UNICID 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

• 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

• Allergic conditions
• Autoimmune diseases
• Asthma and chronic obstructive pulmonary disease (COPD)
• Certain cancers (e.g., leukemia, lymphoma)
• Skin conditions (e.g., dermatitis)
• Inflammatory bowel disease
• Multiple sclerosis exacerbations
• Severe infections requiring immunosuppression

Dosage

Children: Refer to BNF for Children for specific dosing; doses vary significantly based on the child's age, weight, and condition being treated.

Adults: Refer to BNF for specific dosing; typically, initial doses range from 4 to 48 mg depending on the severity of the condition.

Mechanism of action

Methylprednisolone exerts its effects by binding to glucocorticoid receptors, leading to the modulation of gene expression. This interaction influences the transcription of anti-inflammatory proteins while suppressing the expression of pro-inflammatory genes, ultimately resulting in reduced inflammation and immune response.

Pharmacodynamics

The pharmacodynamic effects of methylprednisolone are characterized by its ability to decrease inflammation, suppress the immune response, and affect carbohydrate metabolism. Therapeutic doses lead to various systemic effects, including modification of leukocyte distribution and inhibition of cytokine production.

Pharmacokinetics

Methylprednisolone is well absorbed after oral administration, with a bioavailability of approximately 50%. It has a volume of distribution that reflects extensive tissue binding. The drug is metabolized primarily in the liver through conjugation and reduction, and its metabolites are excreted in urine. The half-life varies based on the route of administration but is generally around 18 to 36 hours.

Adverse effects

• Increased blood pressure
• Hyperglycemia
• Weight gain
• Mood changes
• Insomnia
• Gastrointestinal disturbances
• Increased susceptibility to infections

Interactions

• methylphenidate+apraclonidine: Severe (decreases effects)
• methylthioninium chloride+bupropion: Severe (increases risk of severe hypertension)
• methylphenidate+linezolid: Severe (increases risk of elevated blood pressure)
• rasagiline+methylphenidate: Severe (increases risk of a hypertensive crisis)
• mao-inhibitors+methylphenidate: Severe (increases risk of a hypertensive crisis)
• dronedarone+methylprednisolone: Moderate (increases exposure)
• miconazole+methylprednisolone: Moderate (increases concentration)
• antifungals, azoles+methylprednisolone: Moderate (increases exposure)
• crizotinib+methylprednisolone: Moderate (increases exposure)

Precautions

• Use with caution in patients with hypertension
• Monitor blood glucose levels in diabetic patients
• Consider potential for infection risk due to immunosuppression
• Evaluate for psychiatric effects in susceptible individuals

Pregnancy

Corticosteroids may be used during pregnancy if the potential benefit justifies the risk to the fetus. Careful monitoring is advised.

Breast-feeding

Corticosteroids are excreted in breast milk; caution is advised. Monitor the infant for potential effects.

Storage

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

Formulations

• Tablets
• Injectable solutions
• Topical preparations

Mechanism of action

Methylsulphate functions as a methylating agent, transferring a methyl group to nucleophiles. This process involves the formation of a sulfonium ion, which is highly reactive and can readily react with nucleophilic sites on various substrates, leading to methylation reactions.

Pharmacodynamics

The pharmacodynamics of methylsulphate is primarily related to its role as a methylating agent in biochemical reactions. It can alter the structure and function of biological molecules, potentially affecting cellular processes and signaling pathways. However, detailed pharmacodynamic studies specific to therapeutic use are limited.

Pharmacokinetics

There is limited information on the pharmacokinetics of methylsulphate, given its typical use as a reagent in laboratory settings rather than a clinical drug. When used in chemical reactions, its reactivity and transformation into other compounds would dictate its pharmacokinetic profile, which could vary significantly based on the specific context of use.

Pregnancy

There is limited data on the use of methylsulphate in pregnancy. Consult relevant guidelines.

Breast-feeding

Data on the excretion of methylsulphate in human milk is not available. Caution is advised.

Storage

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

Indications

• Relief of symptoms associated with excessive gas in the gastrointestinal tract
• Treatment of foaming in gastrointestinal disorders

Dosage

Children: Refer to specific product guidelines or consult the BNF for Children for appropriate dosing information, as it may vary based on formulation and indication.

Adults: Refer to specific product guidelines or consult the BNF for appropriate dosing information, as it may vary based on formulation and indication.

Mechanism of action

Polysiloxane acts primarily by reducing the surface tension of liquids, which decreases the formation of bubbles or foam. This property is beneficial in formulations where excessive foam could interfere with the delivery or effectiveness of a drug. The compound's siloxane backbone provides flexibility and stability, contributing to its efficacy as an anti-foaming agent.

Pharmacodynamics

The pharmacodynamic properties of polysiloxane relate to its surface-active characteristics. By adsorbing at the air-liquid interface, it disrupts the formation of stable foam, thereby facilitating smoother administration of oral or injectable formulations. Its action is generally localized to the gastrointestinal tract when used as an anti-foaming agent, with minimal systemic effects.

Pharmacokinetics

Polysiloxane is not absorbed significantly into the systemic circulation when administered orally. It passes through the gastrointestinal tract largely unchanged, which is beneficial for its function as an anti-foaming agent. The elimination of polysiloxane occurs through fecal excretion.

Adverse effects

• Nausea
• Vomiting
• Diarrhea
• Abdominal discomfort

Precautions

• Use with caution in patients with gastrointestinal obstruction.
• Assess for allergies to silicone or related compounds.

Pregnancy

Polysiloxane is generally considered safe for use during pregnancy; however, consult a healthcare provider for personalized advice.

Breast-feeding

Polysiloxane is unlikely to affect breastfed infants; consult a healthcare provider for specific recommendations.

Storage

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

Formulations

• Oral suspension
• Chewable tablets
• Capsules

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