ESKAFULVIN TABLETS

Dosage

Children: Refer to specific drug information for detailed dosage recommendations.

Adults: Refer to specific drug information for detailed dosage recommendations.

Mechanism of action

The mechanism of action varies depending on the specific drug that 'contains' certain active ingredients. Each compound will have its own unique pharmacological pathway and target within the body, which can include receptor modulation, enzyme inhibition, or other biochemical interactions.

Pharmacodynamics

Pharmacodynamics will depend on the active ingredients in the formulation. It generally encompasses the biochemical and physiological effects of the drug and its mechanisms of action, including the relationship between drug concentration and effect.

Pharmacokinetics

Pharmacokinetics involves the absorption, distribution, metabolism, and excretion of the specific active ingredients within the formulation. This can vary significantly based on the drug's chemical properties, route of administration, and individual patient factors.

Pregnancy

Consult with a healthcare provider before use, as safety during pregnancy has not been established.

Breast-feeding

Consult with a healthcare provider before use, as it is not known if this drug is excreted in human milk.

Storage

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

Indications

• Dermatophyte infections of the skin
• Tinea capitis caused by Trichophyton tonsurans

Mechanism of action

Griseofulvin is fungistatic, inhibiting fungal cell mitosis primarily by binding to and interfering with the function of spindle and cytoplasmic microtubules, particularly by binding to alpha and beta tubulin. This action disrupts the mitotic spindle structure, arresting the cell division process during metaphase. Additionally, griseofulvin binds to keratin in human cells, and once it reaches the fungal site of action, it binds to fungal microtubules, altering the process of mitosis in fungi. As infected keratin is shed, it is replaced with healthy tissue, rendering the keratin resistant to further fungal invasion.

Pharmacodynamics

Griseofulvin has demonstrated in vitro activity against various species of dermatophytes including Microsporum, Epidermophyton, and Trichophyton. The drug is tightly bound to new keratin, making it highly resistant to fungal invasion. While it is effective against dermatophytes, it has no antibacterial properties and does not affect other genera of fungi. The clinical efficacy is enhanced by its preferential deposition in keratin precursor cells of the skin, hair, and nails.

Pharmacokinetics

Griseofulvin is administered orally and is absorbed from the gastrointestinal tract. Its absorption can be enhanced when taken with fatty foods. The drug is widely distributed in body tissues and has a high affinity for keratin. It undergoes hepatic metabolism and is excreted primarily via the urine. The half-life of griseofulvin varies but is generally around 24 hours. Caution should be exercised in patients with renal impairment, and dose adjustments may be necessary based on creatinine clearance.

Contra-indications

• Acute porphyrias
• Systemic lupus erythematosus

Adverse effects

• Diarrhoea
• Epigastric discomfort
• Headache
• Nausea
• Vomiting
• Decreased appetite
• Confusion
• Coordination abnormalities
• Dizziness
• Drowsiness
• Insomnia
• Irritability
• Peripheral neuropathy
• Photosensitivity reactions
• Skin reactions

Interactions

• Griseofulvin may decrease the anticoagulant effect of coumarins

Precautions

• Use with caution in patients with renal impairment
• Avoid contact with eyes and mucous membranes
• Monitor liver and kidney function during treatment

Pregnancy

Griseofulvin is not recommended during pregnancy due to potential risks to the fetus.

Breast-feeding

Griseofulvin is excreted in breast milk; caution should be exercised when administering to nursing mothers.

Storage

Store at room temperature, away from moisture and heat.

Formulations

• Oral suspension
• Tablets

Mechanism of action

Griseofulvin is fungistatic, however the exact mechanism by which it inhibits the growth of dermatophytes is not clear. It is thought to inhibit fungal cell mitosis and nuclear acid synthesis. It also binds to and interferes with the function of spindle and cytoplasmic microtubules by binding to alpha and beta tubulin. It binds to keratin in human cells, then once it reaches the fungal site of action, it binds to fungal microtubes thus altering the fungal process of mitosis. Fungistatic; griseofulvin inhibits fungal cell mitosis by causing disruption of the mitotic spindle structure, thereby arresting the metaphase of cell division. It is deposited in varying concentrations in the keratin precursor cells of skin, hair, and nails, rendering the keratin resistant to fungal invasion. As the infected keratin is shed, it is replaced with healthy tissue.

Pharmacodynamics

Griseofulvin is a mycotoxic metabolic product of <i>Penicillium spp.</i> It was the first available oral agent for the treatment of dermatophytoses and has now been used for more than forty years. Griseofulvin is fungistatic with in vitro activity against various species of Microsporum Epidermophyton, and Trichophyton. It has no effect on bacteria or on other genera of fungi. Following oral administration, griseofulvin is deposited in the keratin precursor cells and has a greater affinity for diseased tissue. The drug is tightly bound to the new keratin which becomes highly resistant to fungal invasions. Once the keratin-Griseofulvin complex reaches the skin site of action, it binds to fungal microtubules (tubulin) thus altering fungal mitosis.