Drenison Tape

Drenison Tape Uses, Dosage, Side Effects, Food Interaction and all others data.

A corticosteroid used topically in the treatment of various skin disorders. It is usually employed as a cream or an ointment, and is also used as a polyethylene tape with an adhesive. (From Martindale, The Extra Pharmacopoeia, 30th ed, p733)

Drenison Tape is primarily effective because of its anti-inflammatory, antipruritic, and vasoconstrictive actions.

Trade Name Drenison Tape
Availability Prescription only
Generic Flurandrenolide
Flurandrenolide Other Names Fludroxicortida, Fludroxicortide, Fludroxycortid, Fludroxycortide, Fludroxycortidum, Flurandrenolide, Flurandrenolone
Related Drugs Humira, Cosentyx, Dupixent, prednisone, methotrexate, Remicade, Stelara, cyclosporine, infliximab, Temovate
Type Topical application
Formula C24H33FO6
Weight Average: 436.5136
Monoisotopic: 436.226116993
Protein binding

Corticosteroids are bound to plasma proteins in varying degrees.

Groups Approved
Therapeutic Class
Manufacturer
Available Country United States
Last Updated: September 19, 2023 at 7:00 am
Drenison Tape
Drenison Tape

Uses

Drenison Tape is a corticosteroid used to treat corticosteroid-responsive dermatoses.

For relief of the inflammatory and pruritic manifestations of corticosteroid-responsive dermatoses, particularly dry, scaling localized lesions

Drenison Tape is also used to associated treatment for these conditions: Dermatosis

How Drenison Tape works

Drenison Tape is a topical corticosteroid. It is normally applied to a plastic tape called Cordran. Cordran is primarily effective because of its anti-inflammatory, antipruritic, and vasoconstrictive actions. Drenison Tape, which is slowly released from the Cordran tape, binds to the cytosolic glucocorticoid receptor. After binding the receptor the newly formed receptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes preventing the phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. Cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In another words, the two main products in inflammation Prostaglandins and Leukotrienes are inhibited by the action of Glucocorticoids. Glucocorticoids also stimulate the lipocortin-1 escaping to the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines etc.) from neutrophils, macrophages and mastocytes. Additionally the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding. Like other glucocorticoid agents Fluocinolone acetonide acts as a physiological antagonist to insulin by decreasing glycogenesis (formation of glycogen). It also promotes the breakdown of lipids (lipolysis), and proteins, leading to the mobilization of extrahepatic amino acids and ketone bodies. This leads to increased circulating glucose concentrations (in the blood). There is also decreased glycogen formation in the liver.

Toxicity

Systemic absorption of topical corticosteroids has produced reversible hypothalamic-pituitary- adrenal (HPA) axis suppression, manifestations of Cushing's syndrome, hyperglycemia, and glucosuria in some patients

Food Interaction

No interactions found.

Elimination Route

Once absorbed through the skin, topical corticosteroids are handled through pharmacokinetic pathways similar to those of systemically administered corticosteroids

Elimination Route

Topical corticosteroids can be absorbed from normal intact skin. They are metabolized primarily in the liver and then excreted in the kidneys. Some of the topical corticosteroids and their metabolites are also excreted into the bile.

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