NOVAGEL 2.4%W/V,5%W/V SUSPENSION

Indications

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

Dosage

Children: Refer to the BNF for Children for appropriate dosing guidelines for paediatric patients, as dosing will depend on the child's age, weight, and specific indications.

Adults: Refer to the BNF for specific dosing recommendations for adults, as doses may vary based on the formulation and clinical condition being treated.

Mechanism of action

Alumina works by neutralizing gastric acid through a chemical reaction that forms aluminum chloride and water, thereby increasing the pH level in the stomach. This action alleviates symptoms associated with hyperacidity, such as heartburn and dyspepsia, by reducing the acidity of the stomach contents and promoting a more favorable environment for gastric mucosa.

Pharmacodynamics

Alumina exhibits its pharmacological effects primarily through its antacid properties. It binds to gastric acid in the stomach, leading to a decrease in acidity and helping to relieve discomfort from acid-related conditions. The effectiveness of alumina as an antacid is influenced by its ability to form complexes with hydrochloric acid, which decreases the overall acid concentration in the gastrointestinal tract.

Pharmacokinetics

Alumina is not significantly absorbed in the gastrointestinal tract, which limits its systemic effects. The pharmacokinetic profile indicates that alumina acts locally in the stomach and intestines, where it neutralizes acid without being absorbed into the bloodstream. The elimination of aluminum from the body occurs primarily through the kidneys, and when used as directed, it typically does not lead to toxicity.

Pregnancy

Safety in pregnancy has not been established. Use only if clearly needed and the potential benefits outweigh the risks.

Breast-feeding

Safety during breastfeeding is not established. Caution is advised.

Storage

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

Formulations

• Powder
• Suspension

Indications

• Gastric hyperacidity
• Heartburn
• Indigestion
• Gastritis
• Peptic ulcers

Dosage

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

Adults: Refer to specific product guidelines for dosing, as it may vary based on formulation.

Mechanism of action

Trisilicate works by reacting with hydrochloric acid in the stomach to form neutral compounds, which reduces acidity. This action helps to alleviate symptoms of acid-related disorders by increasing the pH level in the stomach.

Pharmacodynamics

Trisilicate exhibits its therapeutic effects primarily through acid neutralization. By decreasing the acidity of gastric contents, it provides symptomatic relief from conditions such as gastritis, gastroesophageal reflux disease (GERD), and peptic ulcers. The onset of action is typically rapid, with effects lasting for a few hours.

Pharmacokinetics

The pharmacokinetics of trisilicate involve minimal systemic absorption since the drug primarily acts locally within the gastrointestinal tract. The compound is excreted unchanged in the feces. Its onset of action is usually within minutes after administration, with a duration of effect that can last several hours, depending on gastric emptying and the formulation used.

Pregnancy

Trisilicate is not recommended for use during pregnancy unless the potential benefit justifies the potential risk to the fetus.

Breast-feeding

Trisilicate may be used during breastfeeding, but it is advisable to consult a healthcare professional before use.

Storage

Store in a cool, dry place, protected from light.

Mechanism of action

... Six 8 wk old female Swiss Webster mice were fed for 10 weeks 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 ... 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 /group/ brain homogenates than in the ... /control/ group (4.9 vs 3.9 nmol 2-thiobarbituric acid reactive subtances/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 /diet/ 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. /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 a 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 of magnesium into brain neurons. The hypothesis has advanced 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/ 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 exchanges between the central nervous system and peripheral circulation. The blood brain barrier owes its unique properties to the integrity of cell membranes that comprise it. Aluminum affects some of the membrane-like functions of the blood brain barrier. It increases the rate of transmembrane diffusion and selectively changes saturable transport systems without disrupting the integrity of the membranes or altering CNS hemodynamics. Such alterations in the access to the brain of nutrients, hormones, toxins, and drugs could be the basis of CNS dysfunction. Aluminum is capable of altering membrane function at the blood-brain barrier; many of its effects on the CNS as well as peripheral tissues can be explained by its actions as a membrane toxin. /Aluminum/ Chronic, oral administration of aluminum to rats increases the in vivo concentration of cyclic AMP and the phosphorylation of microtubule-associated protein-2 and the 200 kd neurofilament subunit. In the present study, the effect of t