Vitamin A Palmitate BP 1000IU/g, Vitamin D3 BP 30IU/g, Urea BP 5.0% w/w, Aloe vera Extract 5.0% w/w, Magnesium Lactate Dihydrate BP 2.0% w/w and Zinc Oxide BP 2.0% w/w

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

• Vitamin D deficiency
• Rickets
• Osteomalacia
• Osteoporosis
• Hypoparathyroidism

Dosage

Adults: The usual adult dose for vitamin D deficiency is 800 to 2000 IU daily, depending on the severity of deficiency and clinical condition. Higher doses may be used under medical supervision.

Mechanism of action

Cholecalciferol is converted to its active forms, 25-hydroxyvitamin D in the liver and 1,25-dihydroxyvitamin D in the kidneys. These metabolites enhance the intestinal absorption of calcium and phosphorus, increase serum calcium levels, and mobilize these minerals from bone. This process is regulated by parathyroid hormone, which influences calcium and phosphate metabolism, particularly in the kidneys.

Pharmacodynamics

The pharmacodynamics of cholecalciferol involve its conversion to active metabolites that play a significant role in calcium and phosphorus homeostasis. The metabolites facilitate intestinal absorption of these minerals, promote bone mineralization, and influence renal reabsorption. The onset of action occurs within 10 to 24 hours following administration, as metabolic activation is required for its biological effects.

Pharmacokinetics

Cholecalciferol is absorbed in the gastrointestinal tract, and its absorption is enhanced by the presence of dietary fats. It is transported in the bloodstream bound to vitamin D-binding protein. Once in the liver, it undergoes hydroxylation to form 25-hydroxyvitamin D, which is further converted in the kidneys to the active form, 1,25-dihydroxyvitamin D. The elimination half-life of cholecalciferol varies, typically spanning several days, and it is primarily excreted in bile and urine.

Adverse effects

• Hypercalcemia
• Hypercalciuria
• Nausea
• Vomiting
• Constipation
• Weakness
• Fatigue

Interactions

• May enhance the effects of thiazide diuretics, leading to increased risk of hypercalcemia
• Anticonvulsants may increase metabolism of vitamin D, leading to reduced effectiveness
• Cholestyramine may reduce absorption of vitamin D

Precautions

• Monitor serum calcium levels in patients with renal impairment
• Caution in patients with a history of hypercalcemia or hyperparathyroidism
• Use with caution in patients taking other medications that affect calcium metabolism

Pregnancy

Cholecalciferol can be used during pregnancy if indicated, as vitamin D is essential for fetal bone development.

Breast-feeding

Cholecalciferol is excreted in breast milk, but is generally considered safe during breastfeeding.

Storage

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

Formulations

• Capsules
• Tablets
• Liquid formulations

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

• Metabolic acidosis
• Lactic acidosis
• Energy substrate in critical illness
• Monitoring tissue perfusion and oxygenation

Dosage

Children: Refer to the BNF for Children for appropriate dosing in paediatric patients.

Adults: Refer to specific guidelines based on clinical context as dosing is highly variable and situation-dependent.

Mechanism of action

Lactate acts as a signaling molecule and energy substrate in various physiological and pathological processes. It is involved in the modulation of several metabolic pathways, including the Cori cycle and Krebs cycle. Lactate also participates in metabolic reprogramming, especially in cancer cells, where it can promote tumor growth and survival by providing an alternative energy source and influencing cellular signaling pathways such as the PI3K/AKT/mTOR pathway.

Pharmacodynamics

Lactate plays a vital role in energy metabolism. It can be oxidized back to pyruvate by lactate dehydrogenase, entering the Krebs cycle for ATP production. In addition to serving as an energy substrate, lactate impacts pH regulation and can influence the function of various immune cells. Its levels can indicate the state of oxygen delivery and utilization in tissues, thus serving as a marker for metabolic stress.

Pharmacokinetics

Lactate is produced primarily in the cytoplasm during glycolysis, with its concentration in the blood reflecting the balance between production and clearance. It is metabolized predominantly in the liver, where it can be converted back to glucose or utilized in the Krebs cycle. Lactate levels can vary based on factors such as exercise, tissue hypoxia, and metabolic conditions.

Pregnancy

Lactate is generally regarded as safe during pregnancy as it is a naturally occurring metabolite in the body, but specific clinical advice should be sought.

Breast-feeding

Lactate is considered safe during breastfeeding as it is a normal component of human metabolism, but consult a healthcare provider for personalized advice.

Storage

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

Mechanism of action

Oxides do not have a single mechanism of action as they are a broad category of compounds. However, in general, metal oxides can exhibit catalytic properties, while non-metal oxides may participate in biochemical reactions by forming acids or bases upon dissolution in water.

Pharmacodynamics

The pharmacodynamics of oxides depend on the specific type of oxide and its interaction with biological systems. For instance, metal oxides may have antimicrobial properties, while certain non-metal oxides can influence metabolic pathways through their acid-base chemistry. The effects vary widely, necessitating specific studies for each oxide's role in therapeutic contexts.

Pharmacokinetics

The pharmacokinetics of oxides are also variable. Many metal oxides are poorly soluble and thus have limited absorption when ingested. Non-metal oxides, such as carbon dioxide, can be readily absorbed and utilized in metabolic processes. The distribution, metabolism, and excretion of oxides depend on their chemical form and the biological system in which they are involved.

Pregnancy

Not applicable as oxide is not a drug but a class of chemical compounds.

Breast-feeding

Not applicable as oxide is not a drug but a class of chemical compounds.

Storage

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

Mechanism of action

Excessive palmitoylcarnitine formation and exhausted L-carnitine stores lead to energy depletion, which, along with attenuated acetylcholine synthesis and oxidative stress, are main mechanisms behind palmitate-induced neuronal loss. High levels of palmitate exposure are suggested to contribute to diabetic neuropathy and gastrointestinal dysregulation. Additionally, palmitate negatively regulates acetyl-CoA carboxylase, thereby preventing further palmitate generation.

Pharmacodynamics

Palmitate is the first fatty acid generated during lipogenesis and serves as a precursor for the synthesis of longer fatty acids. The presence of palmitate inhibits acetyl-CoA carboxylase, reducing the conversion of acetyl-ACP to malonyl-ACP, which subsequently decreases the synthesis of new palmitate. This feedback mechanism is crucial for maintaining lipid homeostasis within the body.

Pharmacokinetics

Palmitate is absorbed from dietary sources and can also be synthesized endogenously in the liver and adipose tissue. Once in circulation, it is transported via chylomicrons or albumin. The metabolism of palmitate occurs primarily in the mitochondria through fatty acid oxidation, generating acetyl-CoA, which can enter the citric acid cycle for energy production. The overall kinetics of palmitate are influenced by dietary intake, metabolic demand, and hormonal regulation.

Pregnancy

Palmitate is classified as a category C drug. Animal reproduction studies have not been conducted, and there are no adequate and well-controlled studies in pregnant women. It should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus.

Breast-feeding

There are no data on the excretion of palmitate in human milk. Caution should be exercised when administering to nursing mothers.

Storage

Store at room temperature, away from light and moisture. Keep the container tightly closed.

Formulations

• Palmitate 500 mg softgel
• Palmitate 1000 mg softgel

Indications

• Dry skin
• Ichthyosis
• Eczema
• Psoriasis
• Dermatitis

Dosage

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

Adults: Refer to the specific product information for dosing instructions, as doses may vary based on formulation and intended use.

Mechanism of action

The primary mechanism of ammonia toxicosis appears to be inhibition of the citric acid cycle. There is an increase in anaerobic glycolysis, blood glucose, and blood lactate. Acidosis is manifested. The exact means by which ammonia blocks the citric acid cycle is not known. It is postulated that ammonia saturation of the glutamine-synthesizing system causes a backing-up in the citrate cycle, a decrease in its intermediates, and a decrease in energy production and cellular respiration, which leads to convulsions. The decrease of citrate cycle intermediates is postulated to result from reamination of pyruvic, ketoglutaric, and oxaloacetic acids.

Pharmacodynamics

Urea is a keratolytic emollient that works to treat or prevent dry, rough, scaly, itchy skin. Its emollient properties help to maintain skin hydration and improve the overall condition of the skin.

Pharmacokinetics

Urea is absorbed through the skin and metabolized in the body. It does not have significant systemic effects when used topically, as it primarily acts locally to alter the moisture content of the stratum corneum, thereby enhancing the skin's barrier function and improving hydration.

Adverse effects

• Skin irritation
• Burning sensation
• Dryness
• Redness

Precautions

• Use with caution in individuals with renal impairment
• Avoid contact with eyes
• Discontinue use if severe irritation occurs

Pregnancy

Consult healthcare provider before use, safety in pregnancy not established.

Breast-feeding

Consult healthcare provider before use, safety in breastfeeding not established.

Storage

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

Formulations

• Topical cream
• Topical ointment
• Topical lotion

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

Indications

• Vitamin deficiency syndromes (e.g., scurvy for vitamin C deficiency, rickets for vitamin D deficiency)
• Support for immune function
• Antioxidant support
• Bone health maintenance
• Vision health
• Energy metabolism support

Dosage

Children: Refer to the BNF for Children for specific vitamin dosing guidelines, which depend on age and nutritional requirements.

Adults: Refer to specific vitamin guidelines as dosage varies significantly depending on the type of vitamin and individual needs.

Mechanism of action

Vitamins function primarily as coenzymes or precursors for coenzymes in enzymatic reactions. For instance, B vitamins are involved in energy metabolism, while vitamins A, C, D, E, and K support various physiological functions including vision, antioxidant activity, calcium regulation, and blood clotting. Each vitamin has a unique mechanism of action based on its structure and role in the body.

Pharmacodynamics

Vitamins exert their effects at the cellular level, influencing metabolic pathways, gene expression, and immune responses. For example, vitamin D regulates calcium and phosphate homeostasis, while vitamin A is crucial for vision and immune function. Deficiencies in vitamins can lead to a range of disorders, highlighting their importance in maintaining health.

Pharmacokinetics

The pharmacokinetics of vitamins vary widely. Fat-soluble vitamins (A, D, E, and K) are stored in liver and adipose tissues and can be released into circulation as needed. Water-soluble vitamins (B-complex and C) are not stored and must be consumed regularly, with excess amounts excreted in urine. Absorption rates, half-lives, and distribution can also differ based on the specific vitamin and individual metabolic factors.

Interactions

• tretinoin+vitamin: Severe (increases risk of vitamin toxicity)
• retinoids+vitamin: Severe (increases risk of vitamin toxicity)
• retinoids+vitamin: Moderate (increases risk of toxicity)
• carbamazepine+vitamin: Unknown (decreases effects)
• cobicistat+vitamin: Unknown (increases exposure)
• vitamin D substances+digoxin: Unknown (increases risk of toxicity)
• idelalisib+vitamin: Unknown (increases exposure)
• clarithromycin+vitamin: Unknown (increases exposure)

Pregnancy

Consult healthcare professional before use. Vitamin supplementation during pregnancy should be carefully managed to avoid hypervitaminosis.

Breast-feeding

Consult healthcare professional before use. Some vitamins can pass into breast milk and may affect the infant.

Storage

Store in a cool, dry place, away from direct sunlight. Ensure it is kept out of reach of children.

Formulations

• {'name': 'Vitamin A', 'form': 'Capsule', 'strength': '10000 IU'}
• {'name': 'Vitamin D', 'form': 'Tablet', 'strength': '1000 IU'}
• {'name': 'Vitamin E', 'form': 'Softgel', 'strength': '400 IU'}

Mechanism of action

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 stimulate 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. In particular, calcitriol interacts with vitamin D receptors in the small intestine to enhance the efficiency of intestinal calcium and phosphorous absorption from about 10-15% to 30-40% and 60% increased to 80%, respectively. Furthermore, calcitriol binds with vitamin D receptors in osteoblasts to stimulate a receptor activator of nuclear factor kB ligand (or RANKL) which subsequently interacts with receptor activator of nuclear factor kB (NFkB) on immature preosteoclasts, causing them to become mature bone-resorbing osteoclasts. Such mature osteoclasts ultimately function in removing calcium and phosphorus from bone to maintain blood calcium and phosphorus levels. Moreover, calcitriol also stimulates calcium reabsorption from the glomerular filtrate in the kidneys. Additionally, it is believed that when calcitriol binds with nuclear vitamin D receptors, that this bound complex itself binds to retinoic acid X receptor (RXR) to generate a heterodimeric complex that consequently binds to specific nucleotide sequences in the DNA called vitamin D response elements. When bound, various transcription factors attach to this complex, resulting in either up or down-regulation of the associated gene's activity. It is thought that there may be as much as 200 to 2000 genes that possess vitamin D response elements or that are influenced indirectly to control a multitude of genes across the genome. It is in this way that cholecalciferol is believed to function in regulating gene transcription associated with cancer risk, autoimmune disorders, and cardiovascular disease linked to vitamin D deficiency. In fact, there has been some research to suggest calcitriol may also be able to prevent malignancies by inducing cellular maturation and inducing apoptosis and inhibiting angiogenesis, exhibit anti-inflammatory effects by inhibiting foam cell formation and promoting angiogenesis in en

Pharmacodynamics

The in vivo synthesis of the predominant two biologically active metabolites of vitamin D occurs in two steps. The first hydroxylation of vitamin D3 cholecalciferol (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 cholecalciferol 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.

Mechanism of action

... Excessive palmitoylcarnitine formation and exhausted L-carnitine stores leading to energy depletion, attenuated acetylcholine synthesis and oxidative stress to be main mechanisms behind PA-induced neuronal loss.High PA exposure is suggested to be a factor in causing diabetic neuropathy and gastrointestinal dysregulation. ... First phase insulin release response was lost in these islets. FFAs slightly increased the insulin output of normal fresh pancreas beta-cells. However, chronic exposure to FFAs resulted in loss of first phase insulin release and blunted insulin secretion response to various levels of D-glucose stimulation.

Pharmacodynamics

Palmitic acid is the first fatty acid produced during lipogenesis (fatty acid synthesis) and from which longer fatty acids can be produced. Palmitate negatively feeds back on acetyl-CoA carboxylase (ACC) which is responsible for converting acetyl-ACP to malonyl-ACP on the growing acyl chain, thus preventing further palmitate generation

Mechanism of action

... The primary mechanism of ammonia toxicosis appears to be inhibition of the citric acid cycle. There is an increase in anaerobic glycolysis, blood glucose, and blood lactate ... . Acidosis is manifested. The exact means by which ammonia blocks the citric acid cycle is not known. It is postulated that ammonia saturation of the glutamine-synthesizing system causes a backing-up in the citrate cycle, a decrease in its intermediates, and a decrease in energy production and cellular respiration, which leads to convulsions ... . The decrease of citrate cycle intermediates is postulated to result from reamination of pyruvic, ketoglutaric, and oxaloacetic acids.

Pharmacodynamics

Urea is a keratolytic emollient that works to treat or prevent dry, rough, scaly, itchy skin.