Bufacort-N

Uses

Hydrocortisone Acetate is used for:

• Primary irritant dermatitis
• Contact allergic dermatitis
• Eczema: atopic, infantile, discoid, stasis
• Seborrheic dermatitis
• Lichen simplex and pruritus ani
• Flexural psoriasis
• Skin irritations, itching and rashes, for example those caused by insect bites, minor thermal burns, sunburn, etc

Bufacort-N is also used to associated treatment for these conditions: Acute, Inflammatory Superficial Cutaneous Lesions caused by susceptible bacteria, Adrenal cortical hypofunctions, Anal Fissures, Anal inflammation, Androgenital syndrome, Conjunctivitis, Conjunctivitis allergic, Corneal Inflammation, Dermatitis infected, Diaper Dermatitis, Eczema infected, Episcleritis, Hemorrhoids, Iridocyclitis, Iritis, Ocular Inflammation, Ocular Irritation, Postoperative pain, Proctitis, Pruritus, Pruritus Ani, Radiation Induced Proctitis, Rheumatoid Arthritis, Scleritis, Skin Infections, Skin Irritation, Superficial ocular bacterial infections caused by susceptible bacteria, Thyroiditis, Ulcerative Colitis, Anal eczema, Bacterial blepharitis, Corneal clouding, Corticosteroid responsive Dermatosis of the anal region, Corticosteroid-responsive dermatoses, Cryptitis, Localized uninfected hemorrhoids, Mild Anal Fissures, Pruritus associated with bowel movements, Skin and skin-structure infections caused by susceptible bacteria, Postoperative Eye Care

How Bufacort-N works

Hydrocortisone 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. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other 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.

Dosage

Bufacort-N dosage

Hydrocortisone cream should be applied in a thin smear to the affected area one to two times per day or as directed by the physician. The recommended duration of treatment is usually two weeks. For rectal use apply to the irritated anorectal tissue in the morning and at evening and after each bowel movement for two to six days.

Side Effects

Hydrocortisone Acetate 1% cream is usually well-tolerated, but if signs of hypersensitivity appear, application should be stopped.

Toxicity

Side effects include inhibition of bone formation, suppression of calcium absorption and delayed wound healing

Precaution

In infants and children, long-term continuous topical therapy should be avoided where possible, as adrenal suppression can occur. As with all corticosteroids, prolonged application to the face is undesirable.

Elimination Route

Topical corticosteroids can be absorbed from normal intact skin. Inflammation and/or other disease processes in the skin increase percutaneous absorption.

Half Life

6-8 hours

Elimination Route

Corticosteroids are metabolized primarily in the liver and are then excreted by the kidneys. Some of the topical corticosteroids and their metabolites are also excreted into the bile.

Pregnancy & Breastfeeding use

There is inadequate evidence for safety in human pregnancy. It is recommended that topical corticosteroids should not be used extensively during pregnancy. It is highly unlikely that sufficiently high blood levels of Hydrocortisone are achieved during topical therapy to reach breast milk.

Contraindication

Contraindicated in infections (bacterial; viral; fungal), skin ulcers, hypersensitivity to the preparation

Acute Overdose

Acute overdosage is very unlikely to occur, however, in the case of chronic overdosage or misuse, the features of hypercorticism may appear and in this situation topical steroids should be discontinued

Storage Condition

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

Innovators Monograph

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