Komfoderm K, cream 0.1% 30 g

Pharmacotherapeutic group:

Glucocorticosteroid for topical use

ATC code:

D07AA01

Pharmacological action

Pharmacodynamics

The active ingredient of Comfoderm® K, methylprednisolone aceponate, is a nonhalogenated synthetic steroid.

When applied topically, Comfoderm® K suppresses inflammatory and allergic skin reactions as well as reactions associated with increased proliferation, which results in reduction of objective symptoms of inflammation (erythema, edema, mottling) and subjective sensations (itching, irritation, pain, etc.).

When methylprednisolone aceponate is applied topically at the recommended dose, systemic effects are minimal in both humans and animals. After repeated application of methylprednisolone aceponate on large surfaces (40-60% of the skin surface), and also when used under the occlusive dressing no adrenal disturbances are noted: plasma cortisol level and its circadian rhythm remain within normal limits, there is no reduction of cortisol level in daily urine.

Methylprednisolone aceponate (especially its main metabolite, 6α-methylprednisolone-17-propionate) binds to intracellular glucocorticoid receptors. The steroid-receptor complex binds to specific DNA sites of immune response cells, thus causing a series of biological effects.

In particular, binding of the steroid-receptor complex to the DNA of the immune response cells leads to induction of macrocortin synthesis. Macrocortin inhibits the release of arachidonic acid and thus the formation of inflammatory mediators such as prostaglandins and leukotrienes. Inhibition by glucocorticosteroids of the synthesis of vasodilatory prostaglandins and potentiation of the vasoconstrictor effect of adrenaline, lead to a vasoconstrictor effect.

Pharmacokinetics

In external use methylprednisolone aceponate is hydrolyzed in the epidermis and dermis.
The main and most active metabolite is 6α-methylprednisolone-17-propionate, which has a significantly higher affinity for glucocorticosteroid receptors in the skin, indicating the presence of its “bioactivation” in the skin.

The extent of percutaneous absorption depends on the skin condition and the route of application (with or without an occlusive dressing). Percutaneous absorption in children and adults with atopic dermatitis (neurodermatitis) and psoriasis is less than 2.5%, which is only slightly higher compared to healthy volunteers (0.5-1.5%).

After entering the systemic bloodstream 6α-methylprednisolone-17-propionate rapidly conjugates with glucoronic acid, and thus in the form of 6α-methylprednisolone-17-propionate glucuronide is inactivated.
Metabolites of methylprednisolone aceponate are eliminated mainly by kidneys with the elimination half-life of about 16 hours. Methylprednisolone aceponate and its metabolites do not cumulate in the body.

Indications

Inflammatory skin diseases sensitive to therapy with topical glucocorticosteroids:

Active ingredient

Composition

How to take, the dosage

Special Instructions

In the presence of bacterial dermatoses and/or dermatomycoses, specific antibacterial or antimycotic treatment is required in addition to therapy with Comfoderm® K .

The drug is not intended for use in ophthalmology. Contact with the eyes and mucous membranes should be avoided. As with systemic GCS, glaucoma may develop after external use (e.g., when using high doses, very prolonged use of occlusive dressings or application to the skin around the eyes).

Influence on driving and operating ability

Have not been identified.

Synopsis

Features

Absorption and distribution

The extent of percutaneous absorption depends on the skin condition and the route of administration (with or without an occlusive dressing). Percutaneous absorption in children and adults with atopic dermatitis (neurodermatitis) and psoriasis is less than 2.5%, which is only slightly higher than in healthy volunteers (0.5-1.5%). After entering the systemic bloodstream, 6α-methylprednisolone-17-propionate rapidly conjugates with glucoronic acid and is thus inactivated in the form of 6α-methylprednisolone-17-propionate glucuronide.

Methylprednisolone aceponate and its metabolites do not cumulate in the body.

Metabolism and excretion

Methylprednisolone aceponate is hydrolyzed in the epidermis and dermis when applied externally. The main and most active metabolite is 6α-methylprednisolone-17-propionate, which has a significantly higher affinity for glucocorticoid receptors in the skin, indicating the presence of its “bioactivation” in the skin.

Methylprednisolone aceponate metabolites are eliminated primarily by the kidneys with a T1/2 of approximately 16 h.

Contraindications

Side effects

Overdose

In studies of acute toxicity of methylprednisolone aceponate, no risk of acute intoxication was found with excessive single cutaneous administration (application of the drug to a large area under conditions favorable for absorption) or unintentional oral administration.

Symptoms:In excessive long-term and/or intensive external use of GCS, skin atrophy (skin thinning, telangiectasia, stretch marks) may develop.

Treatment:In case of signs of skin atrophy, the drug should be discontinued.

Pregnancy use

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