Relcer Gel suspension

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

• Gastroesophageal reflux disease (GERD)
• Peptic ulcer disease
• Heartburn
• Dyspepsia
• Acid indigestion

Dosage

Children: Refer to pediatric dosing guidelines in the relevant pediatric reference materials.

Adults: Refer to specific product guidelines for dosing instructions; typical adult doses vary based on formulation and indication.

Mechanism of action

Hydroxide compounds neutralize gastric acid through a chemical reaction, resulting in the formation of water and other neutral salts. This raises the pH of the stomach contents, providing symptomatic relief from acidity, and promoting healing of the gastric mucosa.

Pharmacodynamics

Hydroxide compounds decrease gastric acidity, which can help alleviate symptoms of acid-related gastrointestinal conditions. They also can stimulate mucus secretion and increase the rate of gastric emptying, contributing to their therapeutic effects.

Pharmacokinetics

Hydroxide compounds generally have low systemic absorption; they mainly act in the gastrointestinal tract. After oral administration, they react with gastric acid in the stomach. The onset of action is typically rapid, with effects lasting for a few hours, depending on the formulation and the presence of food.

Adverse effects

• Gastrointestinal irritation
• Constipation
• Diarrhea
• Nausea
• Electrolyte imbalance

Precautions

• Use with caution in patients with renal impairment
• Monitor electrolyte levels in patients using high doses or prolonged therapy
• Avoid concurrent use with other medications that can cause gastrointestinal irritation

Pregnancy

Use only if clearly needed, as safety in pregnancy has not been established.

Breast-feeding

Consult healthcare provider before use, as it may pass into breast milk.

Storage

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

Formulations

• Oral tablets
• Suspensions
• Chewable tablets

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

• Cough and respiratory tract disorders
• Peptic ulcer disease
• Gastroesophageal reflux disease (GERD)
• Adrenal insufficiency
• Inflammatory conditions

Dosage

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

Adults: Refer to reputable clinical guidelines or pharmacopoeias for appropriate dosing.

Mechanism of action

Glycyrrhizin inhibits the enzyme 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2), which typically converts active cortisol to its inactive form, cortisone. This inhibition leads to increased cortisol levels, resulting in mineralocorticoid-like effects such as sodium retention and potassium excretion, which can influence blood pressure and fluid balance. Additionally, liquorice exhibits antioxidant properties and may modulate immune responses.

Pharmacodynamics

Liquorice displays a variety of pharmacological effects including anti-inflammatory, antiviral, and gastroprotective actions. Its anti-inflammatory effects are attributed to the inhibition of pro-inflammatory cytokines and the suppression of immune cell activation. The antiviral properties are primarily linked to its action against viruses such as herpes simplex and hepatitis C. Moreover, liquorice can enhance mucus secretion in the respiratory tract, facilitating the expulsion of phlegm.

Pharmacokinetics

Liquorice is absorbed from the gastrointestinal tract, with glycyrrhizin being the most bioactive compound. Its metabolites can be detected in the plasma, and the elimination half-life is variable, generally between 6 to 12 hours. The metabolism of glycyrrhizin occurs primarily in the liver, and it undergoes phase I and phase II metabolic processes. Excretion mainly occurs through urine, with both active and inactive metabolites present.

Contra-indications

• Hypersensitivity to liquorice or any of its components
• Severe hypertension
• Heart disease
• Kidney disease
• Cirrhosis of the liver

Adverse effects

• Hypertension
• Hypokalemia
• Edema
• Headache
• Fatigue
• Gastrointestinal disturbances
• Muscle weakness
• Arrhythmias

Interactions

• Corticosteroids - may enhance the effects of corticosteroids
• Digoxin - may increase the risk of digoxin toxicity due to hypokalemia
• Diuretics - may reduce effectiveness of potassium-sparing diuretics and increase potassium loss
• Antihypertensives - may counteract the effects of antihypertensive medications

Precautions

• Use with caution in patients with hypertension
• Monitor electrolytes, particularly potassium levels in long-term use
• Avoid excessive consumption, particularly in patients with underlying cardiovascular conditions

Pregnancy

Use during pregnancy is not well studied; consult a healthcare provider before use.

Breast-feeding

Limited information available; consult a healthcare provider before use.

Storage

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

Formulations

• Dried root
• Powder
• Extracts
• Syrups

Indications

• Dermatitis
• Eczema
• Psoriasis
• Wound care
• Skin infections
• Burns
• Irritation or inflammation of the skin

Dosage

Children: For paediatric use, apply a thin layer of paste to the affected area as needed, following guidance from a healthcare professional or as directed in pediatric dosing guidelines.

Adults: Apply a thin layer of paste to the affected area as needed, ensuring to follow the specific instructions provided with the formulation or as directed by a healthcare professional.

Mechanism of action

The mechanism of action of paste depends on its active ingredients. Generally, pastes provide a protective barrier, reduce moisture loss, and may deliver anti-inflammatory or antimicrobial agents to the skin. The combination of ingredients can enhance the therapeutic effect, leading to improved healing and symptom relief.

Pharmacodynamics

Pharmacodynamics of paste formulations involves the interaction of its components with skin receptors and the local environment. Active ingredients may exert anti-inflammatory, antimicrobial, or soothing effects. The occlusive nature of pastes can enhance drug absorption and prolong the action of therapeutic agents, leading to improved efficacy in treating skin conditions.

Pharmacokinetics

Pastes are primarily applied topically, and their absorption can vary based on the formulation, the condition of the skin, and the presence of occlusive agents. Systemic absorption is generally minimal, although it can occur, especially with certain active ingredients. The onset of action can vary, typically providing localized effects within a short period after application.

Pregnancy

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

Breast-feeding

Consult a healthcare provider before use during breastfeeding, as safety is not well-established.

Storage

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

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.