Prednisonum ( genus Prednisoni)
Pharmacological action – anti-inflammatory, anti-allergic, glucocorticoid .
Stabilizes cell membranes, including lysosomal, reduces the release of proteolytic enzymes from lysosomes (inhibition of the alteration phase and limitation of the focus of inflammation), inhibits phospholipase A 2 , disrupts the liberalization of arachidonic acid and, as a result, inhibits the synthesis of PG, hydroxy acids and leukotrienes, inhibits the activity of hyaluronidase and reduces the permeability of capillaries (inhibition of the exudation phase), the activity of fibroblasts (inhibition of the proliferation phase). Antiallergic properties are due to impaired mast cell degranulation, a decrease in the synthesis of leukotrienes and suppression of antibody production, anti-shock – to the retention of sodium and water, an increase in the response of blood vessels to endogenous and exogenous vasoconstrictors and a stimulating effect on cardiac activity, antitoxic – to accelerate the inactivation of toxic substances in the liver, decrease permeability of cell membranes.
When taken orally, it is easily absorbed, C max in the blood plasma is observed after 1-2 hours. Bioavailability exceeds 90%. It undergoes biotransformation, mainly in the liver, excreted mainly by the kidneys. With an increase in dose, T 1/2 increase, total clearance, volume of distribution and degree of binding to proteins. Affects carbohydrate, protein, fat and water-salt metabolism. Increases blood glucose, promotes the accumulation of glycogen in the liver, enhancing gluconeogenesis. It activates the processes of catabolism, slows down the regeneration, controls the deamination of amino acids in the liver, promotes the redistribution of adipose tissue, retains sodium and water in the body, enhances the excretion of potassium; it stimulates the cardiovascular system, increases the tone of arterioles and myocardial contractility, increases stroke and minute volume, stimulates the central nervous system, has antitoxic and immunosuppressive effects, causes increased secretion of the gastric mucosa and acidity of gastric juice.
Use of prednisone
Rheumatism, rheumatoid arthritis, dermatomyositis, periarteritis nodosa, scleroderma, ankylosing spondylitis, bronchial asthma, allergic diseases, Addison’s disease, acute adrenal cortical insufficiency, adrenogenital syndrome, hepatitis, hepatic coma, hypoglycemic nephrosis, various types of lymphoid leukemic leukemosis, lymphoid leukemia leukemia, , thrombocytopenic purpura, hemolytic anemia, infectious mononucleosis, acute pancreatitis, pemphigus, eczema, pruritus, exfoliative dermatitis, psoriasis, pruritus , seborrheic dermatitis, lupus erythematosus, erythroderma, alopecia; prevention and treatment of shock.
Hypersensitivity, peptic ulcer of the stomach and duodenum in the exacerbation phase, osteoporosis, Itsenko-Cushing’s disease, tendency to thromboembolism, renal failure, severe arterial hypertension, systemic mycoses, viral infections, vaccination period, the active form of tuberculosis, productive symptoms of psychosis.
Diabetes mellitus, non-specific infections, latent forms of tuberculosis, pregnancy (especially the first trimester).
Side effects of the substance prednisone
Decreased resistance to infection, hyperglycemia up to the development of steroid diabetes, negative nitrogen balance, osteoporosis, aseptic necrosis of the bones, increased acidity of the gastric juice, ulcerogenic effect on the gastrointestinal tract , hypokalemia, sodium and water retention, edema, arterial hypertension, increased blood coagulability, Itsenko syndrome – Cushing’s, weight gain, “moon-shaped” face, steroid cataract, latent glaucoma, menstrual irregularities in women, insomnia, muscle weakness; withdrawal syndrome associated with inhibition of function or atrophy of the adrenal cortex.
It accelerates the elimination of barbiturates, digitoxin, penicillin, chloramphenicol. Phenobarbital, diphenin, diphenhydramine, ephedrine increase the rate of biotransformation. The risk of hypokalemia increases when combined with amphotericin and cardiac glycosides. NSAIDs increase (mutually) ulcerogenicity. When combined with acetylsalicylic acid, the development of hypoprothrombinemia is possible.
Route of administration