PRENATAL

Mechanism of action

Carbonate ions participate in buffering reactions that help maintain pH homeostasis in biological systems. They can react with acids to form bicarbonate and carbon dioxide, thus neutralizing excess acidity in the body. This mechanism is crucial in processes such as respiration and metabolism.

Pharmacodynamics

As a buffer, carbonate helps to stabilize pH levels in different biological environments, preventing excessive acidity or alkalinity that could impair cellular functions. It is involved in the transport of carbon dioxide in the blood and plays a role in maintaining the acid-base equilibrium necessary for physiological processes.

Pharmacokinetics

Carbonate ions are readily absorbed in the gastrointestinal tract when ingested and can be found in various body fluids. They are involved in the bicarbonate buffering system, where they are converted to bicarbonate (HCO3-) and carbon dioxide (CO2) through reactions with acids. The kidneys regulate the levels of bicarbonate and carbonate in the body, excreting or reabsorbing them as needed to maintain homeostasis.

Pregnancy

There is no specific information available regarding the use of carbonate compounds during pregnancy. Consult a healthcare provider for advice.

Breast-feeding

There is no specific information available regarding the use of carbonate compounds while breastfeeding. Consult a healthcare provider for advice.

Storage

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

Indications

• Copper deficiency
• Occipital Horn Syndrome
• Menke's disease
• Contraception (via copper IUD)

Dosage

Children: Refer to the BNF for Children for specific dosing information.

Adults: Refer to the relevant clinical guidelines and BNF for specific dosing information.

Mechanism of action

Copper is absorbed from the gastrointestinal tract via high affinity copper uptake proteins and low affinity copper uptake proteins, likely being reduced to the Cu1+ form prior to transport. Inside enterocytes, it binds to the copper transport protein ATOX1, which facilitates its transport to copper transporting ATPase-1 on the Golgi membrane for incorporation into the Golgi apparatus. Once in systemic circulation, copper binds primarily to ceruloplasmin, albumin, and alpha 2-macroglobulin. It acts as a cofactor in a variety of oxidase enzymes and also influences sperm motility when released from copper IUDs, contributing to its contraceptive effect.

Pharmacodynamics

Copper is essential for the activity of many enzymes and plays a vital role in processes such as iron metabolism, neurotransmitter synthesis, and antioxidant defense. Copper ions, particularly when released from intrauterine devices, have been shown to decrease sperm viability, thereby impacting fertility.

Pharmacokinetics

Copper is absorbed from the gut and is predominantly transported in the plasma bound to proteins such as ceruloplasmin and albumin. The absorption efficiency can vary; however, a significant portion of dietary copper is usually absorbed. The body regulates copper levels through hepatic excretion and storage mechanisms, ensuring homeostasis. Excess copper can lead to toxicity, while deficiency results in various health issues.

Pregnancy

Copper is considered essential during pregnancy, but excessive intake should be avoided due to potential toxicity.

Breast-feeding

Copper is excreted in breast milk, and adequate maternal intake is important for infant development.

Storage

Store in a cool, dry place, away from moisture and heat.

Indications

• Acne vulgaris
• Rosacea
• Skin irritation
• Atopic dermatitis
• Seborrheic dermatitis
• General skin health and maintenance

Dosage

Children: Refer to specific product guidelines or consult a healthcare professional for dosing information.

Adults: Refer to specific product guidelines or consult a healthcare professional for dosing information.

Mechanism of action

Nicotinamide, or niacinamide, functions by inhibiting the production of pro-inflammatory cytokines and enhancing skin barrier function. It promotes keratinocyte differentiation, reduces transepidermal water loss, and has antioxidant properties. Calcium plays a critical role in cell signaling and is vital for various cellular processes, including skin cell proliferation and differentiation. The synergistic effect of these two components may lead to enhanced skin repair and reduced inflammation.

Pharmacodynamics

The pharmacodynamics of enicotinamidecalcium is characterized by its ability to modulate skin responses to inflammatory stimuli. Nicotinamide acts to suppress the release of mediators involved in the inflammatory response, leading to reduced redness and irritation. Calcium contributes to maintaining skin integrity and hydration, promoting a healthy skin barrier. Together, these actions help in improving skin conditions such as acne, rosacea, and general skin irritation.

Pharmacokinetics

The pharmacokinetics of nicotinamide indicate that it is readily absorbed through the skin when applied topically, with systemic absorption being minimal. It is metabolized in the liver and excreted primarily through the urine. The calcium component is also absorbed and utilized in metabolic processes, but the specific pharmacokinetics of enicotinamidecalcium as a combined entity is not well-documented. The half-life and bioavailability would depend on the formulation and mode of application.

Pregnancy

There is limited data on the use of enicotinamidecalcium during pregnancy. It should only be used if the potential benefit justifies the potential risk to the fetus.

Breast-feeding

It is not known whether enicotinamidecalcium is excreted in human milk. Caution should be exercised when administering to a breastfeeding woman.

Storage

Store at room temperature, away from moisture and heat. Keep out of reach of children.

Indications

• Iodine deficiency
• Goiter
• Hypothyroidism
• Thyroiditis
• Fibrocystic breast disease

Dosage

Children: Refer to the BNF for Children for appropriate dosing guidelines based on age and weight.

Adults: Refer to the BNF for appropriate dosing guidelines based on condition and clinical judgment.

Mechanism of action

Molecular iodine inhibits the induction and promotion of carcinogenesis in mammary tissues and has shown beneficial effects in fibrocystic breast disease. It temporarily decreases thyroid hormone production through the acute Wolff-Chaikoff effect, followed by a return to normal hormone synthesis due to down regulation of the sodium-iodide symport. This mechanism can lead to a transient hypothyroid state in some individuals with underlying thyroid conditions.

Pharmacodynamics

Iodine is vital for the synthesis of thyroid hormones thyroxine (T4) and triiodothyronine (T3). It affects the metabolism of amine-derived hormones and plays a role in amino acid metabolism. The acute excess of iodide can lead to decreased circulating levels of T4 and T3 in susceptible individuals, while most people can escape this effect and maintain normal thyroid function.

Pharmacokinetics

Iodine is absorbed primarily in the gastrointestinal tract and is distributed throughout the body, particularly in the thyroid gland, where it is concentrated for hormone synthesis. The kidney plays a significant role in the excretion of excess iodine. The half-life of iodine in the body varies and can be influenced by dietary intake and underlying health conditions.

Adverse effects

• Hypothyroidism
• Hyperthyroidism
• Iodine allergy
• Gastrointestinal disturbances

Interactions

• Thyroid hormones
• Antithyroid drugs
• Lithium
• Diuretics

Precautions

• Use with caution in patients with thyroid dysfunction
• Monitor thyroid function periodically during treatment
• Pregnant or breastfeeding women should consult a healthcare provider before use

Pregnancy

Iodine is essential for fetal thyroid hormone synthesis, but excessive iodine intake should be avoided.

Breast-feeding

Iodine is excreted in breast milk; consult a healthcare provider regarding supplementation.

Storage

Store in a cool, dry place away from light.

Formulations

• Iodine solution
• Iodine tincture
• Potassium iodide tablets

Indications

• Manganese deficiency
• Bone health and development
• Antioxidant support
• Enzyme cofactor in metabolic processes

Dosage

Children: Refer to the BNF for Children for appropriate dosing recommendations.

Adults: Refer to specific clinical guidelines or the BNF for appropriate dosing recommendations.

Mechanism of action

Manganese serves as a cofactor for several enzymes, including manganese superoxide dismutase (MnSOD), which protects cells from oxidative stress by catalyzing the dismutation of superoxide radicals into oxygen and hydrogen peroxide. It also participates in the activation of enzymes involved in carbohydrate, fat, and protein metabolism.

Pharmacodynamics

Manganese plays a role in various biochemical pathways, particularly in the metabolism of amino acids, cholesterol, glucose, and carbohydrates. It is crucial for bone formation and the maintenance of cartilage. Manganese also aids in the synthesis of glycosyltransferases, which are important for the formation of glycoproteins and proteoglycans.

Pharmacokinetics

Manganese is absorbed primarily in the small intestine, with absorption efficiency influenced by dietary factors and the presence of competing minerals. It is transported in the bloodstream bound to proteins such as alpha-2-macroglobulin and transferrin. Manganese is stored in the liver, pancreas, and bones, and is excreted primarily through bile and to a lesser extent in urine. Its half-life in the human body is not well defined due to its trace nature and variable absorption.

Pregnancy

Manganese is classified as a dietary mineral that is essential for human health, but excessive intake should be avoided during pregnancy as it may affect fetal development.

Breast-feeding

Manganese is present in breast milk, and normal dietary intake is considered safe during breastfeeding. However, excessive supplementation should be avoided.

Storage

Store in a cool, dry place, away from direct light and moisture.

Indications

• Vitamin deficiency syndromes
• Anemia due to folic acid deficiency
• Pregnancy and lactation support
• Support in cases of malabsorption syndromes

Dosage

Children: Refer to specific guidelines or product labeling, as doses can vary based on indication.

Adults: Refer to specific guidelines or product labeling, as doses can vary based on indication.

Mechanism of action

Pantothenic acid is converted to coenzyme A, which is essential for the metabolism of carbohydrates, fats, and proteins. Folic acid is converted to tetrahydrofolate, which serves as a cofactor in the synthesis of nucleotides, crucial for DNA and RNA synthesis. This combination supports cellular division and growth, particularly in rapidly dividing tissues.

Pharmacodynamics

The pharmacodynamics of pantothenatefolic involve the bioavailability of its components. Pantothenic acid aids in the production of energy from fats and carbohydrates, while folic acid is crucial for nucleic acid synthesis. Adequate levels of these vitamins are necessary for normal physiological function, particularly in the formation of blood cells and cellular metabolism.

Pharmacokinetics

Pantothenic acid is absorbed in the intestine and is widely distributed in body tissues. It undergoes metabolism to coenzyme A and is excreted in urine primarily as metabolites. Folic acid is also absorbed in the intestine and is converted in the liver to its active forms. It has a half-life of around 6 hours and is primarily excreted in urine. Both vitamins do not accumulate in the body, as excess amounts are readily excreted.

Adverse effects

• Allergic reactions (e.g., rash, itching)
• Gastrointestinal disturbances (e.g., nausea, vomiting)
• Headache
• Fatigue

Interactions

• Anticonvulsants may reduce the effectiveness of folate
• Some antibiotics (e.g., chloramphenicol) can interfere with folate metabolism
• Alcohol can impair absorption and utilization of folate

Precautions

• Use with caution in patients with a history of allergic reactions to vitamins
• Monitor in patients with renal impairment
• Caution in individuals with a history of seizures, especially if taking anticonvulsants

Pregnancy

Folic acid supplementation is recommended during pregnancy to reduce the risk of neural tube defects. Consult healthcare providers for appropriate dosing.

Breast-feeding

Folate is essential during breastfeeding; supplementation may be necessary. Consult healthcare providers for guidance.

Storage

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

Formulations

• Tablets
• Capsules
• Oral solutions

Indications

• Hypokalemia (low serum potassium levels)
• Hypertension (as part of dietary management)
• Heart disease (to prevent arrhythmias)
• Muscle cramps (related to low potassium levels)

Dosage

Children: Refer to guidelines for specific dosing recommendations based on age and clinical condition.

Adults: Dosage varies based on clinical condition and serum potassium levels. Refer to established guidelines for specific dosing recommendations.

Mechanism of action

Potassium ions are crucial for the generation and conduction of action potentials in neurons and muscle cells. They help to maintain the membrane potential and are involved in the repolarization phase of the action potential. Additionally, potassium plays a role in enzymatic reactions and the synthesis of proteins.

Pharmacodynamics

Potassium participates in numerous physiological processes, including muscle contraction, nerve transmission, and cardiac function. Adequate levels of potassium help to prevent arrhythmias and support overall cardiovascular health. It also influences the function of the kidneys, adrenal glands, and other organs involved in electrolyte and fluid balance.

Pharmacokinetics

Potassium is absorbed in the gastrointestinal tract, with the majority of absorption occurring in the small intestine. The distribution of potassium within the body is primarily intracellular, with most of it located within cells. The kidneys regulate potassium levels through filtration and reabsorption, with excess potassium being excreted in urine. Factors such as diet, renal function, and hormonal regulation can impact potassium homeostasis.

Contra-indications

• Hyperkalemia
• Severe renal impairment
• Untreated Addison's disease
• Acute dehydration

Adverse effects

• Hyperkalemia
• Cardiac arrhythmias
• Muscle weakness
• Nausea
• Vomiting
• Diarrhea
• Abdominal cramping

Interactions

• Angiotensin-converting enzyme (ACE) inhibitors may increase potassium levels
• Potassium-sparing diuretics can lead to hyperkalemia
• Non-steroidal anti-inflammatory drugs (NSAIDs) may reduce renal excretion of potassium
• Digoxin toxicity may occur with elevated potassium levels

Precautions

• Monitor serum potassium levels regularly
• Use with caution in patients with renal dysfunction
• Consider dietary potassium intake in patients on potassium supplements
• Be cautious in patients with cardiac disease

Pregnancy

Potassium is essential during pregnancy, but supplementation should only be done under medical supervision to avoid hyperkalemia.

Breast-feeding

Potassium is present in breast milk and is important for nursing infants, but additional supplementation should be approached with caution.

Storage

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

Formulations

• Oral tablets
• Oral liquid
• Intravenous solution
• Effervescent tablets

Indications

• Vitamin deficiency
• Nutritional supplementation
• Prevention of certain diseases
• Supporting metabolic functions

Dosage

Children: Refer to specific guidelines for individual vitamins or consult a healthcare professional for personalized dosing recommendations.

Adults: Refer to specific guidelines for individual vitamins or consult a healthcare professional for personalized dosing recommendations.

Mechanism of action

Vitamins function primarily as coenzymes or precursors for enzyme cofactors in various metabolic pathways. For instance, B vitamins are involved in energy metabolism by assisting in the conversion of carbohydrates, fats, and proteins into energy. Vitamin C acts as an antioxidant, protecting cells from damage, and is also crucial for collagen synthesis. Fat-soluble vitamins like A are involved in vision and immune function, while vitamin D regulates calcium and phosphate metabolism.

Pharmacodynamics

Vitamins exert their effects by participating in biochemical reactions and influencing metabolic pathways. For example, vitamin A is vital for vision and immune response, while vitamin D is important for maintaining bone health through its role in calcium absorption. The effects of vitamins can vary significantly depending on their solubility, with water-soluble vitamins typically being excreted more readily than fat-soluble ones, which can accumulate in the body.

Pharmacokinetics

The absorption of vitamins varies; water-soluble vitamins are generally absorbed in the small intestine and excreted in urine, while fat-soluble vitamins require dietary fats for absorption and are stored in the liver and fatty tissues. The bioavailability of vitamins can be affected by dietary composition, age, and health status. Elimination half-lives also differ; for instance, vitamin C has a shorter half-life compared to vitamin A, which can persist in the body for longer periods.

Adverse effects

• Nausea
• Vomiting
• Diarrhea
• Constipation
• Headache
• Fatigue
• Allergic reactions

Interactions

• Fat-soluble vitamins (A, D, E, K) can accumulate and cause toxicity when taken in excess, especially with other supplements
• Certain medications (e.g., anticoagulants) may interact with vitamin K
• Vitamin C can enhance the absorption of iron supplements

Precautions

• Use caution in patients with kidney disease when taking vitamin D
• Monitor for signs of toxicity with high-dose vitamin supplementation
• Consider dietary sources of vitamins before recommending supplements

Pregnancy

Vitamins are generally considered safe during pregnancy when taken at recommended dosages. However, excessive intake, particularly of fat-soluble vitamins, should be avoided.

Breast-feeding

Most vitamins are safe during breastfeeding at recommended doses, but excessive amounts can affect breast milk composition.

Storage

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

Formulations

• Tablets
• Capsules
• Soft gels
• Powders
• Liquid solutions
• Chewable tablets

Mechanism of action

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. The reason for the less severe reaction when the foreign body is at a distance from the retina has been proposed to be ... that near the retina & its blood vessels there is greater oxygen tension than at a distance, which causes metallic copper to oxidize to toxic copper compounds more rapidly close to or in contact with the retina than at a distance. Furthermore, the abscess formation that is characteristic of copper undergoing oxidation close to the retina & choroiod can be attributed to attraction of polymorphonuclear leukocytes from these nearby vascular tissues, which become heavily infiltrated. Liquefaction & disorganization of the vitreous body has been explained on the basis of copper catalysis of oxidation of ascorbic acid, leading to depolymerization of the hyaluronic acid of the vitreous humor. Changes in protein & hexosamine content have also been related to decrease in viscosity of the vitreous humor. Increased content of amino acids in the vitreous humor has been consistent with proteolysis of the vitreous body, but decreased concentration in the aqueous humor has suggested suppression of secretion of amino acids by the ciliary body under the influence of copper.

Pharmacodynamics

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.

Mechanism of action

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. An acute iodide excess (above the preexisting dietary intake) transiently decreases the production of thyroid hormones in the thyroid gland; this is referred to as the acute Wolff-Chaikoff effect. In normal people, this is followed by a return to normal levels of hormone synthesis, referred to as escape from the acute Wolff-Chaikoff effect, without a significant change in circulating hormone levels. Escape is thought to be the result of down regulation of the sodium-iodide symport (NIS), the iodide transporter in the thyroid gland, resulting in a decrease in the intrathyroidal iodine and the resumption of normal hormone synthesis. An acute or chronic excess of iodide can also decrease circulating T4 and T3 levels and induce a hypothyroid state in some people who have underlying thyroid disorders. These effects are the result of a failure to escape from the acute Wolff-Chaikoff effect. Most people who experience iodine-induced hypothyroidism recover when the excess iodine intake is discontinued.