responsible for the neurological manifestations of B12 deficiency. Succinyl-CoA is also necessary for the synthesis of hemoglobin. In tissues, vitamin B12 is required for the synthesis of _methionine_ from homocysteine. Methionine is required for the formation of S-adenosylmethionine, a methyl donor for nearly 100 substrates, comprised of DNA, RNA, hormones, proteins, as well as lipids. Without vitamin B12, tetrahydrofolate cannot be regenerated from 5-methyltetrahydrofolate, and this can lead to functional folate deficiency,. This reaction is dependent on methylcobalamin (vitamin B12) as a co-factor and is also dependent on folate, in which the methyl group of methyltetrahydrofolate is transferred to homocysteine to form _methionine_ and _tetrahydrofolate_. Vitamin B12 incorporates into circulating folic acid into growing red blood cells; retaining the folate in these cells. A deficiency of vitamin B12 and the interruption of this reaction leads to the development of megaloblastic anemia.

Pharmacodynamics

**General effects** Cyanocobalamin corrects vitamin B12 deficiency and improves the symptoms and laboratory abnormalities associated with pernicious anemia (megaloblastic indices, gastrointestinal lesions, and neurologic damage). This drug aids in growth, cell reproduction, hematopoiesis, nucleoprotein, and myelin synthesis. It also plays an important role in fat metabolism, carbohydrate metabolism, as well as protein synthesis. Cells that undergo rapid division (for example, epithelial cells, bone marrow, and myeloid cells) have a high demand for vitamin B12. **Parenteral cyanocobalamin effects** The parenteral administration of vitamin B12 rapidly and completely reverses the megaloblastic anemia and gastrointestinal symptoms of vitamin B12 deficiency. Rapid parenteral administration of vitamin B12 in deficiency related neurological damage prevents the progression of this condition. **Nasal spray effects** In 24 vitamin B12 deficient patients who were already stabilized on intramuscular (IM) vitamin B12 therapy, single daily doses of intranasal cyanocobalamin for 8 weeks lead to serum vitamin B12 concentrations that were within the target therapeutic range (>200 ng/L).