GINOVERA MULTIVITAMIN AND MINERAL ​​CAPSULES

Indications

• Papulopustular rosacea
• Inflammatory acne vulgaris

Dosage

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

Adults: For papulopustular rosacea, apply daily for up to 4 months. The treatment course may be repeated; discontinue if no improvement is observed after 3 months. For inflammatory acne vulgaris, apply twice daily, reduced to once daily or alternate days if irritation occurs.

Mechanism of action

Nicotinamide exhibits anti-inflammatory effects by inhibiting the release of pro-inflammatory cytokines and enhancing the barrier function of the skin. It is also involved in the NAD salvage pathway, which is essential for maintaining cellular energy levels and promoting cell repair mechanisms. Additionally, nicotinamide contributes to the synthesis of coenzymes involved in metabolic processes, including the conversion of niacin into NAD+.

Pharmacodynamics

Nicotinamide is known for its ability to improve skin hydration and reduce transepidermal water loss. It has been shown to decrease the appearance of acne lesions and rosacea by modulating inflammatory responses and accelerating cell turnover. Its antioxidant properties also help to protect the skin from oxidative stress and UV damage.

Pharmacokinetics

When applied topically, nicotinamide is absorbed through the skin layers, with minimal systemic absorption. Its peak plasma concentrations are generally low, and the drug has a half-life that varies depending on the route of administration. The metabolism of nicotinamide occurs primarily in the liver, where it is converted into its active forms, including NAD+. The elimination route is via the kidneys, with metabolites excreted in urine.

Contra-indications

• Pregnancy
• Severe acne involving large areas
• Severe skin reactions

Adverse effects

• Sunburn
• Skin reactions (common or very common)
• Cheilitis
• Eyelid oedema
• Flushing
• Dry skin
• Eye irritation
• Photosensitivity reactions
• Transient skin pigmentation changes

Interactions

• Clindamycin
• Topical retinoids
• Abrasive cleaners
• Comedogenic cosmetics

Precautions

• Avoid exposure to UV light, including sunlight and sunlamps
• Wash hands immediately after use
• Avoid contact with eyes and mucous membranes
• Use moisturizers to reduce the risk of skin irritation
• Discontinue treatment if severe irritation occurs

Pregnancy

Avoid use during pregnancy due to potential risks, as limited information is available regarding toxicity.

Breast-feeding

Amount of drug in milk after topical application is probably too small to be harmful; ensure infant does not come in contact with treated areas.

Storage

Store at room temperature away from moisture and light.

Formulations

• Cream
• Gel

Indications

• Skin burns and wounds
• Sunburn
• Acne
• Psoriasis
• Digestive disorders
• Constipation

Dosage

Children: For topical use, apply Aloe vera gel as needed on the affected area. For oral formulations, consult product-specific dosing recommendations tailored to children's needs.

Adults: For topical use, apply Aloe vera gel directly to the affected area as needed. For oral consumption, refer to specific product guidelines, as formulations vary widely.

Mechanism of action

The primary mechanism of action of Aloe vera involves its anti-inflammatory and immunomodulatory properties. The polysaccharides, such as acemannan, enhance immune function and promote wound healing. Aloe also exhibits antimicrobial activity, which can help in preventing infections in wounds. In the gastrointestinal tract, Aloe may exert a laxative effect by stimulating intestinal peristalsis and enhancing mucosal secretions.

Pharmacodynamics

Aloe vera gel has demonstrable effects on skin hydration, wound healing, and anti-inflammatory responses. Its polysaccharide content is responsible for its ability to retain moisture and promote cell proliferation and migration, essential processes in tissue repair. Additionally, Aloe has shown potential in modulating inflammatory cytokines, which may contribute to its soothing effects when applied topically.

Pharmacokinetics

Aloe vera is typically administered topically or orally. When applied to the skin, it is absorbed locally, facilitating its effects on the epidermis and dermis. Oral consumption of Aloe products leads to absorption of its active compounds in the gastrointestinal tract, where they may exert systemic effects. The half-life and metabolism of Aloe components can vary depending on the formulation and route of administration, with the laxative effects usually occurring within a few hours after oral intake.

Adverse effects

• Abdominal cramps
• Diarrhea
• Electrolyte imbalance
• Dehydration
• Allergic reactions

Interactions

• May interact with diuretics, increasing the risk of electrolyte imbalance
• May affect the absorption of other medications due to its laxative effects

Precautions

• Use with caution in individuals with gastrointestinal disorders
• Not recommended for long-term use due to potential for dependence
• Avoid in cases of known allergy to aloe or its components

Pregnancy

Aloe is not recommended during pregnancy due to potential uterine stimulation and risks of miscarriage.

Breast-feeding

Aloe should be avoided during breastfeeding as safety has not been established.

Storage

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

Formulations

• Aloe vera gel
• Aloe vera juice
• Aloe extracts in capsules or tablets

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

• General wellness support
• Anti-inflammatory effects
• Antioxidant activity
• Digestive aid
• Support for immune function

Dosage

Children: Paediatric dosing should be determined based on the specific extract and its intended use. Consultation with a healthcare provider is recommended for accurate dosing.

Adults: Dosage varies widely depending on the specific extract and formulation. It is essential to follow the manufacturer's instructions or consult a healthcare professional for appropriate dosing.

Mechanism of action

The mechanism of action of herbal extracts can vary significantly based on their constituents. Commonly, they exert their effects through multiple pathways including modulation of neurotransmitter systems, interference with inflammatory processes, or direct antioxidant activity. Some extracts may activate certain receptors or inhibit enzymes related to disease processes.

Pharmacodynamics

The pharmacodynamics of extracts is complex due to the presence of multiple active compounds which can have synergistic or antagonistic effects. These compounds may influence cellular signaling pathways, alter gene expression, or modulate immune response. The overall pharmacological profile is determined by the specific composition of the extract, its concentration, and the biological target it interacts with.

Pharmacokinetics

The pharmacokinetics of extracts involves absorption, distribution, metabolism, and excretion of the active compounds. Generally, herbal extracts are absorbed in the gastrointestinal tract, with bioavailability influenced by factors such as formulation, the presence of food, and individual metabolic differences. Compounds may undergo hepatic metabolism, and elimination can occur through urine or feces, depending on their chemical nature.

Pregnancy

Consult a healthcare professional before use, as the safety of the extract during pregnancy has not been established.

Breast-feeding

Consult a healthcare professional before use, as the safety of the extract during breastfeeding has not been established.

Storage

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

Indications

• Fatigue
• Stress management
• Cognitive enhancement
• Immune support
• General well-being

Dosage

Children: Refer to specific product guidelines, as dosing in children should be determined by a healthcare professional.

Adults: Refer to specific product guidelines, as dosing can vary based on formulation and intended use.

Mechanism of action

Ginseng is thought to exert its effects through several mechanisms, including modulation of the hypothalamic-pituitary-adrenal (HPA) axis, enhancement of antioxidant activity, and regulation of neurotransmitter levels. Ginsenosides, the active compounds in ginseng, may influence cellular signaling pathways, promote neuroprotection, and enhance immune responses.

Pharmacodynamics

The pharmacodynamic effects of ginseng are attributed primarily to its active constituents, ginsenosides, which interact with various receptors and enzymes in the body. These interactions can lead to increased energy metabolism, improved cognitive function, enhanced physical performance, and modulation of the immune system. Ginseng may also exhibit adaptogenic properties, helping the body to maintain homeostasis under stress.

Pharmacokinetics

Ginsenosides undergo extensive metabolism in the body, primarily by the liver. Bioavailability can vary significantly based on the specific ginsenoside and the method of administration. Ginseng is usually administered orally, with effects typically observed within several hours after ingestion. The elimination half-life of ginsenosides can vary based on the specific compound and individual metabolism, with some studies suggesting that effects may persist for several hours to days.

Adverse effects

• Insomnia
• Headache
• Gastrointestinal disturbances
• Nervousness
• Hypertension
• Allergic reactions

Interactions

• May interact with anticoagulants (e.g., warfarin)
• May enhance the effects of caffeine
• May affect insulin levels and blood sugar control
• Potential interaction with immunosuppressants

Precautions

• Use with caution in patients with hypertension
• May cause sleep disturbances; avoid use before bedtime
• Should be used cautiously in patients with diabetes
• Consult a healthcare provider before use in individuals with autoimmune conditions

Pregnancy

Limited data available. Generally not recommended due to potential hormonal effects.

Breast-feeding

Limited data available. Consult a healthcare provider before use.

Storage

Store in a cool, dry place, away from direct sunlight.

Formulations

• Dried root
• Powdered extract
• Capsules
• Tinctures
• Teas

Indications

• Pantothenate deficiency
• Support in energy metabolism
• Adjuvant therapy in chronic conditions requiring enhanced energy production

Dosage

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

Adults: Refer to the BNF for specific dosing information, generally 5-10 mg daily for adults.

Mechanism of action

Pantothenate functions primarily as a precursor to coenzyme A (CoA), which is vital for various biochemical reactions in the body. CoA is involved in the metabolism of fatty acids, the synthesis of cholesterol and steroid hormones, and the acetylation of various substrates, which is crucial for energy production and metabolic processes.

Pharmacodynamics

Pantothenate plays a significant role in energy metabolism, cellular respiration, and the biosynthesis of fatty acids. It facilitates the transfer of acyl groups, which is critical for the metabolism of carbohydrates and fats, thereby influencing the overall energy production in cells. Adequate levels of pantothenate are necessary for maintaining metabolic homeostasis and supporting growth and development.

Pharmacokinetics

Pantothenate is well absorbed from the gastrointestinal tract, with a bioavailability of approximately 70%. Once absorbed, it is widely distributed throughout the body, particularly in the liver, adrenal glands, and kidneys. The vitamin is metabolized primarily in the liver, where it is converted to coenzyme A. Excess pantothenate is excreted in the urine as pantothenic acid and its metabolites. The half-life of pantothenate in the body is not well-defined but is generally considered to be relatively short due to its water-soluble nature.

Pregnancy

Pantothenic acid (Vitamin B5) is generally regarded as safe during pregnancy. It is important to maintain adequate levels for fetal development.

Breast-feeding

Pantothenic acid is excreted in breast milk in small amounts. Adequate intake is important for breastfeeding mothers, but supplementation is typically not necessary.

Storage

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

Formulations

• Pantothenate tablets
• Pantothenic acid capsules
• Pantothenate injections

Indications

• Phosphorus deficiency
• Bone health maintenance
• Nutritional supplementation
• Metabolic bone diseases

Dosage

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

Adults: Refer to the BNF for specific dosing information.

Mechanism of action

Phosphorus decreases the absorption of intercellular calcified cartilage matrix by osteoclasts in the metaphyseal region of growing bones. This results in the formation of 'phosphorus bands' of increased bone density and thickness. Additionally, exposure to white phosphorus impairs protein synthesis by damaging the rough and smooth endoplasmic reticulum, leading to an accumulation of triglycerides in the liver and resulting in hepatic steatosis and fibrosis.

Pharmacodynamics

Phosphorus is vital for the formation of hydroxyapatite in bone, which is necessary for maintaining bone density and strength. It also plays a significant role in energy transfer through ATP and in cellular signaling pathways. The balance of phosphorus in the body is tightly regulated, as both deficiency and excess can lead to serious health issues, including bone disorders and metabolic dysfunctions.

Pharmacokinetics

Phosphorus is absorbed primarily in the intestines, with bioavailability influenced by dietary factors. It is distributed throughout the body and is predominantly found in bones and teeth. Phosphorus is excreted mainly via the kidneys, with regulation occurring through various hormonal mechanisms, including parathyroid hormone and calcitriol. The half-life can vary depending on dietary intake and individual metabolism.

Pregnancy

Phosphorus is generally regarded as safe during pregnancy when consumed in appropriate dietary amounts. However, excessive phosphorus intake should be avoided as it may lead to complications.

Breast-feeding

Phosphorus is excreted in breast milk, but it is essential for the health of both the mother and the infant. Supplementation should be considered carefully.

Storage

Store in a tightly closed container, in a cool, dry place away from direct sunlight.

Indications

• Hypertension
• Angina pectoris
• Supraventricular tachycardia
• Atrial fibrillation
• Atrial flutter

Dosage

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

Adults: Refer to the BNF for specific dosing guidelines based on the condition being treated and patient characteristics.

Mechanism of action

Verapamil works by selectively blocking L-type calcium channels, which are essential for the influx of calcium ions during depolarization in cardiac and vascular smooth muscle cells. This blockade decreases intracellular calcium levels, resulting in reduced cardiac contractility (negative inotropic effect), decreased heart rate (negative chronotropic effect), and vasodilation, which collectively help in managing conditions like hypertension and angina.

Pharmacodynamics

Verapamil exhibits dose-dependent effects on cardiac conduction and vascular tone. It slows conduction through the atrioventricular (AV) node, which is beneficial in treating certain types of supraventricular tachycardias. Its vasodilatory effects lead to a reduction in peripheral vascular resistance, contributing to its antihypertensive properties. The onset of action occurs within 1 hour after oral administration, with effects lasting for several hours.

Pharmacokinetics

Verapamil is well absorbed from the gastrointestinal tract but undergoes extensive first-pass metabolism in the liver, leading to variable bioavailability (usually 20-35%). It is highly protein-bound (90-95%), primarily to albumin. The elimination half-life ranges from 3 to 7 hours, with metabolites also exhibiting pharmacological activity. Renal excretion accounts for the elimination of both unchanged drug and metabolites, necessitating caution in patients with renal impairment.

Contra-indications

• Severe hypotension
• Cardiogenic shock
• Severe left ventricular dysfunction
• Second- or third-degree AV block (unless a functioning pacemaker is present)

Adverse effects

• Hypotension
• Bradycardia
• Heart block
• Peripheral edema
• Constipation
• Headache
• Dizziness
• Fatigue

Interactions

• amiodarone+verapamil: Severe (increases risk of cardiodepression)
• verapamil+betablockers, non-selective: Severe (increases risk of cardiovascular adverse effects)
• intravenous dantrolene+verapamil: Severe (increases risk of acute hyperkalaemia and cardiovascular collapse)
• grapefruit juice+verapamil: Severe (increases exposure)
• miconazole+verapamil: Moderate (increases exposure)
• verapamil+bictegravir: Moderate (increases exposure)
• verapamil+panobinostat: Moderate (increases exposure)
• verapamil+thrombin inhibitors: Moderate (increases exposure)
• verapamil+dabigatran: Moderate (increases exposure)
• enzalutamide+verapamil: Unknown (decreases exposure)

Precautions

• Use with caution in patients with hepatic impairment
• Monitor heart rate and blood pressure regularly
• Caution in patients with a history of heart failure

Pregnancy

Use in pregnancy only if the potential benefit justifies the potential risk to the fetus. Consult local guidelines.

Breast-feeding

Verapamil is excreted in breast milk, caution is advised when used during breastfeeding.

Storage

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

Formulations

• Tablets
• Sustained-release tablets
• Injection

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

Phosphorus apparently decreases the absorption of intercellular calcified cartilage matrix by osteoclasts, in the metaphyseal region of growing bones. Administration of phosphorus to growing animals or children produces "phosphorus bands" of increased bone density and thickness that are visible grossly or from radiograms. The "phosphorus bands" are observed in the metaphyseal region of growing bones, and represent areas of decreased absorption of the calcified cartilage matrix. Exposure to white phosphorus has been shown to damage the rough endoplasmic reticulum and cause a disaggregation of polyribosomes. This damage results in impairment of protein synthesis, in particular, a decrease in the synthesis of the apolipoprotein portion of very low density lipoproteins (VLDL), which are required for the transport of triglycerides. A significant decrease in protein synthesis has been detected as early as 3 hours after oral exposure. The smooth endoplasmic reticulum is also involved in the formation of the VLDLs, and damage to the smooth endoplasmic reticulum also impairs the formation of VLDLs. The net result of these ultrastructural changes is an accumulation of triglycerides in the liver. This results in steatosis and fibrosis, which is one of the mechanisms involved in the hepatotoxicity of white phosphorus. The mechanism behind the damage to the endoplasmic reticulum is not known; also, it is not known whether white phosphorus itself or a metabolite of white phosphorus is the damaging agent. In addition to these damages, white phosphorus or a metabolite causes damage to the mitochondria and nuclei in the livers of animals orally exposed to white phosphorus. The damage to the mitochondria may impair the cell's ability to produce ATP, thus resulting in necrosis of the cell. Fatty infiltration and/or cellular damage has also been observed in the kidney, brain, and heart. It is possible that white phosphorus (or a metabolite) also impairs the ability of cells in these organs to produce ATP. The mitochondrial damage may also inhibit fatty acid oxidation (also contributing to the decreased availability of ATP) which could result in an accumulation of fat in the organs.