Locid 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

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

• Ocular implants
• Dermal fillers
• Controlled drug delivery systems
• Surgical adhesives

Dosage

Children: Refer to specific formulations and therapeutic indications for guidance as doses will vary depending on the application and product.

Adults: Refer to specific formulations and therapeutic indications for guidance as doses will vary depending on the application and product.

Mechanism of action

Polymethyl compounds, such as PMMA, function as inert materials that provide structural support in biomedical applications. They do not exhibit pharmacological activity in the traditional sense, but their effectiveness in drug delivery is attributed to their ability to form a stable matrix that can encapsulate drugs and release them over time, dependent on factors such as polymer composition and environmental conditions.

Pharmacodynamics

Due to the nature of polymethyl compounds, they do not interact with biological receptors or pathways in a pharmacodynamic manner. Instead, their properties allow for the controlled release of encapsulated substances, affecting the pharmacokinetics of the drug being delivered. They may influence the drug's bioavailability and therapeutic effects through modulation of release rates.

Pharmacokinetics

Polymethyl compounds are generally not absorbed into systemic circulation due to their inert nature. When used in drug delivery systems, the pharmacokinetics of the encapsulated drug is primarily determined by the release characteristics of the polymer matrix. Factors such as polymer molecular weight, porosity, and the presence of additives can affect the rate of drug release and subsequent absorption, distribution, metabolism, and excretion of the drug.

Pregnancy

Polymethyl is not typically recommended during pregnancy due to limited safety data. Consult healthcare providers for risk assessment.

Breast-feeding

Limited data is available on the excretion of polymethyl in human milk. Use caution and consult healthcare providers.

Storage

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

Mechanism of action

Siloxanes function primarily through their physical properties rather than a specific biochemical mechanism of action. They exhibit low surface tension and high hydrophobicity, which allows them to form protective barriers and reduce friction. In biomedical applications, siloxanes can be used as carriers for drug molecules, enhancing their solubility and stability.

Pharmacodynamics

The pharmacodynamics of siloxanes are largely related to their chemical structure, which influences their interactions with biological membranes and other compounds. Their ability to modify surface properties and create hydrophobic environments can affect drug absorption and distribution within biological systems. Additionally, siloxanes can influence the release profiles of drugs when used in controlled-release formulations.

Pharmacokinetics

The pharmacokinetics of siloxanes depend on their specific formulation and the presence of other compounds. Generally, siloxanes are poorly absorbed when ingested and are not expected to accumulate in the body. They are often metabolized in the liver, with elimination primarily occurring through urine. Their low toxicity profile makes them suitable for various applications, but specific pharmacokinetic data may vary based on the molecular structure of the specific siloxane compound being used.

Pregnancy

There are no adequate and well-controlled studies in pregnant women. Siloxane should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus.

Breast-feeding

It is not known whether siloxane is excreted in human milk. Caution should be exercised when siloxane is administered to a nursing woman.

Storage

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

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