Brands, Medical Use, Clinical Data
Drug Category
Dosage Forms
Brands / Synonyms
11beta-Hydroxycortisone; 17alpha-Hydroxycorticosterone; A-Hydrocort; Acticort; Aeroseb HC; Aeroseb-HC; Ala-cort; Ala-Scalp; Alacort; Algicirtis; Alphaderm; Amberin; Analpram HC; Anflam; Anti-inflammatory hormone; Anusol HC; Aquacort; Aquanil HC; Balneol-hc; Barseb HC; Basan-Corti; Bencort; Beta-hc; CaldeCORT Spray; Cetacort; Cipro HC; Clear aid; Cleiton; Cobadex; Colocort; Compound F; Cort-Dome; Cort-Quin; Cortaid; Cortanal; Cortef; Cortef Acetate; Cortenema; Cortesal; Corticreme; Cortifan; Cortifoam; Cortiment; Cortisol; Cortisol alcohol; Cortisolonum; Cortisone, tetrahydro-; Cortisporin; Cortisporin Otico; Cortisporin-TC; Cortispray; Cortolotion; Cortonema; Cortoxide; Cortril; Cremesone; Cremicort-H; Cutisol; Delacort; Derm-Aid; Dermacort; Dermasorb AF Complete KIT; Dermaspray; Dermazene; Dermil; Dermocortal; Dermolate; Dihydrocostisone; Dioderm; Dome-cort; Domolene-HC; Dricort; Drotic; EF corlin; Efcorbin; Efcortelan; Efcortelin; Eldecort; Eldercort; Epicort; Epiderm H; Epifoam; Esiderm H; Evacort; Ficortril; Fiocortril; Flexicort; Foille Insetti; Genacort; Glycort; Gyno-Cortisone; H-Cort; Heb Cort; Heb-Cort; Hemsol-HC; Hi-cor; Hidalone; Hidro-Colisona; Hidrocortisona [INN-Spanish]; Hycort; Hycortol; Hycortole; Hydracort; Hydrasson; Hydro-adreson; Hydro-colisona; Hydrocort; Hydrocortal; Hydrocorticosterone; Hydrocortisone Acetate; Hydrocortisone alcohol; Hydrocortisone and Acetic Acid; Hydrocortisone Base; Hydrocortisone Butyrate; Hydrocortisone free alcohol; Hydrocortisone Sodium Phosphate; Hydrocortisone Sodium Succinate; Hydrocortisone Valerate; Hydrocortisone [BAN:INN:JAN]; Hydrocortisonum [INN-Latin]; Hydrocortistab; Hydrocortisyl; Hydrocortone; Hydroskin; Hydroxycortisone; Hysone; Hytisone; Hytone; Hytone lotion; Idrocortisone [DCIT]; Incortin-H; Incortin-hydrogen; Kendall's compound F; Komed HC; Kyypakkaus; Lacticare HC; Lacticare-HC; Lactisona; Locoid; Locoid Lipocream; Lubricort; Maintasone; Medicort; Meusicort; Micort-hc; Mildison; Milliderm; Neomycin and Polymyxin B Sulfates and Bacitracin Zinc with Hydrocortisone; Neomycin and Polymyxin B Sulfates and Hydrocortisone; Neosporin-H Ear; Nogenic HC; Nutracort; Nystaform-HC; Optef; Orabase HCA; Otalgine; Otobiotic; Otocort; Otosone-F; Pandel; Pediotic Suspension; Penecort; Permicort; Polcort H; Pramosone; Preparation H Hydrocortisone Cream; Prepcort; Prevex HC; Proctocort; Proctofoam; Proctofoam HC; Protocort; Racet; Rectoid; Reichstein's Substance M; Remederm HC; Sanatison; Scalpicin Capilar; Schericur; Scheroson F; Sigmacort; Signef; Solu-cortef; Stie-cort; Stiefcorcil; Synacort; Systral Hydrocort; Tarcortin; Terra-Cortril; Tetrahydro E; Tetrahydrocompound E; Texacort; Texacort lotion 25; THE; Thyrotropic-releasing factor; Timocort; Topicort; Transderma H; Traumaide; Uniderm; Urocortisone; Vioform-Hydrocortisone; VoSol HC; Vytone; Westcort; Xerese; Zenoxone
Indications
For the relief of the inflammatory and pruritic manifestations of corticosteroid-responsive dermatoses. Also used to treat endocrine (hormonal) disorders (adrenal insufficiency, Addisons disease). It is also used to treat many immune and allergic disorders, such as arthritis, lupus, severe psoriasis, severe asthma, ulcerative colitis, and Crohn's disease.
Pharmacology
Hydrocortisone is the most important human glucocorticoid. It is essential for life and regulates or supports a variety of important cardiovascular, metabolic, immunologic and homeostatic functions. Topical hydrocortisone is used for its anti-inflammatory or immunosuppressive properties to treat inflammation due to corticosteroid-responsive dermatoses. Glucocorticoids are a class of steroid hormones characterised by an ability to bind with the cortisol receptor and trigger a variety of important cardiovascular, metabolic, immunologic and homeostatic effects. Glucocorticoids are distinguished from mineralocorticoids and sex steroids by having different receptors, target cells, and effects. Technically, the term corticosteroid refers to both glucocorticoids and mineralocorticoids, but is often used as a synonym for glucocorticoid. Glucocorticoids suppress cell-mediated immunity. They act by inhibiting genes that code for the cytokines IL-1, IL-2, IL-3, IL-4, IL-5, IL-6, IL-8 and TNF-alpha, the most important of which is the IL-2. Reduced cytokine production limits T cell proliferation. Glucocorticoids also suppress humoral immunity, causing B cells to express lower amounts of IL-2 and IL-2 receptors. This diminishes both B cell clonal expansion and antibody synthesis. The diminished amounts of IL-2 also leads to fewer T lymphocyte cells being activated.
Mechanism of Action
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 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.
Absorption
Topical corticosteroids can be absorbed from normal intact skin. Inflammation and/or other disease processes in the skin increase percutaneous absorption.
Toxicity
Side effects include inhibition of bone formation, suppression of calcium absorption and delayed wound healing
Biotrnasformation / Drug Metabolism
Primarily hepatic via CYP3A4
Contraindications
Topical corticosteroids are contraindicated in those patients with a history of hypersensitivity to
any of the components of the preparation.
Drug Interactions
No information available.
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