LILU CREAM

Indications

• Skin disinfection
• Preparation of skin before injections
• Cleansing minor wounds

Dosage

Children: Apply to the skin as required; consult product literature for specific guidance.

Adults: Apply to the skin as required for disinfection.

Mechanism of action

Alcohol exerts its antiseptic effect by denaturing proteins, disrupting cell membranes, and dehydrating microbial cells, leading to cell lysis and death.

Pharmacodynamics

Alcohol has broad-spectrum antimicrobial activity, effective against bacteria, fungi, and viruses. Its efficacy is influenced by concentration, with higher concentrations generally being more effective.

Pharmacokinetics

Alcohol is rapidly absorbed through the skin and mucous membranes. It is metabolized primarily in the liver, with a half-life that varies based on the individual's metabolic rate and the amount consumed.

Contra-indications

• Concomitant use with lithium
• Regular use in neonates
• Patients with severe burns when diathermy has been preceded by application of alcoholic skin disinfectants

Adverse effects

• Eye erythema
• Punctate keratitis
• Cytotoxicity
• Eye discolouration

Interactions

• Increases risk of visual disturbances with antiepileptics
• Increases concentration with methylphenidate
• Increases risk of facial flushing and skin irritation with topical pimecrolimus
• Increases concentration with retinoids
• Increases concentration with acitretin
• Increases risk of facial flushing and skin irritation with topical tacrolimus
• Decreases antidiuretic effect with vasopressin

Precautions

• Avoid regular application to inflamed or broken skin or mucosa
• Avoid broken skin
• Flammable

Pregnancy

Sufficient iodine may be absorbed to affect the fetal thyroid in the second and third trimester.

Breast-feeding

Avoid regular or excessive use.

Storage

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

Formulations

• Betadine 2.5% dry powder spray
• Industrial methylated spirit
• Povidone-Iodine 25 mg per 1 gram

Indications

• Food preservative
• Treatment of urea cycle disorders
• Metabolic disorders involving benzoyl-CoA

Dosage

Children: Refer to the BNF for Children for specific dosing guidelines based on condition.

Adults: Refer to the BNF for specific dosing guidelines based on condition.

Mechanism of action

Benzoate acts mainly by inhibiting the growth of bacteria and fungi through its ability to lower the pH, creating an environment that is less favorable for microbial growth. It is also involved in metabolic pathways where it helps in the conjugation of toxic substances, facilitating their excretion from the body.

Pharmacodynamics

Benzoate is known for its antimicrobial properties, which are particularly effective against a wide range of fungi and bacteria. Its efficacy as a preservative is due to its ability to penetrate microbial cell membranes and disrupt their metabolic processes. Additionally, it has been observed to modulate various metabolic pathways, particularly those associated with aromatic compound degradation.

Pharmacokinetics

After ingestion, benzoate is rapidly absorbed in the gastrointestinal tract. It is metabolized primarily in the liver, where it undergoes conjugation with glycine to form hippurate, which is then excreted in the urine. The half-life of benzoate varies depending on individual metabolic rates but is generally short due to its efficient conversion and excretion.

Pregnancy

There is limited data on the use of benzoate in pregnancy. Consultation with healthcare professionals is advised before use.

Breast-feeding

Limited data is available on the excretion of benzoate in breast milk. Caution is recommended when administering to nursing mothers.

Storage

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

Indications

• Bacterial infections
• Pneumonia
• Meningitis
• Syphilis
• Endocarditis
• Skin and soft tissue infections

Dosage

Children: Paediatric dosing for benzylpenicillin is determined by the child's weight and the severity of the infection. Refer to the BNF for Children for specific dosing guidelines.

Adults: The usual adult dose for benzylpenicillin varies based on the type and severity of the infection. It is generally administered via intramuscular or intravenous routes. For severe infections, doses may range from 1 to 4 million units every 4 to 6 hours.

Mechanism of action

Benzylpenicillin exerts its antibacterial effects by inhibiting the synthesis of bacterial cell walls. It binds to penicillin-binding proteins (PBPs) located inside the bacterial cell wall, disrupting the transpeptidation process, which is crucial for cross-linking peptidoglycan layers. This inhibition leads to cell lysis and death of the bacteria.

Pharmacodynamics

Benzylpenicillin demonstrates time-dependent bactericidal activity, meaning its effectiveness is related to the duration of time the drug concentration remains above the minimum inhibitory concentration (MIC) for the target bacteria. It has a narrow spectrum of activity, primarily targeting Gram-positive cocci and some Gram-negative rods.

Pharmacokinetics

Benzylpenicillin is typically administered parenterally due to poor oral absorption. It is rapidly distributed throughout the body and can penetrate various tissues, including the central nervous system during inflammation. The drug is primarily eliminated by renal excretion, with a half-life of approximately 30 minutes to 1 hour in healthy individuals. Dosage adjustments may be necessary in patients with renal impairment.

Interactions

• leflunomide+benzylpenicillin: Unknown (increases exposure)
• nitisinone+benzylpenicillin: Unknown (increases exposure)
• teriflunomide+benzylpenicillin: Unknown (increases exposure)

Pregnancy

Benzylpenicillin is generally considered safe to use during pregnancy, as it is a penicillin antibiotic and has a long history of use.

Breast-feeding

Benzylpenicillin is excreted in breast milk in small amounts, but it is not expected to have adverse effects on a nursing infant.

Storage

Store in a cool, dry place, protected from light. Reconstituted solutions should be used promptly or stored in a refrigerator and used within a limited time frame.

Formulations

• Benzylpenicillin injection

Dosage

Children: Refer to specific formulations and usages, as dosing can vary widely depending on the application and regulatory guidelines.

Adults: Refer to specific formulations and usages, as dosing can vary widely depending on the application and regulatory guidelines.

Mechanism of action

Butylated hydroxyanisole (BHA) and butylated hydroxytoluene (BHT) act as antioxidants by inhibiting the oxidation of lipids. They scavenge free radicals and donate hydrogen atoms to reactive species, thus stabilizing and preventing oxidative damage to cellular components. This action helps to protect the integrity of cell membranes and prevent the formation of harmful peroxides.

Pharmacodynamics

The pharmacodynamic properties of butylated compounds are primarily related to their antioxidant activity. They exhibit a dose-dependent ability to inhibit lipid peroxidation, which is crucial in protecting cells from oxidative stress. Furthermore, they may modulate certain biochemical pathways involved in cell signaling and apoptosis, although these effects are less well-characterized.

Pharmacokinetics

Butylated compounds are absorbed from the gastrointestinal tract following oral ingestion. They undergo metabolic processing primarily in the liver, where they are conjugated and excreted in urine. The half-life of butylated compounds in humans is variable, influenced by factors such as dosage and individual metabolism. Accumulation in tissues is generally low, but prolonged exposure may lead to higher tissue concentrations.

Adverse effects

• Gastrointestinal disturbances
• Allergic reactions
• Potential carcinogenic effects with prolonged exposure

Precautions

• Use with caution in patients with a history of hypersensitivity to butylated compounds
• Avoid prolonged exposure due to potential toxicity

Pregnancy

Limited data available, use only if the benefits outweigh the risks.

Breast-feeding

Unknown, exercise caution and consult a healthcare provider.

Storage

Store in a cool, dry place away from light.

Formulations

• Butylated hydroxytoluene (BHT)
• Butylated hydroxyanisole (BHA)

Indications

• Nutritional supplementation
• Antimicrobial therapy
• Ketogenic dietary applications
• Potential adjunct in metabolic disorders

Dosage

Children: For pediatric use, consult specific pediatric guidelines and literature, as no standardized dosing recommendations are available.

Adults: For general use, refer to specific guidelines on capric acid supplementation and dietary applications, as there are no standard dosing recommendations established.

Mechanism of action

Capric acid is thought to exert its effects through several mechanisms. It can be metabolized to generate energy, particularly in the liver, where it undergoes beta-oxidation. Additionally, it has been shown to have antimicrobial activity by disrupting the cell membrane of bacteria and fungi, leading to cell lysis. Capric acid may also influence lipid metabolism and insulin sensitivity, contributing to its potential benefits in metabolic conditions.

Pharmacodynamics

Capric acid demonstrates various pharmacodynamic effects, including the modulation of lipid profiles and improvement of insulin sensitivity. Its medium-chain length allows for rapid absorption and metabolism, providing a quick source of energy. The antimicrobial properties of capric acid make it effective against certain pathogens, which can be beneficial in preventing infections. Furthermore, it may have anti-inflammatory effects, potentially aiding in the management of inflammatory conditions.

Pharmacokinetics

Capric acid is absorbed efficiently in the gastrointestinal tract due to its medium-chain structure. Once absorbed, it is transported directly to the liver, where it is rapidly oxidized to produce energy. The half-life of capric acid is relatively short, and it is primarily excreted through urine and breath as carbon dioxide after metabolism. The bioavailability of capric acid is high, allowing for effective utilization by the body.

Pregnancy

There is limited information available regarding the safety of capric in pregnancy. Consult a healthcare provider for advice.

Breast-feeding

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

Storage

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

Indications

• Nutritional supplementation
• Potential neuroprotective agent
• Anti-inflammatory applications

Dosage

Children: Refer to BNF for Children for specific pediatric dosing information.

Adults: Refer to BNF for specific dosage information, as caprylic acid is often used in dietary supplements and the appropriate dosage may vary based on formulation and indication.

Mechanism of action

Caprylic acid induces neuronal differentiation in PC12 cells, a model for studying nerve growth factors. It has been shown to promote the growth of neurite processes in these cells, particularly in the presence of inducers. The fatty acid also influences interleukin-8 production in human intestinal epithelial cells, suggesting a role in modulating inflammatory responses.

Pharmacodynamics

As a medium-chain fatty acid, caprylic acid is rapidly absorbed and metabolized in the body. It is utilized for energy production and has a role in various metabolic pathways, including fatty acid oxidation and biosynthesis. Its effects on neuronal differentiation indicate potential neuroprotective properties, while its ability to modulate inflammatory cytokines highlights its anti-inflammatory potential.

Pharmacokinetics

Caprylic acid is absorbed in the gastrointestinal tract and transported directly to the liver, where it undergoes rapid metabolism. The short chain length allows for efficient absorption and utilization as an energy source. Its pharmacokinetic profile supports its quick action compared to long-chain fatty acids, which require more complex digestion and transport mechanisms.

Pregnancy

There are no well-controlled studies of caprylic acid in pregnant women. Use only if clearly needed.

Breast-feeding

Caprylic acid is likely safe during breastfeeding; however, consult a healthcare provider.

Storage

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

Formulations

• Capsules
• Liquid

Indications

• Electrolyte replacement
• Volume expansion in hypovolemic patients
• Management of hyponatremia
• Support in intravenous fluid therapy

Dosage

Children: Refer to the BNF for Children for appropriate dosing in paediatric patients, as dosages may vary based on the formulation and clinical condition.

Adults: Refer to specific product information or clinical guidelines for dosage recommendations, as disodium is often part of combination products.

Mechanism of action

Disodium compounds often function by providing sodium ions that are essential for various physiological processes. Sodium ions play a critical role in maintaining osmotic balance, nerve impulse transmission, and muscle contraction. In the context of intravenous solutions, disodium helps to restore electrolyte balance in patients.

Pharmacodynamics

The pharmacodynamics of disodium is primarily related to its role in electrolyte balance and fluid homeostasis. Sodium ions are vital for the function of excitable tissues, including neurons and muscle cells. Changes in sodium levels can affect blood pressure, hydration status, and overall cellular function.

Pharmacokinetics

The pharmacokinetics of disodium compounds depend on their specific formulation and route of administration. When administered intravenously, disodium is rapidly distributed in the extracellular fluid, where it helps to maintain osmotic pressure. Sodium is primarily excreted by the kidneys, and its levels can be influenced by fluid intake, dietary sodium, and renal function.

Pregnancy

Use with caution. Consult a healthcare provider for specific guidance.

Breast-feeding

Use with caution. Consult a healthcare provider for specific guidance.

Storage

Store at room temperature, away from moisture and direct sunlight.

Indications

• Lead poisoning
• Mercury poisoning
• Calcium overload
• Certain diagnostic procedures involving heavy metals

Dosage

Children: Refer to the BNF for Children for appropriate dosing information tailored for paediatric patients.

Adults: Refer to the BNF for specific dosing guidelines based on the condition being treated, considering factors such as the severity of metal poisoning and renal function.

Mechanism of action

Edetate functions by forming stable complexes with divalent and trivalent metal ions, including lead and calcium, through its multiple carboxylate and amine groups. This chelation renders the metals more soluble and promotes their renal excretion, thereby reducing their toxic effects in the body.

Pharmacodynamics

The chelation of metals by edetate decreases the free metal concentration in the bloodstream, which mitigates the toxic effects associated with heavy metal accumulation. The efficacy of edetate in removing metals such as lead has been well documented, and its ability to bind calcium can influence calcium homeostasis in certain clinical scenarios.

Pharmacokinetics

Edetate is administered intravenously, with rapid distribution throughout the extracellular fluid. It is primarily excreted unchanged by the kidneys. The onset of action occurs quickly after administration, and the duration depends on the dose and the patient's renal function. The elimination half-life is approximately 1 hour but may vary based on renal clearance.

Contra-indications

• Hypersensitivity to edetate or any component of the formulation
• Severe renal impairment
• Active bleeding disorders

Adverse effects

• Hypocalcemia
• Nausea
• Vomiting
• Diarrhea
• Abdominal pain
• Headache
• Rash
• Fever

Interactions

• May enhance the effects of anticoagulants
• Concurrent use with calcium supplements may reduce effectiveness
• May interfere with the absorption of certain medications due to changes in gastrointestinal motility

Precautions

• Use with caution in patients with renal impairment
• Monitor electrolyte levels, particularly calcium, during treatment
• Assess the patient's hydration status before administration

Pregnancy

Limited data on the use of edetate in pregnancy. Use only if the potential benefit justifies the potential risk to the fetus.

Breast-feeding

Caution is advised as it is not known whether edetate is excreted in human milk. Weigh the risks and benefits before use.

Storage

Store in a cool, dry place, protected from light. Do not freeze.

Formulations

• Edetate disodium injection
• Edetate calcium disodium injection

Dosage

Children: Refer to the BNF for Children for appropriate dosing information in paediatric cases, especially in instances of overdose.

Adults: Refer to the BNF for specific dosing information based on clinical circumstances, particularly in cases of overdose.

Mechanism of action

Ethylene glycol is metabolized by alcohol dehydrogenase to glycoaldehyde, which is subsequently converted to glycolic, glyoxylic, and oxalic acids. These metabolites contribute to anion gap metabolic acidosis and are responsible for tissue injury through the formation of insoluble calcium oxalate crystals.

Pharmacodynamics

The toxicity of ethylene glycol arises from its metabolites, particularly glycolic and oxalic acids. These compounds induce metabolic acidosis, lead to renal failure through calcium oxalate crystal deposition in the kidneys, and can cause neurological impairment. The anion gap increases due to the accumulation of these acids, leading to complications such as cardiovascular instability and potential multi-organ failure.

Pharmacokinetics

Ethylene glycol is rapidly absorbed after oral ingestion. It undergoes first-pass metabolism primarily in the liver, where it is converted into its toxic metabolites. The elimination half-life of ethylene glycol varies but is generally prolonged in cases of renal impairment. Renal excretion of metabolites contributes to the duration of toxicity, necessitating prompt medical intervention in cases of overdose.

Adverse effects

• Metabolic acidosis
• Renal failure
• CNS depression
• Hypocalcemia
• Cardiovascular collapse
• Pulmonary edema

Precautions

• Use with caution in patients with renal impairment
• Monitor for signs of metabolic acidosis
• Evaluate electrolyte levels, particularly calcium

Pregnancy

There is limited data on the safety of ethylene glycol in pregnancy. It should only be used if clearly needed.

Breast-feeding

It is unknown if ethylene glycol is excreted in human milk. Caution is advised.

Storage

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

Formulations

• Liquid

Indications

• Anxiety disorders
• Nausea and vomiting
• Allergic conditions
• Preoperative sedation
• Pruritus

Dosage

Children: Refer to the BNF for Children for appropriate dosing recommendations based on age and weight.

Adults: Refer to the BNF for specific dosing guidelines based on the indication and patient characteristics.

Mechanism of action

Hydroxyzine works by antagonizing the H1 histamine receptors, leading to a reduction in the effects of histamine in the body. This action helps alleviate symptoms of allergic reactions and promotes sedation. Additionally, it may exert effects on serotonin and adrenergic receptors, which could contribute to its anxiolytic properties. Hydroxyzine is also involved in various metabolic pathways, including selenium metabolism and the degradation of reactive oxygen species.

Pharmacodynamics

The pharmacodynamic effects of hydroxyzine include sedation, anxiolysis, and reduction of allergic symptoms. Its sedative effects can make it useful in managing anxiety and inducing sleep, while its antihistaminic properties help to relieve symptoms such as itching and rashes associated with allergic reactions. The onset of action is typically within 15 to 30 minutes when taken orally, with peak effects occurring within 1 to 2 hours.

Pharmacokinetics

Hydroxyzine is well absorbed from the gastrointestinal tract, with peak plasma concentrations occurring approximately 2 hours after oral administration. It is extensively metabolized in the liver, with metabolites, including cetirizine, possessing their own therapeutic effects. Hydroxyzine has a half-life of approximately 20 hours, allowing for once or twice daily dosing. It is primarily excreted in the urine, with less than 1% of the unchanged drug found in urine.

Interactions

• hydroxyzine+antiepileptics: Severe (increases risk of overheating and dehydration)
• hydroxyzine+zonisamide: Severe (increases risk of overheating and dehydration)
• hydroxychloroquine+penicillamine: Severe (increases risk of haematological toxicity)
• hydroxychloroquine+agalsidase alfa: Unknown (decreases effects)
• hydroxychloroquine+agalsidase beta: Unknown (decreases exposure)
• hydroxychloroquine+oral cholera vaccine: Unknown (decreases efficacy)
• live vaccines+hydroxy carbamide: Unknown (increases risk of generalised infection (possibly life-threatening))
• lanthanum+hydroxychloroquine: Unknown (decreases absorption)
• macrolides+hydroxychloroquine: Unknown (increases risk of serious cardiovascular adverse effects)
• hydroxychloroquine+remdesivir: Unknown (decreases effects)

Pregnancy

Safety in pregnancy has not been established. Use only if the potential benefit justifies the potential risk to the fetus.

Breast-feeding

Use with caution. Hydroxychloroquine is excreted in breast milk, and effects on the infant are unknown.

Storage

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

Formulations

• Tablets
• Oral solution

Indications

• Head lice infestation
• Body lice infestation
• Scabies

Dosage

Children: Refer to BNF for Children for specific dosing information.

Adults: Refer to BNF for specific dosing information.

Mechanism of action

Benzyl alcohol, a component of hydroxytoluene, inhibits lice from closing their respiratory spiracles. This action allows the vehicle to obstruct the spiracles, leading to asphyxiation of the lice.

Pharmacodynamics

The pharmacodynamics of hydroxytoluene involves its local anesthetic properties and its ability to disrupt the respiratory function of certain parasites. It exerts its effects primarily on ectoparasites like lice, leading to their death through suffocation. Its effectiveness is facilitated by its lipophilicity, which allows it to penetrate the cuticle of the lice and interfere with their respiratory system.

Pharmacokinetics

Hydroxytoluene is absorbed through the skin when applied topically. Its pharmacokinetic profile is influenced by its formulation, with variations in absorption rates based on the vehicle used. Once absorbed, it undergoes metabolic processes primarily in the liver, where it may be conjugated and excreted in urine. The elimination half-life and specific metabolic pathways are not well defined, requiring further research for comprehensive understanding.

Pregnancy

Hydroxytoluene should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus.

Breast-feeding

Caution is advised when administering hydroxytoluene during breastfeeding due to limited data on its excretion in human milk.

Storage

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

Indications

• Antiseptic for skin disinfection
• Solvent in pharmaceutical formulations
• Cleaning agent in laboratories and healthcare settings

Dosage

Children: For pediatric use, consult specific guidelines in the BNF for Children, as dosing may vary based on age, weight, and clinical circumstances.

Adults: For skin antisepsis, apply isopropyl alcohol topically in a concentration of 70% to the affected area. Dosage may vary based on clinical indication and setting.

Mechanism of action

Isopropyl alcohol works primarily as an antiseptic by denaturing proteins and disrupting cell membranes of bacteria, viruses, and fungi, leading to cell lysis and death. Its efficacy is enhanced by the presence of water, which facilitates the penetration of the alcohol into microbial cells.

Pharmacodynamics

Isopropyl alcohol exhibits a rapid onset of action against a variety of pathogens, including gram-positive and gram-negative bacteria, fungi, and some viruses. Its antimicrobial activity is concentration-dependent, with higher concentrations generally providing a broader spectrum of activity. It is commonly used in concentrations ranging from 60% to 90%, with 70% being optimal for disinfection due to its ability to penetrate the cell wall effectively.

Pharmacokinetics

Isopropyl alcohol is readily absorbed through the skin and mucous membranes. After absorption, it is metabolized primarily in the liver to acetone, which is then further metabolized and excreted, mostly via urine. The elimination half-life of isopropyl alcohol varies but is typically around 2 to 3 hours. Its effects can be influenced by factors such as dosage, route of exposure, and individual metabolic differences.

Pregnancy

Isopropyl alcohol should be used with caution during pregnancy. It is a category C drug, indicating that risk cannot be ruled out.

Breast-feeding

Caution is advised when using isopropyl alcohol during breastfeeding, as it is not known if it is excreted in human milk.

Storage

Isopropyl alcohol should be stored at room temperature, away from heat and flame. Keep the container tightly closed and in a well-ventilated area.

Formulations

• Isopropyl alcohol 70% solution
• Isopropyl alcohol 99% solution

Indications

• Tinea corporis
• Tinea cruris
• Tinea pedis
• Dermatophyte infections

Dosage

Children: Refer to the BNF for Children for specific dosing recommendations for pediatric patients.

Adults: Apply a thin layer of luliconazole to the affected area once daily for a duration of 1 to 2 weeks, depending on the specific infection being treated.

Mechanism of action

The exact mechanism of action for luliconazole's antifungal activity is not fully understood, but it is believed to inhibit the enzyme lanosterol demethylase. This enzyme is essential for the synthesis of ergosterol, which is a critical component of fungal cell membranes. By inhibiting this enzyme, luliconazole disrupts the integrity of the fungal cell membrane, leading to cell death.

Pharmacodynamics

Luliconazole demonstrates fungicidal activity against organisms like Trichophyton rubrum and Epidermophyton floccosum. Its action is thought to be primarily through the alteration of fungal cell membranes, which compromises the structure and function of the fungi, ultimately leading to their death.

Pharmacokinetics

Luliconazole is administered topically, which limits its systemic absorption. The pharmacokinetics of luliconazole involve localized action at the site of application, minimizing the risk of systemic side effects. Due to its topical formulation, specific pharmacokinetic parameters such as absorption, distribution, metabolism, and excretion in humans are not extensively detailed in the literature.

Adverse effects

• Application site reactions
• Burning sensation
• Itching
• Erythema

Precautions

• Avoid contact with eyes
• Do not apply to broken skin

Pregnancy

Luliconazole should only be used in pregnancy if the potential benefit justifies the potential risk to the fetus.

Breast-feeding

Caution should be exercised when luliconazole is administered to nursing mothers.

Storage

Store at room temperature, away from moisture and heat.

Formulations

• Topical cream

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

• Acute pain
• Chronic pain
• Inflammatory conditions
• Osteoarthritis
• Rheumatoid arthritis
• Postoperative pain

Dosage

Children: Refer to specific pediatric dosing guidelines as established in authoritative references, ensuring consideration of the child's age, weight, and clinical condition.

Adults: Refer to specific prescribing guidelines or clinical protocols for adult dosing, as it may vary based on the condition being treated and the formulation used.

Mechanism of action

Myristrate acts by inhibiting cyclooxygenase (COX) enzymes, leading to a decrease in the production of prostaglandins. This results in reduced inflammation and pain. The drug may also exert effects on peripheral pain receptors, further contributing to its analgesic properties.

Pharmacodynamics

The pharmacodynamics of myristrate involve its ability to modulate inflammatory pathways and pain signaling. By inhibiting COX enzymes, myristrate decreases the synthesis of pro-inflammatory mediators, leading to a reduction in the clinical manifestations of pain and inflammation. The onset of analgesic effects can occur within a few hours of administration, with peak effects typically seen within several hours.

Pharmacokinetics

Myristrate is generally well absorbed following oral administration, with peak plasma concentrations occurring within 1 to 2 hours. The drug is metabolized primarily in the liver, with various metabolic pathways contributing to its clearance from the body. Its elimination half-life can vary, but it is typically in the range of several hours. Excretion occurs mainly through the urine, with both unchanged drug and metabolites being eliminated.

Pregnancy

There is limited information on the use of myristrate in pregnancy. It is advisable to use caution and consult a healthcare professional before use.

Breast-feeding

Myristrate should be used cautiously during breastfeeding, as its effects on a nursing infant are not well-studied.

Storage

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

Indications

• HIV-1 infection
• Prevention of mother-to-child transmission of HIV

Dosage

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

Adults: Refer to the BNF for specific dosing guidelines based on individual patient circumstances and treatment regimens.

Mechanism of action

Nevirapine works by binding to the reverse transcriptase enzyme, which is crucial for the replication of HIV. By binding to this enzyme, Nevirapine inhibits its function, thereby preventing the conversion of viral RNA into DNA. This action disrupts the HIV replication cycle and reduces the viral load in the body.

Pharmacodynamics

The pharmacodynamic effects of Nevirapine include a decrease in viral load, which is measured by the reduction in the number of HIV RNA copies in the blood. Nevirapine is known for its rapid onset of action and is effective in lowering viral load within a few weeks of initiation. However, resistance can develop if the drug is used alone, hence it is typically used in combination with other antiretroviral agents.

Pharmacokinetics

Nevirapine is well-absorbed after oral administration, with peak plasma concentrations occurring within 4 hours. It has a half-life of approximately 25-30 hours, allowing for once-daily dosing in extended-release formulations. Nevirapine is extensively metabolized in the liver through cytochrome P450 enzymes, primarily CYP3A4, and is eliminated mainly through urine and feces. Its pharmacokinetic profile may be affected by other drugs that induce or inhibit CYP450 enzymes.

Pregnancy

The safety of Nevia during pregnancy has not been established. Use only if the potential benefit justifies the potential risk to the fetus.

Breast-feeding

Caution is advised when using Nevia during breastfeeding. The effects on the nursing infant are unknown.

Storage

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

Indications

• Dry skin
• Atopic dermatitis
• Eczema
• Psoriasis
• Cosmetic skin formulations

Dosage

Children: Refer to specific product guidelines and BNF for Children for pediatric dosing recommendations.

Adults: Olivem is typically used in concentrations ranging from 1% to 10% in topical formulations. Specific dosing depends on the product and condition being treated.

Mechanism of action

Olivem functions by forming a barrier on the skin's surface, which helps to retain moisture and improve the skin's overall hydration. The ingredients in Olivem can also enhance the penetration of other active ingredients in formulations, promoting better absorption and efficacy.

Pharmacodynamics

Olivem demonstrates emollient properties, which help soften and smooth the skin. It may also exhibit anti-inflammatory effects, reducing skin irritation and promoting skin health. The fatty acid content provides nourishment to the skin, supporting its natural barrier function.

Pharmacokinetics

Olivem is applied topically and is designed to act locally at the site of application. Its absorption through the skin can vary depending on the formulation and concentration used. Systemic absorption is minimal, reducing the risk of systemic side effects.

Pregnancy

Olivem is not extensively studied in pregnancy. Caution is advised when administering this drug to pregnant individuals.

Breast-feeding

Limited data available. Caution is advised when administering this drug during breastfeeding.

Storage

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

Indications

• Personal fragrance enhancement
• Mood enhancement
• Social interaction
• Cosmetic use

Dosage

Children: Perfume is not typically recommended for use in children due to the potential for skin irritation and allergic reactions. Refer to guidelines for specific products.

Adults: Perfume is applied as desired, typically in small amounts to pulse points such as the wrists, neck, or behind the ears.

Mechanism of action

The mechanism of action of perfume involves the interaction of volatile aromatic compounds with olfactory receptors in the nasal cavity. These receptors send signals to the brain, which interprets the scent, triggering emotional and physiological responses. Perfumes can influence mood, evoke memories, and enhance social interactions by engaging the limbic system, which is involved in emotion and memory.

Pharmacodynamics

Perfume does not have pharmacodynamic effects in the traditional sense as medicinal drugs do. However, certain components may have mild effects on mood and emotional well-being by stimulating the olfactory system. Essential oils present in some perfumes may also have mild antidepressant or relaxing properties, although these effects are not clinically significant.

Pharmacokinetics

Perfume is primarily applied topically to the skin or clothing, where it evaporates and releases fragrance into the air. The compounds in perfume can be absorbed through the skin, but systemic absorption is generally low. The duration and intensity of fragrance depend on the volatility of the components used and their concentration. The scent usually lasts from a few hours to a day, depending on the formulation and individual skin chemistry.

Adverse effects

• Skin irritation
• Allergic reactions
• Headaches
• Respiratory issues
• Nausea

Precautions

• Use with caution in individuals with sensitive skin or allergies
• Avoid direct contact with eyes
• Use in well-ventilated areas to prevent respiratory irritation

Pregnancy

Generally regarded as safe in pregnancy, but some fragrances may cause allergic reactions or sensitivities.

Breast-feeding

Generally considered safe, but individual fragrances should be assessed for potential allergens.

Storage

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

Formulations

• Eau de parfum
• Eau de toilette
• Cologne
• Perfume oil
• Body spray

Indications

• Hyperthyroidism
• Graves' disease
• Thyroid storm

Dosage

Children: Refer to the BNF

Adults: The usual initial dose of propylthiouracil in adults is 300 mg per day, divided into 3 doses. The maintenance dose is typically 100-150 mg per day, adjusted based on thyroid function tests.

Mechanism of action

Propylthiouracil acts by inhibiting the enzyme thyroid peroxidase, which is involved in the iodination of tyrosine residues in thyroglobulin, a precursor of thyroid hormones. By blocking this enzyme, PTU reduces the production of thyroxine (T4) and triiodothyronine (T3), leading to decreased thyroid hormone levels in circulation. Additionally, PTU inhibits the conversion of T4 to T3 in peripheral tissues, further contributing to its antithyroid effects.

Pharmacodynamics

The pharmacodynamic effects of propylthiouracil are primarily centered around its ability to lower thyroid hormone levels, which helps alleviate symptoms of hyperthyroidism such as increased heart rate, weight loss, and anxiety. The onset of action can vary, but therapeutic effects may be observed within several weeks of initiation. Monitoring thyroid function tests is essential to assess the efficacy and adjust dosing as needed.

Pharmacokinetics

Propylthiouracil is well absorbed from the gastrointestinal tract, though its bioavailability can be affected by factors such as food intake. The drug is extensively metabolized in the liver, and its elimination half-life averages around 1-2 hours. Most of the drug is excreted in urine as metabolites. It is important to note that due to its rapid metabolism, multiple daily doses may be required to maintain therapeutic levels.

Interactions

• propylthiouracil+metyrapone: Severe (decreases effects)

Indications

• Plant growth regulation
• Agricultural applications as a growth inhibitor

Dosage

Children: Not applicable.

Adults: Refer to the relevant agricultural guidelines for specific applications.

Mechanism of action

In an in vitro study, propylene acts as a plant growth inhibitor by inhibiting the oxidation of indole-3-acetic acid by peroxidase in the presence of superoxide anion radicals. This inhibition is linked to the activation of an iron complex (compound III) shuttle, which enhances the reaction rate between superoxide and peroxidase, ultimately affecting plant growth processes. Propylene is a less effective inhibitor compared to ethylene.

Pharmacodynamics

The pharmacodynamic effects of propylene are primarily observed in its role as a growth inhibitor in plants. By modulating the oxidation of phytohormones like indole-3-acetic acid, propylene can influence various growth responses in plants, potentially affecting processes such as cell elongation and division.

Pharmacokinetics

Information on the pharmacokinetics of propylene in humans is not well-documented, as its primary uses are industrial and agricultural. Its metabolism may be influenced by environmental factors, and its effects are primarily studied in the context of plant biology rather than human pharmacology.

Dosage

Children: Refer to specific drug formulations and product labels as purified substances can vary widely in their use and dosing.

Adults: Refer to specific drug formulations and product labels as purified substances can vary widely in their use and dosing.

Mechanism of action

The mechanism of action for purified compounds varies widely depending on the specific substance. Generally, purified drugs exert their effects by interacting with specific biological targets, such as receptors, enzymes, or ion channels, leading to a desired therapeutic effect. This interaction can involve binding to receptors to activate or inhibit signaling pathways, modulating enzymatic activity, or altering physiological processes.

Pharmacodynamics

Pharmacodynamics describes the effects of a drug on the body and the relationship between drug concentration and effect. For purified drugs, this can involve dose-response relationships and the time course of their action. The purified form often enhances potency and reduces variability in response among patients, which can lead to more predictable therapeutic outcomes. The overall effect is determined by the drug's affinity for its target, the efficacy of the drug-receptor interaction, and the downstream signaling pathways activated as a result of this interaction.

Pharmacokinetics

Pharmacokinetics involves the absorption, distribution, metabolism, and excretion (ADME) of a drug. For purified substances, absorption can be more efficient due to the absence of impurities that may affect solubility or stability. Distribution may also be enhanced, leading to higher bioavailability. Metabolism can be influenced by the structure of the purified compound, as it may be metabolized more readily by liver enzymes. Excretion typically occurs through the kidneys or liver, depending on the molecular characteristics of the purified drug.

Pregnancy

Consult with a healthcare professional, as the safety of purified forms of medications during pregnancy may vary depending on the specific substance.

Breast-feeding

Consult with a healthcare professional, as the safety of purified forms of medications during breastfeeding may vary depending on the specific substance.

Storage

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

Indications

• Phenylketonuria (PKU)
• Dopamine deficiency syndromes
• Serotonin deficiency
• Congenital disorders of biopterin metabolism

Dosage

Children: Refer to specific clinical guidelines and literature for appropriate dosing, as it may vary based on the condition being treated.

Adults: Refer to specific clinical guidelines and literature for appropriate dosing, as it may vary based on the condition being treated.

Mechanism of action

Sepi acts by being converted into tetrahydrobiopterin, which is crucial for the activity of several enzymes involved in the biosynthesis of neurotransmitters. Its action enhances the production of these neurotransmitters, thereby influencing mood, cognitive function, and cardiovascular regulation.

Pharmacodynamics

The pharmacodynamics of sepi are linked to its role as a cofactor for aromatic L-amino acid hydroxylases. By facilitating the conversion of phenylalanine to tyrosine and tryptophan to serotonin, sepi contributes to increased levels of neurotransmitters, which can lead to improved mood and cognitive function. Additionally, it may have a role in modulating nitric oxide production, influencing vascular tone and blood pressure.

Pharmacokinetics

Sepi is absorbed following oral administration, with peak plasma concentrations occurring within a few hours. It is subject to metabolism primarily in the liver, where it is converted into tetrahydrobiopterin. The elimination half-life of sepi has not been extensively characterized, but it is believed to be relatively short. Renal excretion plays a significant role in eliminating the compound and its metabolites from the body.

Pregnancy

Safety during pregnancy has not been established. Consult relevant guidelines and consider risk versus benefit.

Breast-feeding

It is not known whether sepi is excreted in human milk. Caution is advised.

Storage

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

Indications

• Transdermal drug delivery systems
• Formulations for poorly soluble drugs
• Topical applications requiring enhanced absorption

Dosage

Children: Refer to specific product guidelines and formulation details as dosing can vary based on the active ingredient and formulation.

Adults: Refer to specific product guidelines and formulation details as dosing can vary based on the active ingredient and formulation.

Mechanism of action

Transcutol P enhances skin permeability by altering the lipid structure of the stratum corneum, which is the outermost layer of the skin. It disrupts the lipid bilayer, allowing larger molecules to pass through more easily. This mechanism increases the absorption of active pharmaceutical ingredients when used in formulations intended for transdermal delivery.

Pharmacodynamics

Transcutol P acts as a skin penetration enhancer, increasing the flux of drugs across the skin barrier. Its efficacy is influenced by factors such as concentration, molecular weight of the drug, and the formulation's overall composition. It is particularly useful for drugs that have low skin permeability, thereby enhancing their therapeutic efficacy when delivered transdermally.

Pharmacokinetics

Transcutol P has a low systemic absorption profile, typically remaining localized at the application site. When used as an excipient, it does not significantly alter the pharmacokinetics of the active ingredient, but it may enhance the bioavailability of drugs that are otherwise poorly absorbed through the skin. The exact pharmacokinetic parameters can vary based on the specific formulation and the drug it is combined with.

Pregnancy

Transcutol P is not recommended during pregnancy due to a lack of sufficient safety data.

Breast-feeding

Caution is advised when using Transcutol P while breastfeeding, as it is unknown if it passes into breast milk.

Storage

Store at room temperature, away from light and moisture.

Formulations

• Transcutol P solution

Indications

• Hypertriglyceridemia
• Metabolic syndrome
• Cardiovascular disease risk assessment

Dosage

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

Adults: Refer to specific guidelines for management of hypertriglyceridemia, including lifestyle modifications and pharmacotherapy as needed.

Mechanism of action

Triglycerides are primarily utilized by the body for energy. They are broken down by lipases into free fatty acids and glycerol, which can then be used for energy production through beta-oxidation in the mitochondria of cells.

Pharmacodynamics

Triglyceride levels in the blood can be influenced by dietary intake, hormonal regulation, and various metabolic pathways. High levels may lead to adverse effects such as atherosclerosis and pancreatitis. The body regulates triglyceride levels through a balance of synthesis in the liver and uptake by peripheral tissues.

Pharmacokinetics

Triglycerides are absorbed from the diet and transported in the bloodstream within lipoproteins. They are metabolized primarily by lipoprotein lipase, which hydrolyzes triglycerides into free fatty acids. The elimination half-life varies depending on the metabolic state and is influenced by factors such as insulin sensitivity and overall lipid metabolism.

Pregnancy

There is limited information on the effects of triglycerides during pregnancy. It is important to consult with a healthcare professional.

Breast-feeding

Consult healthcare provider for advice regarding triglyceride levels and breastfeeding.

Storage

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

Indications

• Used as a thickening agent in food products
• Utilized in pharmaceutical formulations as a stabilizer
• Employed in cosmetics for texture improvement
• Applied in industrial products for its viscosity properties

Dosage

Children: Refer to specific product guidelines for appropriate use. Xanthan is used in formulations as a thickener or stabilizer, and dosage should be evaluated based on the specific product and formulation.

Adults: Refer to specific product guidelines for appropriate use. Xanthan is typically used in small quantities as a thickener or stabilizer in food and pharmaceutical products.

Mechanism of action

Xanthan functions primarily as a thickener and stabilizer. It acts by interacting with water molecules to form a gel-like consistency, which enhances the texture and stability of products. Its unique rheological properties allow it to maintain viscosity under varying conditions, which is beneficial in food and pharmaceutical applications.

Pharmacodynamics

Xanthan's action is primarily physical rather than pharmacological. It does not exert a direct therapeutic effect but influences the delivery and stability of active ingredients in formulations. The gel formation and viscosity changes help ensure the uniform distribution of substances in liquid formulations, which can improve the effectiveness of the drug delivery.

Pharmacokinetics

As xanthan is a polysaccharide, it is not absorbed in the gastrointestinal tract when ingested. It passes through the digestive system largely unchanged. In terms of metabolism, xanthan is broken down by colonic bacteria, resulting in short-chain fatty acids. Its pharmacokinetic profile indicates that it has a low bioavailability due to its large molecular size and structure.

Pregnancy

There is insufficient data on the use of xanthan during pregnancy. Consult a healthcare professional before use.

Breast-feeding

There is insufficient data on the excretion of xanthan in human milk. Consult a healthcare professional before use.

Storage

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

Formulations

• Xanthan gum powder

Mechanism of action

Ethanol affects the brain’s neurons in several ways. It alters their membranes as well as their ion channels, enzymes, and receptors. Alcohol also binds directly to the receptors for acetylcholine, serotonin, GABA, and the NMDA receptors for glutamate. The sedative effects of ethanol are mediated through binding to GABA receptors and glycine receptors (alpha 1 and alpha 2 subunits). It also inhibits NMDA receptor functioning. In its role as an anti-infective, ethanol acts as an osmolyte or dehydrating agent that disrupts the osmotic balance across cell membranes. ... Ethanol is known to affect a large number of membrane proteins that participate in signaling pathways such as neurotransmitter receptors, enzymes, and ion channels, and there is extensive evidence that ethanol interacts with a variety of neurotransmitters. The major actions of ethanol involve enhancing the inhibitory effects of gamma-aminobutyric acid (GABA) at GABAa receptors and blockade of the N-methyl-D-aspartate (NMDA) subtype of glutamate, an excitatory amine acid (EAA) receptor. Animal studies indicate that the acute effects of ethanol result from competitive inhibition of glycine binding to NMDA receptor and disruption of glutamatergic neurotransmission by inhibiting the response of the NMDA receptor. Persistent glycine antagonism and attenuation of glutamatergic neurotransmission by chronic ethanol exposure results in tolerance to ethanol by enhancing EAA neurotransmission and NMDA receptor upregulation. The latter appears to involve selective increases in NMDA R2B subunit concentrations and other molecular changes in specific brain loci. The abrupt withdrawal of ethanol thus produces a hyperexcitable state that leads to the ethanol withdrawal syndrome and excitotoxic neuronal death. GABA-mediated inhibition, which normally acts to limit excitation, is eliminated during ethanol withdrawal syndrome and further intensifies this excitation. In addition, NMDA receptors function to inhibit the release of dopamine in the nucleus accumbens and mesolimbic structures, which modulate the reinforcing action of addictive xenobiotics such as ethanol. By inhibiting NMDA receptor activity, ethanol could increase dopamine release from the nucleus accumbens and ventral tegmental area and could thus create dependence. Chronic ethanol administration also results in tolerance, dependence, and an ethanol withdrawal syndrome, mediated, in part, by desensitization and or downregulation of GABAa receptors. The development of alcoholic ketoacidosis (AKA) requires that a combination of physical and physiologic events occur. The normal response to starvation and depletion of hepatic glycogen stores is for amino acids to be converted to pyruvate. Pyruvate can serve as a substrate for gluconeogenesis, be converted to acetyl-CoA, which can enter the Krebs cycle or can be utilized in various biosynthetic pathways (eg, fatty acid, ketone bodies, cholesterol, and acetylcholine) ... Ethanol metabolism generates NADH, resulting in an excess of reducing potential. This high redox state favors the conversion of pyruvate to lactate, diverting pyruvate from being a substrate for gluconeogenesis. To compensate for the lack of normal metabolic substrates, the body mobilizes fat from adipose tissue and increased fatty acid metabolism as an alternative source of energy. This response is mediated by a decrease in insulin and an increased secretion of glucagon, catecholamines, growth hormone, and cortisol. Fatty acid metabolism results in the formation of acetyl-CoA and it combines with the excess acetate that is generated from ethanol metabolism to form acetoacetate. Most of the acetoacetate is reduced to beta-hydroxybutyrate due to the excess reducing potential or high redox state of the cell. Volume depletion interferes with the renal elimination of acetoacetate and beta-hydroxybutyrate, and contributes to the acidosis. An elevated lactate concentration may result from shunting from pyruvate or

Pharmacodynamics

Alcohol produces injury to cells by dehydration and precipitation of the cytoplasm or protoplasm. This accounts for its bacteriocidal and antifungal action. When alcohol is injected in close proximity to nerve tissues, it produces neuritis and nerve degeneration (neurolysis). Ninety to 98% of ethanol that enters the body is completely oxidized. Ethanol is also used as a cosolvent to dissolve many insoluble drugs and to serve as a mild sedative in some medicinal formulations. Ethanol also binds to GABA, glycine, NMDA receptors and modulates their effects. Ethanol is also metabolised by the hepatic enzyme alcohol dehydrogenase.

Mechanism of action

It has been shown that polyunsaturated fatty acids such as arachidonic and docosahexanoic acids but not monounsaturated and saturated long-chain fatty acids promote basal and nerve growth factor (NGF)-induced neurite extension of PC12 cells, a line derived from a rat pheochromocytoma. On the other hand, short-chain fatty acids and valproic acid (2-propylpentanoic acid) enhance the growth of neurite processes of the cells only in the presence of inducers. In this study, /investigators/ demonstrated that straight medium-chain fatty acids (MCFAs) at millimolar concentrations alone potently induced neuronal differentiation of PC12 cells. ... Nonanoic, decanoic, and dodecanoic acids also induced growth of neurite processes, but their maximal effects were less marked than that of octanoic acid. ... ... the effect of fatty acids on interleukin (IL)-8 production in a human intestinal epithelial cell line (Caco-2) /was investigated/. The cells were cultured as monolayers on microporous membranes in culture inserts. Oleic acid (OA), capric acid (CA), docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) were applied to the apical compartment of Caco-2 cell monolayers. The concentration of IL-8 in the basolateral medium was measured by using enzyme-linked immunosorbent assay, and the expression of IL-8 mRNA was measured by using competitive reverse transcription--polymerase chain reaction. Protein kinase C inhibitors (GF109203X and calphostin C) and H-7 (a protein kinase inhibitor) were used to study the mechanisms by which IL-8 production is stimulated. Both OA and CA enhanced IL-8 production (approximately fivefold), whereas DHA and EPA did not. Both OA and CA also enhanced IL-1-induced IL-8 production. The onset of OA-induced IL-8 production was delayed compared with that of CA-induced IL-8 production. Both OA and CA enhanced IL-8 mRNA expression (approximately fivefold) after 6 and 3 hr, respectively. The protein kinase inhibitor (H-7) reduced both OA- and CA-induced IL-8 production by 88.0 and 85.9%, respectively. The protein kinase C inhibitors (GF109203X and calphostin C) reduced OA-induced IL-8 production by 29.3 and 54.5%, respectively, but showed no effect on CA-induced IL-8 production. These findings suggest that not only OA but also CA stimulates IL-8 production in intestinal epithelial cells, and the mechanisms of action differ between OA and CA.

Mechanism of action

Ethylene glycol is metabolized by alcohol dehydrogenase to glycoaldehyde, which is then metabolized to glycolic, glyoxylic, and oxalic acids. These acids, along with excess lactic acid are responsible for the anion gap metabolic acidosis. Oxalic acid readily precipitates with calcium to form insoluble calcium oxalate crystals. Tissue injury is caused by widespread deposition of oxalate crystals and the toxic effects of glycolic and glyoxylic acids.

Mechanism of action

Benzyl alcohol inhibits lice from closing their respiratory spiracles, allowing the vehicle to obstruct the spiracles and causing the lice to asphyxiate.

Mechanism of action

The exact mechanism of action for luliconazole's anti-fungal activity is still not known, but luliconazole is thought to inhibit the enzyme lanosterol demethylase. Lanosterol demethylase is needed for the synthesis of ergosterol, which is a major component of the fungus cell membranes.

Pharmacodynamics

Luliconazole kills the organisms Trichophyton rubrum and Epidermophyton floccosum, most likely by altering their fungal cell membranes.

Mechanism of action

In an in vitro study of the mechanism of action of ethylene as a plant growth inhibitor, the effects of ethylene and some of its analogs, including propylene, on the oxidation of indole-3-acetic acid were examined. Ethylene and its analogs inhibited the oxidation of indole-3-acetic acid by peroxidase under conditions where the iron complex (compound III, an oxy-ferrous complex of peroxidase) shuttle was activated. Inhibition occurred only in the presence of the superoxide anion radical 02(-). Spectral and kinetic data indicated that ethylene and its analogs enhanced the rate of reaction of 02(-) with peroxidase; ie, the iron complex (compound III) shuttle, resulting in the formation of compound III. Propylene was a less effective inhibitor than ethylene.