Corticosteroid therapy is an adjunct rather than an alternative to traditional treatment. Dermatology diseases Atopic dermatitis (monetoid eczema), neurodermatitis, contact dermatitis, severe solar dermatitis, urticaria, lichen planus, insulin lipodystrophy, nesting alopecia, discoid erythematous lupus, psoriasis, keloid scars, common pemphigus, herpetic dermatitis, cystic acne. Rheumatic disease Rheumatoid arthritis, osteoarthritis, bursitis, tendonitis, tendinitis, peritendinitis, ankylosing spondylitis, epicondylitis, radiculitis, coccidinitis, sciatica, lumbago, torticollis, ganglion cyst, exostosis, fascitis, acute gouty arthritis, synovial cysts, Morton’s disease, inflammation of the cuboid bone, foot diseases, bursitis on the background of a hard corn, spurs, and stiffness of the big toe.
active substance: betamethasone;
1 ml of solution contains 6.43 mg betamethasone dipropionate (equivalent to 5 mg betamethasone) and 2.63 mg betamethasone sodium phosphate (equivalent to 2 mg betamethasone)
sodium phosphate, dihydrate; sodium chloride, Trilon B; polysorbate 80 benzyl alcohol; methyl parahydroxybenzoate (E 218) propyl parahydroxybenzoate (E 216) sodium carboxymethyl cellulose; macrogols; hydrochloric acid; water for injections.
Diprospan Dosage form
Suspension for injection.
Basic physical and chemical properties: transparent, colorless, slightly viscous liquid containing white or almost white particles, easily dispersed, free from impurities.
Systemic corticosteroids. Glucocorticoids. ATX code H02A B01.
Betamethasone is a synthetic glucocorticoid (9 alpha-fluoro-16-beta-methylprednisolone). Betamethasone has a strong anti-inflammatory, anti-allergic and immunosuppressive effect.
Betamethasone has no clinically significant mineralocorticoid effect. GCS spread through cell membranes and form complexes with specific receptors in the cytoplasm. These complexes then penetrate into the cell nucleus, bind to DNA (chromatin) and stimulate the transcription of messenger RNA and further synthesis of proteins of various enzymes. These latter will ultimately be responsible for the actions that are observed with the systematic use of glucocorticoids. In addition to their significant effect on inflammatory and immune processes, glucocorticoids also affect the metabolism of carbohydrates, proteins and lipids. They also affect the cardiovascular system, skeletal muscles and the central nervous system.
Effects on inflammatory and immune processes
It is on the anti-inflammatory, immunosuppressive and antiallergic properties of glucocorticoids that their use in therapeutic practice is based. The main aspects of these properties are: a decrease in the number of immunoactive cells at the level of the focus of inflammation, a decrease in vasodilation, stabilization of lysosomal membranes, inhibition of phagocytosis, a decrease in the production of prostaglandins and related compounds.
The anti-inflammatory effect is about 25 times greater than in hydrocortisone, and 8-10 times more than in prednisolone (in weight ratio).
Corticosteroid therapy is an adjunct and not an alternative to conventional treatment.
Atopic dermatitis (coin-like eczema), neurodermatitis, contact dermatitis, severe solar dermatitis, urticaria, lichen planus, insulin lipodystrophy, alopecia areata, discoid lupus erythematosus, psoriasis, keloid scars, pemphigus common, herpetic ugrimatitis, cystic dermatitis.
Rheumatoid arthritis, osteoarthritis, bursitis, tendosynovitis, tendinitis, peritendinitis, ankylosing spondylitis, epicondylitis, radiculitis, coccidinia, sciatica, lumbago, torticollis, ganglion cyst, exostosis, cystitis arthritis disease, acute gouty disease feet, bursitis against the background of hard calluses, spurs, stiffness of the big toe.
Bronchial asthma, status asthma, hay fever, severe allergic bronchitis, seasonal and aperiodic allergic rhinitis, angioedema, contact dermatitis, atopic dermatitis, serum sickness, hypersensitivity reactions to medications or insect bites.
Systemic lupus erythematosus, scleroderma, dermatomyositis, periarteritis nodosa.
Palliative therapy of leukemia and lymphoma in adults, acute leukemia in children.
Adrenogenital syndrome, ulcerative colitis, Crohn’s disease, sprue, pathological changes in the blood requiring GCS therapy, nephritis, nephrotic syndrome.
Primary and secondary adrenal cortex insufficiency (with the obligatory simultaneous administration of mineralocorticoids).
Hypersensitivity to active substances or to any excipients in the composition of the drug are given in the “Composition” section.
hypersensitivity to GCS.
Systemic fungal infections.
Intramuscular administration to patients with idiopathic thrombocytopenic purpura.