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Manufacturers: Remedica (Cyprus)
Active ingredients
- Triamcinolone
Disease class
- Idiopathic thrombocytopenic purpura
- Asthma
- Crohn's disease [regional enteritis]
- Ulcerative colitis
- Atopic dermatitis
- Dermatitis, unspecified
- Seropositive rheumatoid arthritis
- Systemic lupus erythematosus
- Ankylosing spondylitis
- Nephrotic syndrome
- Other specified general symptoms and signs
- Disorders of plasma protein metabolism, not elsewhere classified
Clinical and pharmacological group
- Not indicated. See instructions
Pharmacological action
- Anti-inflammatory
- Antiallergic
- Immunosuppressive
Pharmacological group
- Glucocorticoids
Indications for use of the drug Triamcinolone
Systemic use - rheumatoid arthritis, rheumatism, systemic lupus erythematosus and other collagenoses, acute allergic and severe skin-allergic reactions, severe forms of asthma, hemorrhagic diathesis, lymphoproliferative processes; intra-articular injection - an inflammatory process in one of several joints during chronic diseases, exudative arthritis, gout, an active form of arthrosis; injection into the affected area - periostitis, bursitis, exostosis, tendovaginitis, lateral brachial epicondylitis ("tennis elbow"), limited nodular skin lesions, isolated psoriatic plaques, etc. Externally - vasculitis, pemphigus, neurodermatitis, eczema, exfoliative dermatitis, diaper rash, psoriasis , prurigo, insect bites.
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Use of the drug Triamcinolone
Orally at a dose of 4–16 mg/day in 2–4 doses. When a therapeutic effect is achieved, the dose is gradually (by 2 mg/day) reduced to a maintenance dose - usually to 1 mg/day. For systemic treatment, adults and adolescents over 16 years of age in the form of a suspension of 40 mg are administered deeply intramuscularly; in severe forms of disease, the dose can be doubled. Deep injection avoids possible tissue atrophy at the injection site. After the injection, you should press a sterile napkin tightly to the injection site for 1–2 minutes to prevent the suspension from leaking out of the injection channel. If it is necessary to perform several injections, an interval of at least 4 weeks should be maintained between them. When used intra-articularly, the dose is determined by the size of the joint and the severity of symptoms; adults and children over 12 years of age are usually prescribed in the following doses: small joints (phalanxes of the fingers of the upper and lower extremities) - 10 mg; medium-sized joints (shoulder, elbow) - 30 mg; large joints (hip, knee) - 40 mg. If multiple joints are affected, the total amount of triamcinolone administered may be 80 mg. For intralesional use for bursitis, periostitis and exostosis, adults and children over 12 years of age, depending on the size and location of the lesions, are administered: for minor lesions - up to 10 mg; for moderate and extensive - from 10 to 40 mg. Locally in the form of 0.1% ointment or cream 2-3 times a day for several days. Occlusive dressings enhance the therapeutic effect. Repeated courses of treatment can be carried out at intervals of several days.
Triamcinolone
When used simultaneously with anabolic steroids and androgens, the risk of developing peripheral edema and acne increases.
When used simultaneously with antithyroid drugs and thyroid hormones, changes in thyroid function may occur.
When used simultaneously with histamine H1 receptor blockers, the effect of triamcinolone is reduced; with hormonal contraceptives - the effect of triamcinolone is potentiated.
Hypocalcemia associated with the use of triamcinolone may lead to an increase in the duration of neuromuscular blockade caused by the action of depolarizing muscle relaxants when used concomitantly.
When used simultaneously with immunosuppressants, the risk of developing bacterial and viral infections increases.
When used simultaneously with potassium-sparing diuretics, hypokalemia is possible.
With simultaneous use, it is possible to reduce the effectiveness of indirect anticoagulants, heparin, streptokinase, urokinase, and increase the risk of erosive and ulcerative lesions and bleeding from the gastrointestinal tract.
When used simultaneously with NSAIDs (including acetylsalicylic acid), the risk of erosive and ulcerative lesions and bleeding from the gastrointestinal tract increases.
With simultaneous use, the effect of oral hypoglycemic agents and insulin is weakened; with laxatives - hypokalemia is possible; with cardiac glycosides - the risk of developing heart rhythm disturbances and other toxic effects of glycosides increases.
When used simultaneously with tricyclic antidepressants, an increase in mental disorders associated with triamcinolone may be possible.
When used simultaneously with m-anticholinergics (including atropine), intraocular pressure may increase.
When used simultaneously with amphotericin B and carbonic anhydrase inhibitors, there is a risk of developing hypokalemia, left ventricular myocardial hypertrophy and circulatory failure.
When used simultaneously with isoniazid, a decrease in the concentration of isoniazid in the blood plasma is possible, mainly in individuals with rapid acetylation.
With simultaneous use, it is possible to accelerate biotransformation and reduce the concentration of mexiletine in the blood plasma.
When used simultaneously with paracetamol, the risk of developing hypernatremia, peripheral edema, increased calcium excretion, hypocalcemia, osteoporosis, and hepatotoxicity of paracetamol increases.
When used simultaneously with rifampicin, phenytoin, carbamazepine, barbiturates, the metabolism of triamcinolone is accelerated due to the induction of microsomal liver enzymes, and its effect is reduced.
When used simultaneously with ephedrine, the metabolism of triamcinolone is accelerated.
Triamsinolone acetonide
GCS inhibits the release of interleukin1, interleukin2, interferon gamma from lymphocytes and macrophages. It has anti-inflammatory, antiallergic, desensitizing, antishock, antitoxic and immunosuppressive effects.
Suppresses the release of ACTH and beta-lipotropin by the pituitary gland, but does not reduce the concentration of circulating beta-endorphin. Inhibits the secretion of TSH and FSH.
Increases the excitability of the central nervous system, reduces the number of lymphocytes and eosinophils, increases the number of red blood cells (stimulates the production of erythropoietins).
Interacts with specific cytoplasmic receptors and forms a complex that penetrates the cell nucleus and stimulates the synthesis of mRNA; the latter induces the formation of proteins, incl. lipocortin, mediating cellular effects. Lipocortin inhibits phospholipase A2, suppresses the formation of arachidonic acid and inhibits the synthesis of endoperoxides, Pg, leukotrienes, which contribute to inflammation, allergies, etc.
Protein metabolism: reduces the amount of protein in plasma (due to globulins) with an increase in the albumin/globulin ratio, increases the synthesis of albumins in the liver and kidneys; enhances protein catabolism in muscle tissue.
Lipid metabolism: increases the synthesis of higher fatty acids and TG, redistributes fat (fat accumulation mainly in the shoulder girdle, face, abdomen), leads to the development of hypercholesterolemia.
Carbohydrate metabolism: increases the absorption of carbohydrates from the gastrointestinal tract; increases the activity of glucose-6-phosphatase, leading to an increase in the flow of glucose from the liver into the blood; increases the activity of phosphoenolpyruvate carboxylase and the synthesis of aminotransferases, leading to the activation of gluconeogenesis.
Water-electrolyte metabolism: retains Na+ and water in the body, stimulates the excretion of K+ (MCS activity), reduces the absorption of Ca2+ from the gastrointestinal tract, “washes out” Ca2+ from the bones, increases the excretion of Ca2+ by the kidneys.
The anti-inflammatory effect is associated with inhibition of the release of inflammatory mediators by eosinophils; inducing the formation of lipocortin and reducing the number of mast cells that produce hyaluronic acid; with a decrease in capillary permeability; stabilization of cell membranes and organelle membranes (especially lysosomal ones).
The antiallergic effect develops as a result of suppression of the synthesis and secretion of allergic mediators, inhibition of the release of histamine and other biologically active substances from sensitized mast cells and basophils, a decrease in the number of circulating basophils, suppression of the development of lymphoid and connective tissue, a decrease in the number of T- and B-lymphocytes, mast cells, reducing the sensitivity of effector cells to allergy mediators, inhibiting antibody formation, changing the body's immune response.
In COPD, the action is based mainly on inhibition of inflammatory processes, inhibition of development or prevention of swelling of the mucous membranes, inhibition of eosinophilic infiltration of the submucosal layer of the bronchial epithelium, deposition of circulating immune complexes in the bronchial mucosa, as well as inhibition of erosion and desquamation of the mucous membrane. Increases the sensitivity of beta-adrenergic receptors of small and medium-caliber bronchi to endogenous catecholamines and exogenous sympathomimetics, reduces the viscosity of mucus by inhibiting or reducing its production.
Antishock and antitoxic effects are associated with an increase in blood pressure (due to an increase in the concentration of circulating catecholamines and restoration of the sensitivity of adrenergic receptors to them, as well as vasoconstriction), a decrease in the permeability of the vascular wall, membrane protective properties, and activation of liver enzymes involved in the metabolism of endo- and xenobiotics.
The immunosuppressive effect is due to inhibition of the release of cytokines (interleukin1, interleukin2; interferon gamma) from lymphocytes and macrophages.
Suppresses the synthesis and secretion of ACTH and, secondarily, the synthesis of endogenous corticosteroids. Inhibits connective tissue reactions during the inflammatory process and reduces the possibility of scar tissue formation.
In terms of anti-inflammatory activity, triamcinolone is close to hydrocortisone; triamcinolone acetonide is 6 times more active. There is virtually no activity on the ISS.
After intramuscular administration, the maximum effect is observed after 24-48 hours, the duration of action with intramuscular administration is 1-6 weeks, in the joint cavity - several weeks.
