DISOGEL

Indications

• Dyspepsia
• Peptic ulcer disease
• Gastroesophageal reflux disease (GERD)
• Heartburn
• Diarrhea
• Mucosal irritations

Dosage

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

Adults: Refer to the BNF for specific dosing recommendations based on the condition being treated.

Mechanism of action

Aluminum acts as an astringent, causing local shrinkage or constriction of body tissues through osmotic flow of fluids away from the area of application. This mechanism assists in reducing mucous secretions and managing conditions such as peptic ulcers and diarrhea. Additionally, it can help in drying and hardening of tissues when applied topically.

Pharmacodynamics

Aluminum-based antacids work by neutralizing gastric acid, leading to an increase in gastric pH. This action helps to alleviate symptoms associated with excess gastric acid, such as heartburn and discomfort. The astringent properties of aluminum also contribute to its therapeutic effects in managing mucosal irritations and secretions.

Pharmacokinetics

Aluminum is absorbed minimally when taken orally, with a bioavailability of about 0.1 to 0.5%. The majority of aluminum is excreted renally, and its half-life can be prolonged in individuals with renal impairment. Long-term use may lead to accumulation and potential toxicity, particularly impacting bone and neurological health.

Interactions

• aluminiumhydroxide+deferasirox: Severe (decreases exposure)
• aluminiumhydroxide+enteralfeeds: Unknown (increases risk of blocked enteral or nasogastric tubes)
• aluminiumhydroxide+roxadustat: Unknown (decreases exposure)

Pregnancy

Aluminum compounds are generally considered safe in pregnancy when used as directed. However, excessive exposure should be avoided.

Breast-feeding

Aluminum is excreted in breast milk; caution is advised when administered to nursing mothers.

Storage

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

Formulations

• aluminium hydroxide suspension
• aluminium hydroxide tablets

Indications

• Gastroesophageal reflux disease (GERD)
• Peptic ulcer disease
• Gastritis
• Dyspepsia
• Mucosal healing

Dosage

Children: Refer to established guidelines or

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

Mechanism of action

Deglycyrrhizinated licorice is believed to exert its effects primarily through the modulation of gastrointestinal mucosal defense mechanisms. It promotes the secretion of mucus and enhances the proliferation of gastric epithelial cells, which aids in the repair of the gastric mucosa. The active compounds in DGL, particularly flavonoids, may also have anti-inflammatory and antioxidant properties, contributing to its protective effects on the gastrointestinal lining.

Pharmacodynamics

DGL exhibits protective effects on the gastrointestinal tract by promoting mucosal healing and reducing inflammation. Its anti-inflammatory properties may help alleviate symptoms associated with conditions such as gastritis and peptic ulcers. The flavonoids present in DGL can enhance blood flow to the gastric mucosa, facilitating healing processes and improving overall gastrointestinal function.

Pharmacokinetics

The pharmacokinetics of deglycyrrhizinated licorice are not extensively studied. However, it is generally considered to have a low bioavailability due to its poor absorption in the gastrointestinal tract. The effects of DGL are primarily localized to the gastrointestinal system, where it acts topically on the mucosal surfaces. The onset of action may vary, but its effects are typically seen after several days of consistent use. Metabolism and excretion pathways for DGL are not well defined, but it is assumed to be processed similarly to other flavonoid compounds in the liver.

Adverse effects

• Headache
• Nausea
• Dizziness
• Gastrointestinal disturbances

Interactions

• May interact with medications that affect the metabolism of certain drugs due to its influence on liver enzymes
• Potential interaction with diuretics or corticosteroids due to its effects on electrolyte balance

Precautions

• Use with caution in patients with underlying liver disease
• Use with caution in patients with hypertension or heart disease

Pregnancy

Safety during pregnancy has not been established. Use only if clearly needed.

Breast-feeding

Consult a healthcare provider before use during breastfeeding.

Storage

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

Formulations

• Tablets
• Capsules
• Liquid extracts

Indications

• Nutritional supplementation
• Herbal therapy for various conditions
• Preservation of medicinal properties of plants

Dosage

Children: Dosage for dried herbal preparations in children should be approached cautiously and is best determined by a healthcare professional. Refer to paediatric guidelines for specific dosing recommendations.

Adults: Dosage for dried herbal preparations varies widely depending on the specific herb and its intended use. Refer to specific guidelines or reputable sources for dosing information.

Mechanism of action

The mechanism of action for dried herbal preparations varies depending on the specific plant material involved. Generally, the active constituents in dried herbs can exert their effects through various pathways, such as modulating neurotransmitter systems, influencing metabolic pathways, and acting on specific receptors in the body. For instance, flavonoids, terpenes, and alkaloids found in certain dried herbs can exhibit anti-inflammatory, antioxidant, or antimicrobial properties.

Pharmacodynamics

The pharmacodynamics of dried drugs depend on their specific chemical constituents. These compounds can affect physiological functions, such as modulating inflammatory responses, enhancing immune function, or affecting neurotransmission. The effects can vary widely based on the type of herb, the method of drying, and the concentration of active ingredients.

Pharmacokinetics

The pharmacokinetics of dried herbal preparations can vary significantly based on the specific herb used. Generally, after ingestion, the active compounds are absorbed in the gastrointestinal tract, metabolized primarily by the liver, and then excreted through urine or feces. The bioavailability of these compounds can be influenced by factors such as the form of the preparation (e.g., powder, extract), the presence of other food substances, and individual patient characteristics.

Pregnancy

Safety during pregnancy has not been established. Consult a healthcare provider before use.

Breast-feeding

Consult a healthcare provider before use during breastfeeding.

Storage

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

Dosage

Children: Refer to specific guidelines for pediatric dosing; consult the BNF for Children for accurate dosage information.

Adults: Refer to specific guidelines for use; dosage may vary based on the context of use.

Mechanism of action

Hydroxide ions act primarily as bases, neutralizing acids to form water and salts. They participate in various biochemical pathways, including selenium metabolism and the degradation of reactive oxygen species. Hydroxide can influence enzyme activity and stability by altering the pH of the environment, thereby affecting metabolic reactions.

Pharmacodynamics

Hydroxide ions can impact biological processes by changing the local pH, which influences enzyme activity, ion transport, and the solubility of other compounds. Their ability to neutralize acids can help regulate physiological pH, contributing to homeostasis in living organisms.

Pharmacokinetics

As an inorganic ion, hydroxide does not undergo traditional pharmacokinetic processes like absorption, distribution, metabolism, or excretion. Instead, it is rapidly equilibrated in biological fluids and participates in acid-base reactions, having immediate effects on the local environment.

Pregnancy

There is limited information regarding the use of hydroxide during pregnancy. Consult a healthcare professional for advice.

Breast-feeding

Limited data is available on the excretion of hydroxide in breast milk. Consult a healthcare professional before use.

Storage

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

Indications

• Chronic cough
• Sore throat
• Gastroesophageal reflux disease (GERD)
• Peptic ulcers
• Adrenal insufficiency
• Inflammatory skin conditions

Dosage

Children: Refer to specific product guidelines or consult a healthcare professional for appropriate dosages.

Adults: Refer to specific product guidelines or consult a healthcare professional for appropriate dosages.

Mechanism of action

Liquorice exerts its effects primarily through the action of glycyrrhizin. It inhibits the enzyme 11β-hydroxysteroid dehydrogenase type 2, leading to increased levels of cortisol. This results in mineralocorticoid-like effects, such as sodium retention and potassium excretion, which can influence blood pressure and fluid balance. Additionally, glycyrrhizin has demonstrated anti-inflammatory and antiviral properties, potentially through modulation of immune responses and inhibition of viral replication.

Pharmacodynamics

Liquorice has several pharmacodynamic properties, including its ability to enhance the effects of corticosteroids, which can be beneficial in conditions requiring anti-inflammatory treatment. It also exhibits expectorant properties, promoting mucus secretion and aiding in respiratory conditions. The sweet taste of liquorice may also stimulate appetite and aid in digestive health.

Pharmacokinetics

The absorption of liquorice occurs mainly in the gastrointestinal tract, with peak plasma concentrations typically reached within 1 to 2 hours after ingestion. Glycyrrhizin is metabolized in the liver to its active components, and its effects can last for several hours. The elimination half-life of glycyrrhizin is approximately 8 to 12 hours, with metabolites primarily excreted in urine. Chronic use may lead to accumulation and associated side effects.

Contra-indications

• Hypersensitivity to liquorice or any of its components
• Severe hypertension
• Diabetes mellitus
• Heart disease
• Renal impairment

Adverse effects

• Hypertension
• Hypokalemia (low potassium levels)
• Edema (swelling due to fluid retention)
• Headache
• Fatigue
• Muscle weakness
• Hormonal imbalances
• Gastrointestinal disturbances

Interactions

• May enhance the effects of corticosteroids and other drugs that affect potassium levels
• May interact with antihypertensive medications, potentially reducing their effectiveness
• May affect the metabolism of certain drugs through cytochrome P450 enzymes
• Concomitant use with diuretics may increase the risk of hypokalemia

Precautions

• Use with caution in patients with cardiovascular diseases
• Monitor blood pressure regularly during prolonged use
• Assess potassium levels in patients on long-term treatment
• Consider potential hormonal effects in patients with endocrine disorders

Pregnancy

Use during pregnancy should be avoided unless clearly needed, as it may affect fetal development and maternal health.

Breast-feeding

Caution is advised when using liquorice while breastfeeding due to potential effects on milk production and infant metabolism.

Storage

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

Formulations

• Dried root
• Powdered extract
• Liquid extract
• Glycyrrhizin (a major active compound)

Indications

• Magnesium deficiency
• Eclampsia
• Torsades de pointes
• Arrhythmias
• Prevention of migraine

Dosage

Children: Refer to the BNF for Children for specific dosing information, as it can vary based on age, weight, and clinical condition.

Adults: Refer to specific guidelines or clinical protocols for dosing as it can vary based on the indication and individual patient factors.

Mechanism of action

Magnesium acts as a cofactor for various enzymatic reactions and is crucial for the function of ion channels, particularly those regulating calcium, sodium, and potassium ions. It stabilizes the structure of ATP and is necessary for cellular energy metabolism. Magnesium also plays a role in neuromuscular transmission and helps to modulate excitatory neurotransmitters, providing a calming effect on the nervous system.

Pharmacodynamics

Magnesium contributes to the maintenance of normal muscle and nerve function, and its deficiency can lead to symptoms such as muscle cramps, seizures, and arrhythmias. It has a role in regulating blood pressure by influencing vascular tone and may have protective effects against cardiovascular diseases. Magnesium is also known to have a role in glucose metabolism, potentially improving insulin sensitivity.

Pharmacokinetics

Magnesium is absorbed in the gastrointestinal tract, primarily in the small intestine. The bioavailability of magnesium can vary based on dietary sources and the presence of other nutrients. The kidneys play a crucial role in regulating magnesium levels in the body, with renal excretion increasing in states of excess and decreasing in deficiency. The half-life of magnesium in the body is variable and can depend on the individual's renal function and dietary intake.

Contra-indications

• Severe renal impairment
• Myasthenia gravis
• Heart block
• Hypersensitivity to magnesium

Adverse effects

• Diarrhea
• Nausea
• Vomiting
• Abdominal cramping
• Hypotension
• Respiratory depression
• Cardiac arrest

Interactions

• Calcium channel blockers (may enhance hypotensive effects)
• Muscle relaxants (may increase neuromuscular blockade)
• Digoxin (may increase risk of digoxin toxicity)

Precautions

• Monitor renal function before and during therapy
• Caution in patients with cardiac disease
• Use with caution in elderly patients due to potential renal impairment

Pregnancy

Magnesium is generally considered safe during pregnancy when used in appropriate doses, but consult healthcare providers for individual recommendations.

Breast-feeding

Magnesium is excreted in breast milk; however, it is not expected to cause adverse effects in breastfed infants when used in normal therapeutic doses.

Storage

Store in a cool, dry place, away from moisture and heat. Keep out of reach of children.

Formulations

• Oral tablets
• Oral solution
• Intravenous injection
• Intramuscular injection

Indications

• Flatulence
• Bloating
• Gastroesophageal reflux disease
• Functional dyspepsia

Dosage

Children: For children, refer to the BNF for Children for specific dosing recommendations.

Adults: The usual adult dose is 40 to 125 mg taken after meals and at bedtime, as needed.

Mechanism of action

Simethicone is a surfactant that decreases the surface tension of gas bubbles in the gastrointestinal tract, facilitating their expulsion. It acts by forming a film of low surface tension that promotes the coalescence of mucus-surrounded gas bubbles, allowing for easier passage of gas.

Pharmacodynamics

Simethicone decreases the surface tension of gas bubbles in the gastrointestinal tract, facilitating their expulsion. Its effects are generally short-lived, as it is typically administered as needed. The therapeutic index is wide since it is not absorbed systemically, making it safe for use in various patient populations.

Pharmacokinetics

Simethicone is not systemically absorbed following oral administration, which contributes to its safety profile. Due to its lack of systemic absorption, specific pharmacokinetic parameters such as half-life, clearance, and volume of distribution are not applicable.

Pregnancy

Simethicone can be used during pregnancy as there are no known risks associated with its use.

Breast-feeding

Simethicone is considered safe to use during breastfeeding, as it is not absorbed systemically.

Storage

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

Formulations

• Oral suspension
• Chewable tablets
• Soft gels

Mechanism of action

Aluminum Acetate is an astringent. An astrignent is a chemical that tends to shrink or constrict body tissues, usually locally after topical medicinal application. The shrinkage or constriction is through osmotic flow of water (or other fluids) away from the area where the astringent was applied. Astringent medicines cause shrinkage of mucous membranes or exposed tissues and are often used internally to check discharge of blood serum or mucous secretions. This can happen with a sore throat, hemorrhages, diarrhea, or with peptic ulcers. Externally applied astringents, which cause mild coagulation of skin proteins, dry, harden, and protect the skin. Acne sufferers are often advised to use astringents if they have oily skin. Astringents also help heal stretch marks and other scars. Mild astringent solutions are used in the relief of such minor skin irritations as those resulting from superficial cuts, allergies, insect bites, or fungal infections such as athlete's foot. Excessive dietary aluminum has been proposed to be a factor contributing to several neurological disorders in humans. Six 8-week-old female Swiss Webster mice were fed for 10 wk purified diets containing 100 (control), 500 or 1000 ug aluminum/g diet. Brain and liver lipid peroxidation was determined by evaluating the production of 2-thiobarbituric acid reactive substances in brain and liver homogenates in the presence or absence of 50 uM ferrous iron. 2-Thiobarbituric acid reactive substances production in the absence of iron in brain homogenates from mice fed the 1000 ug/g diet was higher (30%) than that in the 100 ug/g control group (3.1 vs 2.4 nmol 2-thiobarbituric acid reactive substances/mg protein). The addition of ferrous iron increased 2-thiobarbituric acid reactive substances production in brain homogenates from all 3 dietary groups. The iron induced 2-thiobarbituric acid reactive substances production was 26% higher in the 1000 ug/g brain homogenates than in the 100 ug/g group (4.9 vs 3.9 nmol 2-thiobarbituric acid reactive substances/mg protein). Brain 2-thiobarbituric acid reactive substances production in the presence and absence of iron was similar between the 100 and 500 ug/g aluminum groups. 2-Thiobarbituric acid reactive substances production in liver homogenates measured either with or without iron was similar for the 3 groups. These results show that, in mice, dietary aluminum intoxication leads to increased brain 2-thiobarbituric acid reactive substance production, suggesting that enhanced lipid peroxidation may be one possible mechanism underlying the neurological damage associated with increased tissue aluminum. Evidence is presented indicating that dementias are associated with a relative insufficiency of magnesium in the brain. Such insufficiency may be attributable to low intake or retention of magnesium; high intake of a neurotoxic metal, such as aluminum, which inhibits activity of magnesium requiring enzymes; or impaired transport of magnesium and/or enhanced transport of the neurotoxic metal into brain tissue. It is proposed that Alzheimer's disease involves a defective transport process, characterized by both an abnormally high incorporation of aluminum and an abnormally low incorporation that an altered serum protein contributes to the progression of Alzheimer's disease by having a greater affinity for aluminum than for magnesium, in contrast to the normal protein, which binds magnesium better than aluminum. The altered protein crosses the blood-brain barrier more efficiently than the normal protein and competes with the normal protein in binding to brain neurons. Binding of the altered protein to the target neurons would both facilitate aluminum uptake and impede magnesium uptake. Evidence suggests that albumin is the serum protein that is altered. Aluminum is established as a neurotoxin, although the basis for its toxicity is unknown. It recently has been shown to alter the function of the blood-brain barrier, which regulates ex

Mechanism of action

Simethicone is a surfactant that decreases the surface tension of gas bubbles in the gastrointestinal tract, more easily allowing gas to exit the body. The clinical use of simethicone is based on its antifoam properties. Silicone antifoams spread on the surface of aqueous liquids, forming a film of low surface tension and thus causing collapse of foam bubbles. Simethicone reportedly allows mucus-surrounded gas bubbles in the GI tract to coalesce and be expelled.

Pharmacodynamics

Simethicone decreases the surface tension of gas bubbles in the gastrointestinal tract, facilitating their expulsion. It has a short duration of action as it is generally given as needed, and a wide therapeutic index as it is not systemically absorbed.