Pharmacological form and main properties
Dexamethasone is an injection solution that is widely used in pharmacology. Active ingredient: dexamethasone phosphate, auxiliary ingredients: glycerin, disodium edetate, sodium hydrogen phosphate dihydrate, water. The drug is capable of providing antishock, antiallergic and antitoxic effects. It is produced in ampoules of 5 mg. The cost varies from 25 to 500 rubles.
Main properties of the drug:
- Acceleration of protein production
. Dexamethasone promotes protein production in muscle tissue and increases albumin production in the liver and kidneys. - Acceleration of lipid (fat) metabolism
. The drug affects fat deposits, redistributing cholesterol cells from the subcutaneous area of the extremities to the waist, face and shoulder girdle. - Acceleration of carbohydrate metabolism
. Under the influence of the drug, glucose enters the blood faster from the liver. - Anti-inflammatory effect
. Dexamethasone suppresses acid production in tissues and stabilizes cell membranes, increasing cell resistance to destructive effects. Prevents cell death. - Antiallergic effect
. The drug inhibits the development of the body's allergic reaction and reduces swelling of the mucous membranes.
Dexamethasone can be combined with antibiotics to enhance the drug effect.
Dexamezone can replace taking other antiallergic drugs.
Approximate dosage: 0.5 mg corresponds to 3.5 mg of Prednisolone, 17.5 mg of Cortisone or 15 mg of Hydrocortisone.
Description of the dosage form
Tablets are white, flat-cylindrical with a chamfer.
Pharmacokinetics
Absorption
After oral administration, it is quickly and completely absorbed, the maximum concentration of dexamethasone in the blood plasma is 1-2 hours.
Distribution
In the blood it binds (60–70%) to a specific carrier protein – transcortin. Easily passes through histohematic barriers (including the blood-brain and placental barriers).
Metabolism
Metabolized in the liver (mainly by conjugation with glucuronic and sulfuric acids) to inactive metabolites.
Removal
Excreted by the kidneys (a small amount of dexamethasone passes into breast milk). Half-life is 3-5 hours.
Pharmacodynamics
Dexamethasone is a synthetic glucocorticosteroid (GCS), a methylated derivative of fluoroprednisolone. It has anti-inflammatory, antiallergic, desensitizing, immunosuppressive, antishock and antitoxic effects.
Inhibits the secretion of thyroid-stimulating hormone and follicle-stimulating hormone.
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 erythropoietin). Interacts with specific cytoplasmic receptors and forms a complex that penetrates the cell nucleus, stimulates the synthesis of matrix ribonucleic acid (mRNA); the latter induces the formation of proteins, including lipocortin, that mediate cellular effects. Lipocortin inhibits phospholipase A2, suppresses the release of arachidonic acid and suppresses the synthesis of endoperoxides, prostaglandins, leukotrienes, which contribute to inflammation, allergies and others.
Effect on protein metabolism: reduces the amount of protein in plasma (due to globulins) with an increase in the albumin/globulin ratio, increases albumin synthesis in the liver and kidneys; enhances protein catabolism in muscle tissue.
Effect on lipid metabolism: increases the synthesis of higher fatty acids and triglycerides, redistributes fat (fat accumulation mainly in the shoulder girdle, face, abdomen), leads to the development of hypercholesterolemia.
Effect on carbohydrate metabolism: increases the absorption of carbohydrates from the gastrointestinal tract (GIT); 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, which leads to the activation of gluconeogenesis.
Effect on water-electrolyte metabolism: retains sodium ions and water in the body, stimulates the excretion of potassium ions (mineralocorticosteroid activity), reduces the absorption of calcium ions from the gastrointestinal tract, “washes out” calcium ions from the bones, increases the excretion of calcium ions by the kidneys.
The anti-inflammatory effect is associated with inhibition of the release of inflammatory mediators by eosinophils; inducing the formation of lipocortins 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 allergy 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, suppressing antibody formation, changing the body's immune response.
In chronic obstructive pulmonary disease, the effect 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 bronchial secretions due to inhibition or reduction of 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 (interleukin-1, interleukin-2; interferon gamma) from lymphocytes and macrophages. Suppresses the synthesis and secretion of adrenocorticotropic hormone (ACTH), and secondarily the synthesis of endogenous GCS.
The peculiarity of the action is significant inhibition of pituitary function and the almost complete absence of mineralocorticosteroid activity. Doses of 1-1.5 mg/day inhibit the adrenal cortex; biological half-life is 32-72 hours (duration of inhibition of the hypothalamic-pituitary-adrenal cortex system).
In terms of the strength of glucocorticoid activity, 0.5 mg of dexamethasone corresponds to approximately 3.5 mg of prednisolone, 15 mg of hydrocortisone or 17.5 mg of cortisone for oral dosage forms.
Indications for use
For some diseases, taking medication in tablets is difficult or even impossible. The patient can only tolerate Dexamethasone injections, for which intramuscular injections are prescribed. Indications for this method of drug administration will be:
- Rheumatic diseases
. Dexamethasone alleviates symptoms of bursitis, arthritis, and connective tissue inflammation. - Endocrine diseases
. These include adrenal hyperplasia and thyroiditis. - Malignant tumors
. In the treatment of oncology, Dexamethasone is used as a palliative agent.
To obtain a therapeutic effect as quickly as possible, the drug is administered intravenously. This is necessary in case:
- transient development of shock (traumatic, burn, toxic);
- cerebral edema due to intracranial hemorrhage or traumatic brain injury;
- severe allergies;
- acute renal failure;
- severe pain in the back, neck and chest area: possible
- acute leukemia;
- acute forms of lung diseases;
- severe infectious diseases.
It is also possible to use the medicinal solution locally: it is applied to keloid scars and pathological rashes on the skin.
Breakthrough from the past
Effective: 35 regions will receive the first batches of Avifavir
Deliveries will be made in two weeks
Immunosuppressants, which include the anti-inflammatory drug dexamethasone, can help fight severe coronavirus infection. As Oleg Batishchev, deputy director for scientific work at the Institute of Physics and Chemistry of the Russian Academy of Sciences, told Izvestia, this remedy helps with complications caused by overactivity of the immune system (the so-called cytokine storm).
— As far as I know, quite a lot of drugs were tested that were supposed to help combat the development of this path of the disease. “All of them have existed for a long time, and they were used in the treatment of a number of other, mainly autoimmune, pathologies,” the scientist said. “The fact that dexamethasone showed its effectiveness is certainly an important finding. I hope this will help treat severe forms of COVID-19.
Researchers at the University of Oxford previously announced breakthrough results. A report on their website suggests that inexpensive and long-established dexamethasone reduces mortality in hospitalized patients with severe respiratory complications of COVID-19. British infectious disease specialists conducted a randomized trial in which 2,104 patients received 6 mg of this drug once a day (in tablet form or intravenously) for ten days.
Photo: tass/dpa/Marcel Kusch
The results were so impressive that WHO immediately reported them. This is despite the fact that the study itself has not yet been published. The WHO Director General called the data on the effectiveness of dexamethasone a “scientific breakthrough.” According to him, the anti-inflammatory drug reduces the risk of death of patients with COVID-19 connected to ventilators by 35%. And among patients receiving oxygen - by 20%.
Izvestia Help
Dexamethasone has been widely used since the 1980s. This is a medicine from the group of glucocorticosteroids, which has a pronounced anti-inflammatory, antiallergic, decongestant and immunosuppressive (suppressing immunity) effect on the body. The product is of synthetic origin; in fact, it is an analogue of a person’s own hormones secreted by the adrenal glands. It suppresses the functions of tissue macrophages and also limits the migration of leukocytes to the area of inflammation. As experts emphasize, the use of this drug is dangerous, since all steroids have a large number of serious side effects.
Contraindications for taking Dexamethasone
An absolute contraindication is individual hypersensitivity to the drug. Injections are also prescribed with caution in pathological conditions:
- Gastrointestinal diseases
. During exacerbation of gastritis and peptic ulcers, the risk of perforation (tissue rupture) increases. Dexamethasone can speed up this process and cause internal bleeding. - Infectious and parasitic diseases
. During the development of a disease of a bactericidal or viral nature, any drugs can only be an addition to the main treatment. - Vaccination period
. You must wait 2 to 8 weeks before and after vaccination. Dexamethasone cannot be taken if you have an immunodeficiency state (AIDS or HIV). - Diseases of the cardiovascular system
. A previous heart attack is the main contraindication - the patient may experience an increase in the area of necrosis of cardiac tissue. This slows down the scarring process and leads to rupture of the heart muscle. - Endocrine diseases
. In diabetes mellitus, the drug will provoke the development of obesity.
It is undesirable to take the drug in case of mental pathologies, in particular in acute psychosis. Dexamethasone may increase symptoms and cause hallucinations. Also, the effect of Dexamethasone can increase the manifestation of depression and anxiety.
Contraindications to the use of Dexamethasone
- For short-term use for “life-saving” indications, the only contraindication is hypersensitivity; systemic mycosis;
- simultaneous use of live and attenuated vaccines with immunosuppressive doses of the drug;
- sucrose intolerance, isomaltase/sucrase deficiency, glucose-galactose malabsorption; breastfeeding period; children up to 3 years old.
Carefully:
Parasitic and infectious diseases of a viral, fungal or bacterial nature (currently or recently suffered, including recent contact with a patient) –
- herpes simplex, herpes zoster (viremic phase), chicken pox, measles;
- amebiasis, strongyloidiasis (established or suspected);
- active and latent tuberculosis.
Instructions for use and dosage
The dosage is selected individually depending on the severity of the disease. When administered through a drip, Dexamethasone is administered slowly, drip or stream. Daily dose for adults: from 4 to 20 mg, number of procedures - 3-4. The drug can be administered intravenously for 3-4 days, after which the patient is transferred to the oral form (taking the medicine in tablets). During the acute period, doses may be higher and reach 100-150 mg of the drug per day. After achieving a therapeutic effect, the dose is reduced to a maintenance dose or treatment is stopped.
The drug does not cause water and sodium retention in the body, and no special drinking regimen is required during treatment. But after the introduction of the dropper, the patient may feel a headache, slight dizziness and nausea. In order for the unpleasant symptoms to go away, it is recommended not to get up immediately after the procedure, but to wait 10-15 minutes.
If the drug must be injected, the needle is inserted not under the skin, but into the muscle tissue. It is of great importance how to administer Dexamethasone intramuscularly: quickly or slowly. If Dexamethasone suddenly enters the tissue at the puncture site, a hematoma may appear. To avoid this, the medicine must be administered gradually, monitoring the patient's condition. An allergic reaction to the action of the medicine may appear within 5-10 minutes, so after the injection the patient must be observed for 10-15 minutes.
Dexamethasone
Dexamethasone is a synthetic hormone of the adrenal cortex with glucocorticosteroid action (GCS). It has anti-inflammatory and immunosuppressive effects, and also affects energy metabolism, glucose homeostasis and (via negative feedback) the secretion of hypothalamic activating factor and pituitary adrenocorticotropic hormone.
GCS are fat-soluble substances and therefore easily penetrate into target cells through cell membranes. The binding of a hormone to a receptor causes conformational changes in the receptor and increases its affinity for DNA. The hormone-receptor complex enters the cell nucleus and binds to the regulatory region of the DNA molecule, also known as the glucocorticoid response element (GRE).
The activated receptor binds to GREs or specific genes and regulates messenger RNA (mRNA) transcription. The newly formed mRNA is transported to ribosomes, which then participate in the formation of new proteins. Depending on the type of target cells and cellular processes, the formation of new proteins can be either enhanced (for example, the synthesis of tyrosine transaminase in liver cells) or suppressed (for example, the synthesis of IL-2 in lymphocytes). Since receptors for GCS are found in all tissues, their action is realized in most cells of the body.
Effect on energy metabolism and glucose homeostasis:
Dexamethasone, along with insulin, glucagon and catecholamines, regulates the accumulation and expenditure of energy. In the liver, it stimulates the formation of glucose from pyruvate and amino acids and the formation of glycogen. In peripheral tissues, particularly in muscles, it reduces glucose consumption and mobilizes amino acids (from proteins), which are a substrate for gluconeogenesis in the liver. Direct effects on fat metabolism include central redistribution of adipose tissue and increased lipolysis in response to catecholamines.
Through receptors in the proximal tubules of the kidneys, dexamethasone stimulates renal blood flow and glomerular filtration, inhibits the formation and secretion of vasopressin and improves the ability of the kidneys to excrete acids.
Increases the sensitivity of blood vessels to pressor agents.
In high doses, dexamethasone suppresses the formation of collagen types I and III by fibroblasts and the formation of glycosaminoglycans; by inhibiting the formation of extracellular collagen and matrix, they slow down wound healing. Long-term use of high doses causes progressive bone tissue resorption as an indirect effect, and directly reduces its formation (stimulates the secretion of parathyroid hormone and suppresses the secretion of calcitonin). In addition, it leads to a negative calcium balance, reduces calcium absorption in the intestines and increases its excretion by the kidneys. This usually results in secondary hyperparathyroidism and phosphaturia.
Action on the hypothalamus and pituitary gland:
Dexamethasone has a 30 times more pronounced effect than endogenous cortisol. Therefore, it is a more potent inhibitor of the secretion of corticotropin-releasing factor (CRF) and adrenocorticotropic hormone (ACTH). In pharmacological doses, it inhibits the hypothalamic-pituitary-adrenal system and promotes the development of secondary adrenal insufficiency.
Adrenal insufficiency can develop as early as 5-7 days of dexamethasone administration in daily doses equivalent to 20-30 mg of prednisone or after 30 days of low-dose therapy. After discontinuation of a short course of therapy (up to 5 days) with high doses, the function of the adrenal cortex can be restored within one week; after a long course, normalization occurs later; this process usually takes up to 1 year. Some patients may develop irreversible atrophy of the adrenal cortex.
Anti-inflammatory and immunosuppressive effects
glucocorticosteroids is associated with their molecular and biochemical effects. The molecular anti-inflammatory effect is the result of the interaction of glucocorticosteroids with glucocorticoid receptors and changes in the expression of a number of genes that regulate the formation of many information molecules, proteins and enzymes involved in the process of inflammation. This leads to a decrease or prevention of the tissue response to inflammation: inhibition of the accumulation of macrophages and leukocytes, suppression of phagocytosis and release of lysosomal enzymes, synthesis of inflammatory mediators, blocking of the macrophage inhibitory factor.
Dexamethasone reduces the expansion and permeability of capillaries, reduces the adhesion of leukocytes to the endothelium, and inhibits the synthesis of Pg, leukotrienes, and thromboxanes.
Dexamethasone reduces the formation of leukotrienes by reducing the release of arachidonic acid from cellular phospholipids, which results from inhibition of phospholipase A2 activity. The effect on phospholipase is mediated by an increase in the concentration of lipocortin (macrocortin), which is an inhibitor of phospholipase A2. The suppressive effect of dexamethasone on the synthesis of prostaglandins and thromboxane is the result of a decrease in the synthesis of specific mDNA encoding the formation of cyclooxygenase.
Dexamethasone prevents or inhibits cellular immune reactions (delayed hypersensitivity reactions), reduces the number of T-lymphocytes (T-helper type I), monocytes and eosinophils, the binding of immunoglobulins to their receptors, inhibits the synthesis of interleukins: reduces T-lymphocytic blastogenesis and reduces primary immune answer. Activates humoral immunity by stimulating T-helper type II - enhances the production of antibodies. A significant effect is a decrease in the formation of tumor necrosis factor (TNF) and IL-1.
Side effects
Most patients do not experience side effects from taking Dexamethasone. But some patients may experience reactions from different organ systems:
- Endocrine system: short-term increase in blood pressure, swelling, muscle weakness, increased symptoms of diabetes.
- Digestive system: gastritis, gastric ulcer, bloating, indigestion, pancreatitis, loss of appetite.
- Cardiovascular system: heart rhythm disturbances, risk of thrombosis, feeling of heaviness in the heart area.
- Nervous system: dizziness, headaches, convulsions, depression, hallucinations, nervousness, anxiety, insomnia.
- Sense organs: short-term loss of vision, increased intraocular pressure, increased risk of developing a viral eye infection.
- Metabolism: increased sweating, accelerated excretion of calcium from the body, increased body weight, weakness, fatigue.
- Musculoskeletal system: slowing down the ossification process in children, decreased muscle elasticity, decreased muscle mass, osteochondrosis.
- Skin and mucous membranes: slow healing of wounds, pigmentation on the skin, the appearance of rashes and acne, itching.
During administration of the drug, local reactions may be observed: tingling, numbness, burning. After healing, a scar may form at the injection site. Occasionally, necrosis of the surrounding tissue occurs. Compliance with the rules for administering the drug helps to avoid this: disinfection of the puncture site and slow administration of the drug.
Using Dexamethasone during the development of an infection leads to an exacerbation of symptoms and slows down treatment!
When the drug is administered intravenously, patients with hypersensitivity may suffer from flushing of the face, limb cramps and arrhythmia.
Use during pregnancy
The drug is not recommended to be taken during pregnancy, especially during the first trimester. Dexamethasone can slow down fetal growth and increase the risk of miscarriage. It should be used only in a situation where the therapeutic effect is more important than the potential risks. To understand why Dexamethasone injections are prescribed to pregnant women, you need to assess the severity of the woman’s condition. The drug is prescribed for:
- some cancers;
- exacerbation of rheumatic diseases;
- diseases of the respiratory tract that impede the free circulation of oxygen;
- severe neurological conditions;
- disorders of the endocrine system;
- severe allergic reactions.
Dexamethasone is prescribed to pregnant women who have elevated levels of male hormones. The drug stabilizes the level of ketosteroid production and allows you to carry a child to term. If a woman goes into premature labor, Dexamethasone will suppress contractions and the pregnancy will continue.
The drug may have the greatest negative effect in the third trimester. It can cause the development of atrophy of the adrenal cortex in the fetus. In this case, additional therapy for the newborn will be required. During breastfeeding, taking the drug is prohibited. If long-term treatment is necessary, breastfeeding should be abandoned.
Use of Dexamethasone during pregnancy and children
Dexamethasone crosses the placenta (can reach high concentrations in the fetus) and into breast milk. During pregnancy, especially in the first trimester, or in women planning pregnancy, the use of Dexamethasone is indicated only if the expected therapeutic effect outweighs the risk of negative effects on the mother or fetus. GCS should be prescribed during pregnancy only for absolute indications. With long-term therapy during pregnancy, the possibility of fetal damage cannot be excluded. If used in the third trimester of pregnancy, there is a risk of atrophy of the adrenal cortex in the fetus, which may require replacement therapy in the newborn. If it is necessary to carry out treatment with the drug during breastfeeding, breastfeeding should be stopped.
Special instructions for long-term use
Before starting treatment and after, it is necessary to do a general blood test. During treatment with Dexamethasone, the patient should be under the supervision of an ophthalmologist and monitor blood pressure, calcium and glucose levels in the blood. If side effects occur, the patient should increase the intake of calcium into the body.
To do this, you need to add high-protein foods to the menu and monitor how many carbohydrates the patient consumes per day.
Sudden discontinuation of use, especially at high doses of the drug, can trigger withdrawal syndrome.
A patient with withdrawal syndrome experiences nausea, pain in the limbs, and loss of appetite. He becomes sluggish, absent-minded, and suffers from general weakness. Sometimes taking Dexamethasone provokes an immune response in the body if the immune system recognizes it as a toxic substance. In this case, you need to increase the rate of water consumption to 2-2.5 liters per day in order to quickly remove Dexamethaon from the body.
Long-term use of Dexamethasone is contraindicated for children; it is associated with slower development and growth. Bone fragility increases and the risk of fracture increases. If a child comes into contact with patients with chickenpox during treatment, he needs prophylactic administration of immunoglobulins.
Interaction with other drugs
Taking several drugs at the same time can either enhance their effect and speed up treatment, or cause complications. Dexamethasone in combination with other drugs increases the risk of side effects. Patients may experience various symptoms when taken concomitantly with:
- antipsychotropic drugs - increase the risk of developing glaucoma;
- insulin - decreased effectiveness of the drug;
- hormonal contraceptives (COCs) - acne, thrombosis;
- acetylsalicylic acid - erosion of the stomach walls and bleeding;
- cardiac glycosides - deterioration of tolerability;
- ephedrine - accelerates the excretion of Dexamethasone;
- barbiturates - weakening of the therapeutic effect.
When a patient takes another drug for a long time, Dexamethasone is usually started with a minimum dose. If side effects occur, stop taking. In this case, it is advisable to prescribe to the patient an analogue of the drug that has a similar therapeutic effect.
Analogues and substitutes
A replacement of the drug may be necessary if the patient is intolerant to the main or auxiliary active ingredients. An analogue is selected from the same group of drugs. The form of release is often changed: instead of injections, tablets or ointment are prescribed.
Drug name | Active substance | Manufacturer | Price, rub.) |
Diprospan | betamethasone | Russia, USA, France, India, Slovenia, Ukraine | 300-2000 |
Metipred | methylprednisolone | Belgium, India, Serbia, Italy, USA | 250-1000 |
Hydrocortisone | hydrocortisone | Russia, Poland, Germany, Hungary, Canada, USA | 80-350 |
Prednisolone | prednisolone | Russia, India, Republic of Belarus, Poland, Austria, Switzerland | 70-150 |
Flosteron | betamethasone | Russia, France, India, USA, Ukraine | 1000-1500 |
Dexamethosone analogues may also have side effects. They are observed immediately after administration or several days after the accumulation of the active substance in the body. In case of a severe allergic reaction, use should be stopped immediately.
What else is worth knowing?
Once in the body, Dexamethasone is not completely absorbed. Only 60-70% of the active substance binds to transocrtin, a carrier protein. The drug easily penetrates tissue, including the placental barrier. Metabolism occurs in the liver, the remaining substances are excreted from the body by the kidneys. The disintegration and half-life takes 3-5 hours.
Dexamethasone is a drug that has proven itself as a rapid action against allergies and inflammatory diseases of joint tissue. It is not addictive, injections do not cause any particular pain. Following the instructions reduces the risk of side effects and speeds up the effect of the drug.
Indications for use of Dexamethasone
Systemic connective tissue diseases (systemic lupus erythematosus, scleroderma, periarteritis nodosa, dermatomyositis, rheumatoid arthritis).
Acute and chronic inflammatory diseases of the joints: gouty and psoriatic arthritis, osteoarthritis (including post-traumatic), polyarthritis, glenohumeral periarthritis, ankylosing spondylitis (ankylosing spondylitis), juvenile arthritis, syndrome
Stilla in adults, bursitis, nonspecific tenosynovitis, synovitis and epicondylitis.
Rheumatic fever, acute rheumatic carditis.
Acute and chronic allergic diseases: allergic reactions to drugs and foods, serum sickness, urticaria, allergic rhinitis, angioedema, drug exanthema, hay fever.
Skin diseases: pemphigus, psoriasis, eczema, atopic dermatitis, diffuse neurodermatitis, contact dermatitis (affecting a large surface of the skin), toxicerma, seborrheic dermatitis, exfoliative dermatitis, toxic epidermal necrolysis (Lyell's syndrome), bullous dermatitis herpetiformis, malignant exudative erythema (syndrome) Stevens-Johnson).
Brain edema (only after confirmation of symptoms of increased intracranial pressure by magnetic resonance or computed tomography) caused by a brain tumor and/or associated with surgery or radiation injury.
Allergic eye diseases: allergic corneal ulcers, allergic forms of conjunctivitis.
Inflammatory eye diseases: sympathetic ophthalmia, severe sluggish anterior and posterior uveitis, optic neuritis.
Primary or secondary adrenal insufficiency (including the condition after removal of the adrenal glands).
Congenital adrenal hyperplasia.
Kidney diseases of autoimmune origin (including acute glomerulonephritis); nephrotic syndrome.
Subacute thyroiditis.
Diseases of the hematopoietic organs - agranulocytosis, panmyelopathy, autoimmune hemolytic anemia, acute lymphoid and myeloid leukemia, lymphogranulomatosis, thrombocytopenic purpura, secondary thrombocytopenia in adults, erythroblastopenia (erythrocytic anemia), congenital (erythroid) hypoplastic anemia.
Lung diseases: acute alveolitis, pulmonary fibrosis, stage II-III sarcoidosis. Bronchial asthma (for bronchial asthma, the drug is prescribed only in severe cases, ineffectiveness or inability to take inhaled corticosteroids).
Tuberculous meningitis, pulmonary tuberculosis, aspiration pneumonia (in combination with specific chemotherapy).
Berylliosis, Loeffler's syndrome (not amenable to other therapy).
Lung cancer (in combination with cytostatics).
Multiple sclerosis.
Gastrointestinal diseases: ulcerative colitis, Crohn's disease, local enteritis.
Hepatitis.
Prevention of transplant rejection as part of complex therapy.
Hypercalcemia due to cancer, nausea and vomiting during cytostatic therapy.
Multiple myeloma.
Conducting a test for the differential diagnosis of hyperplasia (hyperfunction) and tumors of the adrenal cortex.