Dexamethasone

Package leaflet (information for patients)

Tradename
Dexamethasone

Dosage form
Tablets 0.5 mg.

Description
Round, flat, beveled to the edge white tablets with an imprint in the form of the brand name "V" on one side.

Structure
Active ingredient: Dexamethasone 0.5 mg.
Excipients: microcrystalline cellulose 102, calcium stearate, aerosil ® 200 (hydrophilic pyrogenic silicon dioxide).

Pharmacotherapeutic group
Glucocorticosteroid

Pharmacological properties
Pharmacodynamics
Dexamethasone is a synthetic adrenal cortex hormone (corticosteroid) with glucocorticoid activity. It has anti-inflammatory and immunosuppressive effects, and also affects metabolism, glucose homeostasis and (through a negative feedback effect) the secretion of hypothalamic releasing hormone and adrenocorticotropic hormone of the adenohypophysis. Until the end, the effect of glucocorticoids has not yet been clarified. Currently, there is sufficient evidence on the mechanism of action of glucocorticoids at the cellular level. There are two well-defined receptor systems in the cytoplasm of cells. Through glucocorticoid receptors, corticosteroids regulate anti-inflammatory andimmunosuppressive effects and glucose homeostasis; through mineralocorticoid receptors they regulate sodium and potassium metabolism, electrolyte and water balance. Glucocorticoids are fat-soluble substances and therefore easily enter target cells through cell membranes. The binding of the hormone to the 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 GRE or specific genes and regulates the transcription of messenger RNA (mRNA). The newly formed mRNA is transported to ribosomes, which are then involved in the formation of new proteins. Depending on the type of target cells and processes, the formation of new proteins can be both enhanced (for example, the synthesis of tyrosine transaminase in liver cells) and suppressed (for example, the synthesis of IL in lymphocytes). Since receptors for glucocorticoids are found in all tissues, their action is realized in most cells of the body.
Effects on glucose metabolism and homeostasis: dexamethasone, along with insulin, glucagon and catecholamines, regulates energy storage and expenditure. In the liver, it stimulates the formation of glucose from pyruvate and amino acids and the formation of glycogen. In peripheral tissues, in particular in muscles, it reduces glucose intake and mobilizes amino acids (from proteins), which are a substrate for gluconeogenesis in the liver. Direct effects on fat metabolism are manifested by central redistribution of adipose tissue and increased lipolysis in response to exposure to catecholamines.
Through receptors in the proximal renal tubules, dexamethasone stimulates renal blood flow and glomerular filtration, inhibits the formation and secretion of vasopressin, and improves the kidney's ability to excrete acids. Increases the sensitivity of blood vessels to pressor agents.
In high doses, dexamethasone inhibits the production of collagen I and III by fibroblasts, as well as glycosaminoglycans ; by inhibiting the formation of extracellular collagen and matrix, they slow down wound healing. Long-term administration of high doses causes progressive resorption of bone tissue 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 - it reduces the absorption of calcium in the intestine and enhances its excretion by the kidneys. This usually leads to secondary hyperparathyroidism and phosphaturia.
Action on the hypothalamus and pituitary gland: Dexamethasone has 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, promotes the development of secondary adrenal insufficiency. Insufficiency of the adrenal cortex can develop as early as 5-7 days of administration of dexamethasone in daily doses equivalent to 20-30 mg of prednisolone or after 30 days of low-dose therapy. After the abolition of a short course of therapy (up to 5 days) with high doses, the function of the adrenal cortex can be restored in one week; after a long course, normalization occurs later, usually this process takes up to 1 year. Some patients may develop irreversible atrophy of the adrenal cortex.
The anti-inflammatory and immunosuppressive effects of glucocorticosteroids are related to their molecular and biochemical effects. The molecular anti-inflammatory effect is the result of the interaction of glucocorticoids 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 macrophage inhibitory factor. Dexamethasone reduces the expansion and permeability of capillaries, reduces the adhesion of leukocytes to the endothelium, inhibits the synthesis of Pg, leukotrienes, thromboxanes. Dexamethasone reduces the formation of leukotrienes by reducing the release of arachidonic acid from their cellular phospholipids, which is the result of suppression of the activity of phospholipase A2. 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 that encodes the formation of cyclooxygenase.
Dexamethasone prevents or inhibits cellular immune responses (delayed-type hypersensitivity reactions), reduces the number of T-lymphocytes (T-helper type I), monocytes and eosinophils, binding,. immunotsl obul ins to their receptors inhibits the synthesis of interleukins : T reduces limfotsitarnyi blastogenesis and reduces primary immune response. Activates humoral immunity by stimulating type II T-helpers - increases the production of antibodies. A significant effect is a decrease in the formation of tumor necrosis factor (TNF) and IL-1.
Pharmacokinetics
Suction
After oral administration, dexamethasone is rapidly and completely absorbed. The bioavailability of dexamethasone tablets is 80% (in the literature, you can find different data on bioavailability, ranging from 53% to 112%). After oral administration, the maximum plasma concentration and the maximum effect are achieved after 1-2 hours; after a single dose, the effect lasts approximately 2.75 days.
Distribution
Approximately 77% of dexamethasone binds to plasma proteins, mainly albumin. Only a small amount of dexamethasone binds to non-albumin proteins. Since dexamethasone is a fat-soluble substance, it can penetrate into the extra- and intracellular space. Metabolism
In the central nervous system (hypothalamus, pituitary gland), its effects are due to binding to membrane receptors. In peripheral tissues, it binds to cytoplasmic receptors. The decay occurs at the place of its action, i.e. in a cage. Basically, the drug is metabolized in the liver, but also metabolized in the kidneys and other tissues. It is excreted mainly in the urine.

Indications for use
Endocrine Disorders:
- Replacement therapy of primary and secondary (pituitary) insufficiency of the adrenal cortex (except for adrenal insufficiency, in which cortisone or hydrocortisone is used due to a strong mineralocorticoid effect).
- Congenital adrenal hyperplasia.
- Subacute thyroiditis and severe forms of radiation thyroiditis.
Rheumatic diseases:
- rheumatoid arthritis (including juvenile chronic arthritis) and extra-articular lesions in rheumatoid arthritis (lungs, heart, eyes, cutaneous vasculitis) as a transitional therapy during a time when the main therapy is not yet effective, as well as therapy for patients in whom nonsteroidal anti-inflammatory drugs have an unsatisfactory analgesic and anti-inflammatory effect.
Systemic connective tissue diseases, vasculitis and amyloidosis (auxiliary and symptomatic treatment under certain conditions that occur during the underlying disease:
- Systemic lupus erythematosus (treatment of polyserositis and dysfunction of internal organs).
- Sjogren 's syndrome (treatment of disorders of the kidneys, lungs and brain).
- Systemic sclerosis (treatment of myositis, pericarditis and alveolitis).
- Polymyositis, dermatomyositis.
- Systemic vasculitis.
- Amyloidosis (replacement therapy for adrenal insufficiency).
Skin diseases:
- Pemphigus.
- Bullous dermatitis herpetiformis.
- Exfoliative dermatitis.
- Exudative erythema (severe forms).
- Erythema nodosum.
- Seborrheic dermatitis (severe).
- Psoriasis (severe forms).
- Eczema (severe forms)
- Urticaria (in the absence of improvement with standard treatment).
- Fungoid mycoses.
- Scleroderma.
- Quincke's edema.
Allergic diseases (not responding to standard therapy):
- Bronchial asthma.
- Contact dermatitis.
- Atopic dermatitis.
- Serum sickness.
- Allergic rhinitis.
- Hypersensitivity to drugs.
- Hives after blood transfusion.
Eye diseases:
- Disorders that threaten with loss of vision (acute central chorioretinitis, optic neuritis), allergic diseases (conjunctivitis, uveitis, scleritis, keratitis, iritis).
- Systemic immune disorders (sarcoidosis, temporal arteritis).
- Proliferative changes in the orbit (endocrine ophthalmopathy, pseudotumor).
- Sympathetic ophthalmia.
- Immunosuppressive therapy for corneal transplantation.
Gastrointestinal Disorders:
- Nonspecific ulcerative colitis (severe exacerbations).
- Crohn's disease (severe exacerbations).
- Chronic autoimmune hepatitis.
- Rejection reactions after liver transplantation.
Respiratory system diseases:
- Acute toxic bronchitis.
- Chronical bronchitis.
- Allergic bronchopulmonary aspergillosis.
- Exogenous allergic alveolitis.
- Idiopathic fibrosing alveolitis.
- Sarcoidosis.
- Eosinophilic infiltrate.
- Fulminant or disseminated pulmonary tuberculosis (in combination with appropriate anti-tuberculosis chemotherapy).
- Tuberculous pleurisy (in combination with appropriate anti-tuberculosis chemotherapy).
- Pleurisy in systemic connective tissue diseases.
- Pulmonary vasculitis.
- Beryllium disease (granulomatous inflammation).
- Obliterating bronchitis due to poisoning with toxic gases.
- Radiation or aspiration pneumonia.
Blood diseases:
- Congenital or acquired aplastic anemia.
- Autoimmune hemolytic anemia.
- Secondary thrombocytopenia in adults.
- Erythroblastopenia.
- Acute lymphoblastic leukemia (induction therapy).
- Myelodysplastic syndrome.
- Angioimmunoblastic malignant T-cell lymphoma (in combination with cytostatics).
- Plasmacytoma (in combination with cytostatics).
- Anemia after myelofibrosis with myeloid metaplasia or lymphoplasmacytoid immunocytoma.
- Systemic histiocytosis (systemic process).
Kidney disease:
- Primary and secondary glomerulonephritis (Goodpasture syndrome).
- Kidney damage in systemic connective tissue diseases (systemic lupus erythematosus, Sjogren's syndrome).
- Systemic vasculitis (usually in combination with cyclophosphamide).
- Glomerulonephritis with polyarteritis nodosa.
- Churg-Strauss syndrome.
- Wegener's granulomatosis.
- Hemorrhagic vasculitis.
- Mixed cryoglobulinemia.
- Kidney damage with Takayasu arteritis.
- Interstitial nephritis.
- Immunosuppressive therapy after kidney transplantation.
- Induction of diuresis or a decrease in proteinuria in idiopathic nephrotic syndrome (without uremia) and in kidney damage associated with systemic lupus erythematosus.
Malignant diseases:
- Palliative therapy for leukemia and lymphoma in adults.
- Acute leukemia in children.
- Hypercalcemia in malignant neoplasms.
Cerebral edema:
- Cerebral edema due to a primary or metastatic brain tumor, craniotomy or traumatic brain injury.
Other indications:
- Tuberculous meningitis with subarachnoid blockade (in combination with adequate anti-tuberculosis therapy).
- Trichinosis with neurological or myocardial manifestations.
- Diagnostic testing of adrenocortical hyperfunction.

Method of administration and dosage
The dose is set individually depending on the disease, the expected duration of treatment, the tolerance of the corticoids and the response of the body.
Treatment
The recommended starting dose for adults is 0.5 mg to 9 mg per day. The usual maintenance dose is 0.5 mg to 3 mg daily. The daily dose can be divided into 2-4 doses. Initially, the dexamethasone dosage is taken until a clinical response is achieved, then the dosage is gradually reduced to the lowest level at which the dose remains clinically effective. If high dose treatment continues for more than a few days, the dose should be reduced over several consecutive days or even over a longer period of time. During long-term ingestion of high doses, it is recommended that dexamethasone be taken with food, and antacids should be taken between meals.
Patients over 65, patients with kidney and liver diseases
For patients over 65 years of age and patients with kidney and liver diseases, the administration of the drug is recommended with extreme caution and followed by careful medical supervision.
Dosage for children
The recommended oral dose for replacement therapy is 0.02 mg / kg body weight or 0.67 mg / m2 body surface divided into three doses, for other indications the recommended dose is 0.08 mg - 0.3 mg / kg body weight body or 2.5 mg - 10 mg / m2 of body surface, divided into three or four doses.
For doses that cannot be achieved with this dosage form, other forms of the drug are available.
Diagnostic tests for hyperfunction of the adrenal cortex
Short 1 mg dexamethasone test: 1 mg dexamethasone by mouth at 11:00 pm; blood sampling for determination of serum cortisol 8.00 the next day. Special 2-day test with 2 mg dexamethasone : 2 mg dexamethasone by mouth every 6 hours for 2 days; 24-hour urine is collected to determine the concentration of 17-hydroxycorticosteroids.

Side effects
Side effects that can occur during treatment with dexamethasone are classified into groups depending on the frequency of occurrence:
- very frequent (≥1 / 10),
- frequent (≥1 / 100 to <1/10),
- infrequent (≥1 / 1000 to <1/100),
- rare (≥ 1/10000 to <1/1000),
- very rare (<1/10000), frequency unknown (cannot be estimated from available data).
Side effects associated with short-term treatment with dexamethasone include:
From the immune system
- infrequent: hypersensitivity reactions.
From the endocrine system
- frequent: transient adrenal insufficiency, impaired glucose tolerance.
Metabolic and nutritional disorders
- frequent: decreased carbohydrate tolerance, increased appetite and weight gain,
- infrequent: hypertriglyceridemia.
Psychiatric disorders
- frequent: mental disorders.
From the digestive system
- infrequent: peptic ulcers and acute pancreatitis.
Side effects associated with long-term dexamethasone treatment include:
From the immune system
- infrequent: decreased immune response and increased susceptibility to infections.
From the endocrine system
- frequent: long-term adrenal insufficiency, growth retardation in children and adolescents.
Metabolic and nutritional disorders
- frequent: upper type of obesity.
Violations of the organ of vision
- infrequent: cataracts, glaucoma.
From the vascular system
- infrequent: arterial hypertension.
On the part of the skin and subcutaneous tissue
- frequent: erythema, thinning and fragility of the skin.
On the part of the musculoskeletal system and connective tissue
- frequent: muscle atrophy, osteoporosis,
- infrequent: aseptic bone necrosis. The following side effects associated with dexamethasone treatment may also occur (presented in decreasing order of importance).
From the lymphatic system and the hematopoietic system
- rare: thromboembolic complications, a decrease in the number of monocytes and / or lymphocytes, leukocytosis, eosinophilia (as in other glucocorticoids), thrombocytopenia and non-thrombocytopenic purpura.
From the immune system
- rare: rash, Quincke's edema, bronchospasm, anaphylactic reactions.
From the side of the heart
- very rare: polyfocal ventricular extrasystoles, transient bradycardia, heart failure, myocardial rupture after a recent acute heart attack.
From the vascular system
- infrequent: hypertensive encephalopathy.
From the nervous system
- infrequently: edema of the papillae of the optic nerve and increased intracranial pressure (pseudotumor of the brain) after discontinuation of therapy, dizziness, headache,
- very rare: convulsions.
Psychiatric disorders
- infrequent: changes in personality and behavior, which are most often manifested by euphoria, insomnia, irritability, hyperkinesia, depression,
- rarely: psychoses.
From the endocrine system
- often: adrenal insufficiency and atrophy (decreased response to stress), Itsenko- Cushing's syndrome, irregularity of the menstrual cycle, hirsutism.
Metabolic and nutritional disorders
- rarely: the transition of latent diabetes mellitus to clinically manifest, increased need for insulin or oral hypoglycemic drugs in patients with diabetes mellitus, sodium and water retention, increased potassium loss,
- very rare: hypokalemic alkalosis, negative nitrogen balance due to protein catabolism.
From the digestive system
- infrequent: nausea, hiccups, stomach or duodenal ulcers,
- very rarely: esophagitis, perforation of ulcers and bleeding of the gastrointestinal tract (hematomesis, melena), pancreatitis, perforation of the gallbladder and intestines (especially in patients with chronic inflammatory diseases of the large intestine).
On the part of the musculoskeletal system and connective tissue
- frequent: muscle weakness, steroid myopathy (muscle weakness due to catabolism of muscle tissue),
- very rare: compression fractures of the vertebrae, tendon ruptures (especially when some quinolines are used together).
On the part of the skin and subcutaneous tissue
- frequent: slowing down the healing of wounds, striae, petechiae and ecchymosis, increased sweating, acne, suppression of skin reactions during allergological tests,
- very rare: allergic dermatitis, urticaria.
Violations of the organ of vision
- infrequent: increased intraocular pressure,
- very rare: exophthalmos.
From the reproductive system and mammary glands
- rarely: impotence
General violations and violations at the injection site
- very rare: edema.
Signs and symptoms of glucocorticosteroid withdrawal syndrome
If a patient who has been taking glucocorticosteroids for a long time, quickly reduce the dose of the drug, signs of adrenal insufficiency, arterial hypotension, and death may develop.
In some cases, withdrawal symptoms may be similar to symptoms and signs of exacerbation or recurrence of the disease for which the patient was receiving treatment.
If severe adverse events develop, treatment should be discontinued.

Contraindication
Hypersensitivity to the active substance or other ingredients of the drug.
Acute viral, bacterial and systemic fungal infections (without appropriate treatment).
Cushing's Syndrome.
Vaccination with a live vaccine.
Simultaneous use of dexamethasone and ritodrin during childbirth.

Overdose
There are isolated reports of cases of acute overdose or death due to acute overdose. Overdose usually manifests itself only after a few weeks of excessive doses and can cause most of the undesirable effects listed in the "Adverse Reactions" section, especially Cushing's syndrome.
A single intake of a large number of tablets does not lead to clinically significant intoxication.
There is no known specific antidote. Treatment is supportive and symptomatic.
Hemodialysis is not effective in accelerating the elimination of dexamethasone from the body.

Precautions
Patients undergoing long-term dexamethasone treatment may experience corticosteroid withdrawal (also without noticeable signs of adrenal insufficiency) after stopping therapy (fever, nasal discharge, conjunctival redness, headache, dizziness, drowsiness or irritability, muscle and joint pain, vomiting, weight loss, weakness, and frequent seizures). Therefore, the dose of dexamethasone should be gradually reduced. Abrupt discontinuation of the drug can be fatal.
If during therapy or when the drug is discontinued, the patient is exposed to severe stress (trauma, surgery, or serious illness), then the dose of dexamethasone should be increased or hydrocortisone or cortisone is prescribed. Patients who have undergone severe stress after long-term withdrawal; taking dexamethasone, dexamethasone should be resumed, since induced adrenal insufficiency may persist for several months after discontinuation of treatment.
Treatment with dexamethasone or natural glucocorticoids may mask signs of existing or new infection and signs of interstitial perforation in patients with ulcerative colitis.
Dexamethasone can exacerbate the course of systemic fungal infections, latent amebiasis and pulmonary tuberculosis.
In patients with active pulmonary tuberculosis, dexamethasone should be prescribed (in combination with anti-tuberculosis therapy) only in cases of fulminant or severe disseminated pulmonary tuberculosis. Patients with inactive tuberculosis who are taking dexamethasone or those with a positive tuberculin reaction should receive chemoprophylaxis.
It is necessary to take special care and conduct close medical supervision of patients with osteoporosis, hypertension, heart failure, tuberculosis, glaucoma, liver failure, renal failure, diabetes, active gastric and duodenal ulcers, fresh intestinal anastomosis, ulcerative colitis and epilepsy. Particular attention should be paid to patients in the first weeks after myocardial infarction, in patients with thromboembolism, myasthenia gravis, glaucoma, hypothyroidism, psychosis or psychoneurosis, and in patients over 65 years of age.
During treatment with dexamethasone, an exacerbation of diabetes or a transition from a latent form to a form of clinical manifestations of diabetes may occur.
Serum potassium should be monitored during long-term treatment.
Vaccination with live vaccines is contraindicated during treatment with dexamethasone.
Immunization with killed viral or bacterial vaccines does not lead to the expected increase in antibodies and does not provide the expected protective effect.
Dexamethasone is usually not given 8 weeks before and 2 weeks after vaccination.
Patients receiving or taking high doses of dexamethasone for a long time should avoid contact with patients with measles; in case of accidental contact, prophylactic treatment with immunoglobulin is recommended.
Caution is required in patients recovering from recent surgery and bone fracture, as dexamethasone can slow the healing of wounds and fractures.
The action of glucocorticoids is potentiated in patients with liver cirrhosis or hypothyroidism.
Corticosteroids can interfere with the results of allergic skin tests.
Severe mental reactions may accompany systemic use of corticosteroids. Symptoms usually appear several days or weeks after starting treatment. The risk of developing these symptoms increases with high doses. Most reactions resolve with dose reduction or drug withdrawal. It is necessary to observe and timely identify changes in the mental state, especially depressive mood, suicidal thoughts and intentions. Corticosteroids should be used with extreme caution in patients with a history of mood disorders, as well as in the immediate family.
To avoid the appearance of undesirable effects, it is recommended to use the minimum effective dose for the shortest possible period. Patients should have a “steroid treatment card” in hand, which provides clear recommendations on the necessary precautions to minimize risk, as well as a description of the medication, dosage and duration of treatment.
Children
Dexamethasone is used in children and adolescents only under strict indications. During treatment with dexamethasone, it is necessary to carefully monitor the development of children and adolescents.

Interaction with other medicinal products
The simultaneous use of dexamethasone and non-steroidal anti-inflammatory drugs increases the risk of gastrointestinal bleeding and ulcers.
The effect of dexamethasone is reduced with the simultaneous administration of drugs that activate the CYP3A4 enzyme (for example, phenytoin, phenobarbitone, carbamazepine, primidone, rifabutin, rifampicin) or that increase the clearance of glucocorticoids (ephedrine and aminoglutethimide); therefore, in these cases, it is necessary to increase the dose of dexamethasone.
Interaction between dexamethasone and the above drugs can distort the results of dexamethasone suppressive tests. If tests with dexamethasone are to be performed during therapy with one of the listed drugs, this interaction should be considered when interpreting the test results.
The simultaneous use of dexamethasone and inhibitors of the isoenzyme CYP 3A4 (for example, ketoconazole, macrolide antibiotics) may lead to an increase in the concentration of dexamethasone in the blood.
Concomitant use of drugs that are metabolized by CYP 3A4 (eg, indinavir, erythromycin) may increase their clearance, which may be accompanied by a decrease in their serum concentrations.
By inhibiting the CYP 3A4 enzyme, ketoconazole can increase plasma concentrations of dexamethasone. On the other hand, ketoconazole can suppress the synthesis of glucocorticoids in the adrenal glands, therefore, with a decrease in the dose of dexamethasone, adrenal insufficiency can develop. Dexamethasone reduces the therapeutic effect of hypoglycemic drugs, antihypertensive drugs, praziquantel and natriuretics (the dosage of these drugs should be increased), but it potentiates the activity of heparin, albendazole and potassium-sparing diuretics (if necessary, the dosage of these drugs should be reduced).
Dexamethasone can alter the action of coumarin anticoagulants ; therefore, during simultaneous use, more frequent monitoring of prothrombin time is recommended.
The combined use of high doses of glucocorticoids and beta - receptor agonists increases the risk of hypokalemia. In patients with hypokalemia, there is an increased arrhythmogenicity and toxicity of cardiac glycosides.
Antacids reduce the absorption of dexamethasone in the stomach. The effect of the combined use of dexamethasone with food or alcohol has not been studied ; however, concomitant use with drugs and foods high in sodium is not recommended. Smoking does not affect the pharmacokinetics of dexamethasone.
Glucocorticoids accelerate the renal clearance of salicylates, so it is sometimes difficult to achieve therapeutic serum salicylates. Caution should be exercised in patients who have been gradually reduced the dose of corticosteroids, since an increase in the concentration of salicylates in the serum and salicylate intoxication may occur.
When taken together with oral contraceptives, the half-life of glucocorticoids may increase, which enhances their biological effect and increases the frequency of side effects.
During childbirth, the combined use of rithodrin and dexamethasone is contraindicated, since this can lead to the death of the mother due to pulmonary edema.
The combined use of dexamethasone and thalidomide can cause toxicodermal necrolysis.
Interactions with possible beneficial therapeutic effects.
The combined use of dexamethasone and metoklopromida, diphenhydramine, prochlorperazine or receptor antagonists, 5-HT3 (serotonin or 5-hydroxytryptamine receptor type 3, such as ondansetron or granisetron) is effective to prevent nausea and vomiting caused by chemotherapy (cisplatin, cyclophosphamide, methotrexate, fluorouracil)...

Special instructions
It should be used with caution in parasitic and infectious diseases of a viral, fungal or bacterial nature (currently or recently transferred, including recent contact with a patient) - herpes simplex, herpes zoster (viremic phase), chickenpox, measles, amebiasis, strongyloidosis (established or suspect), systemic mycosis; active and latent tuberculosis. Application for severe infectious diseases is permissible only against the background of specific therapy.
It should be used with caution within 8 weeks before and 2 weeks after vaccination, with lymphadenitis after BCG vaccination, with immunodeficiency conditions (including AIDS or HIV infection).
It should be used with caution in diseases of the gastrointestinal tract: gastric ulcer and duodenal ulcer, esophagitis, gastritis, acute or latent peptic ulcer, newly created intestinal anastomosis, ulcerative colitis with the threat of perforation or abscess formation, diverticulitis.
It should be used with caution in diseases of the cardiovascular system, incl. after a recent myocardial infarction (in patients with acute and subacute myocardial infarction, it is possible to spread the focus of necrosis, slow down the formation of scar tissue and, as a result, rupture of the heart muscle), with decompensated chronic heart failure, arterial hypertension, hyperlipidemia), with endocrine diseases - diabetes mellitus (in incl. tackle tolerance to carbohydrates), hyperthyroidism, hypothyroidism, diseases Itsenko- Cushing, with severe chronic renal and / or liver failure, nefrourolitiaze at hypoalbuminemia and conditions predisposing to its occurrence, for systemic osteoporosis, myasthenia gravis, acute psychosis,, obesity (III-IV degree) in poliomyelitis (except bulbar form of encephalitis), open-and -closure g laukome.
If necessary, intraarticular injection should be used with caution in patients with a general severe condition, ineffectiveness (or short duration) of the action of 2 previous injections (taking into account the individual properties of the GCS used).
Before and during GCS therapy, it is necessary to monitor a complete blood count, glycemic level and the content of electrolytes in plasma.
With intercurrent infections, septic conditions and tuberculosis, it is necessary to simultaneously carry out antibiotic therapy.
Caused by dexamethasone relative adrenal insufficiency may persist for several months after its cancellation. Taking this into account, in stressful situations that arise during this period, hormonal therapy is resumed with the simultaneous administration of ole and / or mineralocorticoids.
When using dexamethasone in patients with corneal herpes, the possibility of corneal perforation should be borne in mind. During treatment, it is necessary to monitor intraocular pressure and the condition of the cornea.
With the sudden withdrawal of dexamethasone, especially in the case of previous use in high doses, the so-called withdrawal syndrome (not caused by hypocorticism) occurs, manifested by anorexia, nausea, lethargy, generalized musculoskeletal pain, general weakness. After discontinuation of dexamethasone, a relative insufficiency of the adrenal cortex may persist for several months. If during this period stressful situations arise, they are prescribed (according to indications) for the time of GCS, if necessary, in combination with mineralocorticoids.
During the treatment period, monitoring of blood pressure, water-electrolyte balance, peripheral blood picture and glycemic level, as well as observation of an ophthalmologist is required.
In children, during long-term treatment, careful monitoring of the dynamics of growth and development is necessary. Children who, during the period of treatment, were in contact with patients with measles or chickenpox, are prophylactically prescribed specific immunoglobulins.

Pregnancy and elbowing
The drug slows down the intrauterine development of the fetus. Dexamethasone ; should be prescribed to pregnant women only in isolated cases when the expected benefit to the mother justifies the risk to the fetus.
Particular care should be taken with preeclampsia. According to the general recommendations for treatment with glucocorticoids, the lowest effective dose should be used during pregnancy to control the underlying disease. Children whose mothers have taken high doses of corticosteroids for a long time during pregnancy should be closely monitored for possible adrenal insufficiency. Glucocorticosteroids cross the placenta and can reach high concentrations in the fetus. Dexamethasone is less extensively metabolized in the placenta than, for example, with prednisone, so high concentrations of dexamethasone can be determined in the fetus. Therapeutic doses of glucocorticoids can increase the risk of placental insufficiency, oligohydramnios, fetal growth and development retardation or intrauterine death, increase the number of leukocytes (neutrophils) in a child, as well as the risk of developing adrenal insufficiency.
In small amounts, glucocorticoids are excreted in breast milk. Therefore, breastfeeding is not recommended for mothers taking dexamethasone, especially when using high physiological doses (about 1 mg), as this can lead to fetal growth retardation and a decrease in the secretion of endogenous corticosteroids.

Influence on the ability to drive vehicles and work with mechanisms
Does not affect.

Storage conditions
Store in a dry, dark place at a temperature not exceeding 25 ° C, out of the reach of children.

Shelf life
3 years. Do not use after the expiration date printed on the package.

Vacation conditions
On prescription.

Packaging
Dexamethasone 0.5 mg Tablets. There are 25 tablets in a blister. 2 blisters are packed in a cardboard box together with an enclosed leaflet.