Dexamethasone tablets 0.5 mg blister No. 10

Instructions Dexamethasone tablets 0.5 mg blister No. 10

Composition

active ingredient: dexamethasone;

1 tablet contains 0.5 mg of dexamethasone;

excipients: lactose monohydrate, pregelatinized starch, magnesium stearate, colloidal anhydrous silicon dioxide.

Dosage form

Pills.

Main physicochemical properties: round, white or almost white tablets with beveled edges.

Pharmacotherapeutic group

Corticosteroids for systemic use, glucocorticoids.

ATX code H02A B02.

Pharmacological properties

Pharmacodynamics.

Dexamethasone is a semisynthetic adrenal hormone (corticosteroid) with glucocorticoid activity. It has anti-inflammatory and immunosuppressive effects, and also affects energy metabolism, glucose metabolism, and (via negative feedback) the secretion of hypothalamic-activating factor and adenohypophyseal trophic hormone.

The mechanism of action of glucocorticoids is still not fully understood. There are now enough reports on the mechanism of action of glucocorticoids to confirm that they act at the cellular level. There are two well-defined receptor systems in the cytoplasm of cells. By binding to glucocorticoid receptors, corticosteroids exert anti-inflammatory and immunosuppressive effects and regulate glucose metabolism, and by binding to mineralocorticoid receptors, they regulate sodium, potassium metabolism and water-electrolyte balance.

Glucocorticoids are lipid-soluble and readily cross the cell membrane into target cells. Binding of the hormone to the receptor causes a conformational change in the receptor, which increases its affinity for DNA. The hormone/receptor complex enters the nucleus of the cell and binds to a regulatory center of the DNA molecule, also called the glucocorticoid response element (GRE). The activated receptor, bound to the GRE or to specific genes, regulates mRNA transcription, which can be increased or decreased. The newly formed mRNA is transported to the ribosome, after which new proteins are formed. Depending on the target cells and the processes occurring in the cells, protein synthesis can be increased (for example, the formation of tyrosine transaminase in liver cells) or decreased (for example, the formation of IL-2 in lymphocytes). Since glucocorticoid receptors are present in all types of tissues, it can be assumed that glucocorticoids act on most cells of the body.

Impact on energy metabolism and glucose homeostasis

Dexamethasone, together with insulin, glucagon and catecholamines, regulates energy storage and utilization. In the liver, glucose formation from pyruvate or amino acids and glycogen formation are increased. In peripheral tissues, especially in muscle, glucose consumption and mobilization of amino acids (from proteins), which are substrates for gluconeogenesis in the liver, are reduced. Direct effects on fat metabolism are a central distribution of adipose tissue and an increase in the lipolytic response to catecholamines.

Using receptors in the renal proximal tubules, dexamethasone increases renal blood flow and glomerular filtration, inhibits the formation and secretion of vasopressin, and improves the kidneys' ability to excrete acids from the body.

By increasing the number of β-adrenergic receptors and the affinity for β-adrenergic receptors that transmit the positive inotropic effect of catecholamines, dexamethasone directly increases cardiac contractility and peripheral vascular tone.

When used in high doses, dexamethasone inhibits fibroblast production of collagen types I and III and the formation of glycosaminoglycans. Thus, due to the inhibition of the formation of extracellular collagen and matrix, wound healing is delayed. Long-term administration in high doses causes progressive bone resorption by indirect action and reduces osteogenesis by direct action (increased secretion of parathyroid hormone and decreased secretion of calcitonin), and also causes a negative calcium balance by reducing calcium absorption in the intestine and increasing its excretion in the urine. This usually leads to secondary hyperparathyroidism and phosphaturia.

Effects on the pituitary gland and hypothalamus

The anti-inflammatory and immunosuppressive effects of glucocorticoids are based on their molecular and biochemical effects. The molecular anti-inflammatory effect occurs as a result of binding to glucocorticoid receptors and changing the expression of a number of genes that regulate the formation of various information molecules, proteins and enzymes involved in the inflammatory reaction. The biochemical anti-inflammatory effect of glucocorticoids is the result of blocking the formation and functioning of humoral mediators of inflammation: prostaglandins, thromboxanes, cytokines and leukotrienes. Dexamethasone reduces the formation of leukotrienes by reducing the release of arachidonic acid from cellular phospholipids due to inhibition of the activity of phospholipase A2. The effect on phospholipase is achieved not by direct action, but as a result of increasing the concentration of lipocortin (macrocortin), which is an inhibitor of phospholipase A2. Dexamethasone inhibits the formation of prostaglandins and thromboxane by reducing the formation of specific mRNA and, consequently, the amount of cyclooxygenase formed. Dexamethasone also reduces the production of platelet-activating factor (PAF) by increasing the concentration of lipocortin. Other biochemical anti-inflammatory effects include a decrease in the formation of tumor necrosis factor (TNF) and interleukin 1 (IL-1).

Pharmacokinetics.

Dexamethasone is rapidly and almost completely absorbed after oral administration. The bioavailability of dexamethasone tablets is approximately 80% (various literature sources indicate bioavailability from 53 to 112%). The maximum concentration in the blood plasma after oral administration is reached after 1–2 hours, the duration of the effect after taking a single dose is approximately 2.75 days.

In blood plasma, approximately 77% of dexamethasone is bound to plasma proteins, mainly albumin. Only a small amount of dexamethasone is bound to other proteins. Dexamethasone is fat-soluble, so it freely penetrates cells and the intercellular space. In the central nervous system (hypothalamus, pituitary gland), it binds and acts through membrane receptors. In peripheral tissues, it binds and acts through cytoplasmic receptors. Its destruction occurs at the site of action, i.e. in the cell itself. Dexamethasone is primarily metabolized in the liver, but also, possibly, in the kidneys and other tissues. It is excreted mainly in the urine.

Indication

Endocrine disorders:

Replacement therapy for primary or secondary (pituitary) adrenal insufficiency (except acute adrenal insufficiency, in which hydrocortisone or cortisone are the drugs of choice, given their more pronounced hormonal effect); congenital adrenal hyperplasia; thyroiditis, subacute form and severe forms of radiation thyroiditis.

Rheumatic diseases:

rheumatoid arthritis, including juvenile rheumatoid arthritis and extra-articular manifestations of rheumatoid arthritis (rheumatic lung, changes in the heart and eyes, cutaneous vasculitis), as adjunctive therapy in the period when basic therapy has not yet had an effect and in cases where the analgesic and anti-inflammatory effects of non-steroidal anti-inflammatory drugs (NSAIDs) were unsatisfactory.

Systemic connective tissue diseases, vasculitic syndromes and amyloidosis (supportive and symptomatic treatment in certain cases during the underlying disease):

systemic lupus erythematosus (treatment of polyserositis and damage to internal organs); Sjögren's syndrome (treatment of pulmonary, renal and cerebral lesions);

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 forms);

psoriasis (severe forms);

herpes;

hives that do not respond to standard treatment;

mycosis fungoides;

scleroderma;

Quincke's edema.

Allergic diseases (not amenable to standard treatment):

asthma, contact dermatitis, atopic dermatitis, serum sickness, allergic rhinitis, drug allergy, urticaria after blood transfusion.

Diseases of the organs of vision:

inflammatory eye diseases (acute central choroiditis, optic neuritis), allergic diseases (conjunctivitis, uveitis, scleritis, keratitis, iritis);

systemic immune diseases (sarcoidosis, temporal arteritis);

proliferative changes in the orbit (endocrine ophthalmopathy, pseudotumor);

sympathetic ophthalmia;

immunosuppressive therapy during corneal transplantation.

Gastrointestinal diseases:

ulcerative colitis (severe exacerbation), Crohn's disease (severe exacerbation), chronic autoimmune hepatitis, liver transplant rejection.

Respiratory tract diseases:

acute toxic bronchiolitis, chronic bronchitis, allergic bronchopulmonary aspergillosis, exogenous allergic alveolitis, idiopathic fibrosing alveolitis, sarcoidosis, eosinophilic infiltration, focal or disseminated pulmonary tuberculosis (together with appropriate anti-tuberculosis therapy), tuberculous pleurisy (together with appropriate anti-tuberculosis therapy), pleurisy in systemic connective tissue diseases, pulmonary vasculitis, berylliosis (granulomatous inflammation);

radiation or aspiration pneumonitis.

Hematological diseases:

acquired or congenital chronic 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), severe anemia after myelofibrosis with myeloid metaplasia or with lymphoplasmacytoid immunocytoma, systemic histiocytosis (systemic dependence).

Kidney diseases:

primary and secondary glomerulonephritis (Goodpasture syndrome), renal failure in systemic connective tissue diseases (systemic lupus erythematosus, Sjögren's syndrome), systemic vasculitis (usually in combination with cyclophosphamide), glomerulonephritis in polyarthritis nodosa, Churg–Strauss syndrome, Wegener's granulomatosis, Schönlein–Henoch purpura, mixed cryoglobulinemia, renal failure in Tayakasu arteritis, interstitial nephritis, immunosuppressive therapy in kidney transplantation, diuresis induction and proteinuria reduction in idiopathic nephrotic syndrome (without uremia) and renal failure in systemic lupus erythematosus.

Oncological diseases:

palliative treatment of leukemia and lymphoma in adults, acute leukemia in children, hypercalcemia in malignant diseases.

Brain swelling:

cerebral edema due to primary or metastatic brain tumor, craniotomy, and traumatic brain injury.

Other indications:

tuberculous meningitis with subarachnoid block (along with appropriate anti-tuberculosis therapy), trichinosis with neurological symptoms or myocardial trichinosis, diagnostic test for adrenal hyperfunction.

Contraindication

Hypersensitivity to dexamethasone or to any other ingredient of the drug. Acute viral, bacterial or systemic fungal infections (if appropriate therapy is not used), Cushing's syndrome, vaccination with a live vaccine, and breastfeeding (except in urgent cases).

Interaction with other medicinal products and other types of interactions

Concomitant use of dexamethasone and NSAIDs increases the risk of gastrointestinal bleeding and ulceration.

The effect of dexamethasone is reduced by concomitant use of drugs that activate the CYP 3A4 enzyme (phenytoin, phenobarbital, carbamazepine, primidone, rifabutin, rifampicin) or increase the metabolic clearance of glucocorticoids (ephedrine and aminoglutethimide); in these cases, the dose of dexamethasone should be increased. Interactions between dexamethasone and all of the above-mentioned drugs may distort the dexamethasone suppression test. This should be taken into account when interpreting the test results.

Concomitant use of dexamethasone and drugs that inhibit CYP 3A4 enzyme activity (ketoconazole, macrolides) may lead to an increase in serum concentrations of dexamethasone. Dexamethasone is a moderate inducer of CYP 3A4. Concomitant use with drugs that are metabolized by CYP 3A4 (indinavir, erythromycin) may increase their clearance, leading to a decrease in serum concentrations.

By inhibiting the enzyme CYP 3A4, ketoconazole may increase the serum concentration of dexamethasone. On the other hand, ketoconazole may inhibit adrenal synthesis of glucocorticoids, thus, adrenal insufficiency may develop due to a decrease in dexamethasone concentration.

Dexamethasone reduces the therapeutic effect of antidiabetic and antihypertensive drugs, praziquantel and natriuretics (therefore, the dose of these drugs should be increased), but increases the activity of heparin, albendazole and kaliuretics (the dose of these drugs should be reduced if necessary).

Dexamethasone may alter the effect of coumarin anticoagulants, so when using this combination, prothrombin time should be checked more frequently.

Concomitant use of high doses of glucocorticoids and b2-adrenoceptor agonists increases the risk of hypokalemia. In patients with hypokalemia, cardiac glycosides are more likely to cause arrhythmias and are more toxic.

Dexamethasone reduces the therapeutic effect of anticholinesterase agents used for myasthenia gravis.

Antacids reduce the absorption of dexamethasone in the stomach. The effect of dexamethasone when taken with food and alcohol has not been studied, but simultaneous use of the drug and food with a high sodium content is not recommended. Smoking does not affect the pharmacokinetics of dexamethasone.

Glucocorticoids increase renal clearance of salicylate, making it difficult to achieve therapeutic serum concentrations of salicylates. Caution should be exercised in patients who are gradually tapering their corticosteroid dose, as this may result in increased serum salicylate concentrations and intoxication.

If oral contraceptives are used concurrently, the half-life of glucocorticoids may be prolonged, which enhances their biological effects and may increase the risk of side effects.

Concomitant use of dexamethasone and thalidomide may cause toxic epidermal necrolysis.

Types of interactions that have therapeutic benefits: concurrent administration of dexamethasone and metoclopramide, diphenhydramide, prochlorperazine, or 5-HT3 receptor antagonists (serotonin or 5-hydroxytryptamine receptors, type 3, such as ondansetron or granisetron) is effective for the prevention of nausea and vomiting caused by chemotherapy with cisplatin, cyclophosphamide, methotrexate, fluorouracil.

Concomitant use with CYP3A inhibitors, including cobicistat-containing products, is expected to increase the risk of systemic adverse reactions. This combination should be avoided unless the benefit outweighs the risk of systemic corticosteroid adverse reactions. In such cases, patients should be monitored for systemic corticosteroid effects.

Application features

Systemic use of corticosteroids may be associated with severe psychiatric reactions. Symptoms usually appear within a few days or weeks of initiation of treatment. The risk of these symptoms increases with higher doses. Most reactions resolve with dose reduction or discontinuation of the drug. Changes in mental status, especially depressed mood, suicidal thoughts and intentions, should be monitored and promptly identified. Corticosteroids should be used with particular caution in patients with a history of affective disorders, in particular in patients with a history of allergic reactions to any other drugs, or in patients with a family history of such reactions. Undesirable effects can be avoided by using the lowest effective dose for the shortest possible period or by taking the required daily dose once in the morning.

In patients treated with dexamethasone for a long time, upon discontinuation of treatment, a withdrawal syndrome (without visible signs of adrenal insufficiency) may occur with the following symptoms: fever, runny nose, conjunctival redness, headache, dizziness, drowsiness or irritability, muscle and joint pain, vomiting, weight loss, general weakness, and convulsions are also common. Therefore, the dose of dexamethasone should be reduced gradually. Abrupt discontinuation may be fatal.

If the patient is under severe stress (due to trauma, surgery, or serious illness) during therapy, the dose of dexamethasone should be increased, and if this occurs during discontinuation of treatment, hydrocortisone or cortisone should be used.

Patients who have been on dexamethasone for a long time and who experience severe stress after stopping therapy should resume dexamethasone, as the adrenal insufficiency it causes may persist for several months after stopping treatment. Treatment with dexamethasone or natural glucocorticoids may mask symptoms of existing or new infection, as well as symptoms of intestinal perforation.

Dexamethasone may exacerbate systemic fungal infection, latent amebiasis, and pulmonary tuberculosis.

Patients with active pulmonary tuberculosis should receive dexamethasone (along with anti-tuberculosis drugs) only for transient or severe disseminated pulmonary tuberculosis. Patients with inactive pulmonary tuberculosis treated with dexamethasone or patients who respond to tuberculin should receive chemical prophylactics.

Caution and medical supervision are recommended in patients with osteoporosis, arterial hypertension, heart failure, tuberculosis, glaucoma, hepatic or renal failure, diabetes, active peptic ulcer, recent intestinal anastomosis, ulcerative colitis and epilepsy. Special care is required in patients during the first weeks after myocardial infarction, patients with thromboembolism, myasthenia gravis, glaucoma, hypothyroidism, psychosis or psychoneurosis, as well as elderly patients.

During treatment, exacerbation of diabetes or transition from the latent phase to clinical manifestations of diabetes is possible.

During long-term treatment, serum potassium levels should be monitored.

Vaccination with live vaccines is contraindicated during treatment with dexamethasone. Vaccination with inactivated viral or bacterial vaccines does not induce the expected antibody response and does not have the expected protective effect. Dexamethasone should usually be administered 8 weeks before vaccination and not started earlier than 2 weeks after.

Patients who are treated with high doses of dexamethasone for a long time and have never had measles should avoid contact with infected individuals; in case of accidental contact, prophylactic treatment with immunoglobulin is recommended.

Caution is advised in patients recovering from surgery or bone fractures, as dexamethasone may slow wound healing and bone formation.

The effect of glucocorticoids is enhanced in patients with liver cirrhosis or hypothyroidism.

In a post-marketing study in patients with hematological malignancies, tumor lysis syndrome (TLS) was observed after the use of dexamethasone alone or in combination with other chemotherapeutic agents. Patients at high risk of TLS, such as those with high proliferation rate, large tumor mass, and high sensitivity to cytotoxic agents, should be closely monitored and appropriate precautions should be taken.

Vision impairment

Systemic and topical glucocorticoid treatment may cause visual impairment. If blurred or other visual impairment occurs, the patient should be referred for an ophthalmological examination to determine the cause, which may include cataracts, glaucoma, or the rare disease chorioretinopathy, which have been reported with systemic and topical corticosteroid use.

Pheochromocytoma crisis

Pheochromocytoma crisis, which can be fatal, has been reported following the use of systemic corticosteroids. Corticosteroids should be administered to patients with suspected or identified pheochromocytoma only after an appropriate risk/benefit assessment.

Special precautions for excipients

The drug contains lactose, so it should not be taken by patients with rare hereditary problems of galactose intolerance, the Lapp lactase deficiency or glucose-galactose malabsorption.

Use during pregnancy or breastfeeding

Pregnancy

Harmful effects on the fetus and newborn cannot be excluded. The drug inhibits intrauterine development of the child. Dexamethasone should be administered to pregnant women only in exceptional cases of emergency, when the expected benefit to the mother outweighs the potential risk to the fetus. Particular caution is recommended in preeclampsia. In accordance with general recommendations for treatment with glucocorticoids during pregnancy, the lowest effective dose should be used to control the underlying disease. Children whose mothers have taken glucocorticoids during pregnancy should be carefully monitored for adrenal insufficiency.

Glucocorticoids cross the placenta and reach high concentrations in the fetus. Dexamethasone is less extensively metabolized in the placenta than, for example, prednisone. Therefore, high concentrations of dexamethasone may be detected in the fetal serum. According to some data, even pharmacological doses of glucocorticoids may increase the risk of placental insufficiency, oligohydramnios, fetal growth retardation or intrauterine death, increased fetal leukocyte (neutrophil) counts, and adrenal insufficiency. There is no evidence to support the teratogenic effect of glucocorticosteroids. Administration of corticosteroids to pregnant female animals has resulted in fetal malformations, including cleft palate, intrauterine growth retardation, and effects on brain growth and development. There is no evidence that corticosteroids increase the incidence of congenital anomalies such as cleft lip in humans.

It is recommended to use additional doses of glucocorticosteroids during labor for women who took glucocorticosteroids during pregnancy. In case of prolonged labor or planned cesarean section, intravenous administration of 100 mg of hydrocortisone every 8 hours is recommended.

Breast-feeding

Small amounts of glucocorticoids are excreted in breast milk, so women treated with dexamethasone are not recommended to breastfeed, especially when using the drug in excess of physiological norms (about 1 mg). This may lead to a slowdown in the growth of the child and a decrease in the secretion of endogenous corticosteroids.

Ability to influence reaction speed when driving vehicles or other mechanisms

Dexamethasone does not affect the ability to drive a car or other mechanical devices.

Method of administration and doses

The dose should be determined individually according to the specific patient's disease, the intended period of treatment, corticosteroid tolerance, and the body's response.

Treatment

The recommended starting dose for adults is 0.5–9 mg per day. The maintenance dose is usually 0.5–3 mg per day. The daily dose can be divided into 2–4 doses.

Initial doses of dexamethasone should be used until a clinical response is obtained, and then the dose should be gradually reduced to the lowest clinically effective dose. If oral treatment with high doses is continued for more than a few days, the dose should be gradually reduced over several consecutive days or even longer (usually by 0.5 mg over three days). The maximum daily dose is usually 15 mg, the minimum effective dose is 0.5–1 mg per day.

During long-term treatment with high doses, it is recommended to take dexamethasone with food and use antacids between meals.

Dosage for children

The recommended oral dose for replacement therapy is 0.02 mg/kg body weight, or 0.67 mg/m2 body surface area, per day in 3 divided doses.

For all other indications, the initial dose range is 0.08–0.3 mg/kg/day or 2.5–10 mg/m2 body surface area/day in 3–4 divided doses.

The dexamethasone test (Liddle test) is performed in the form of a small and large test.

During the mini-test, dexamethasone is administered at 0.5 mg every 6 hours for 48 hours (namely: at 8 am, 2 pm, 8 pm, and 2 am). Before and after the administration of dexamethasone, the content of 17-hydroxycorticosteroid or free cortisol in the daily urine is determined. The above doses of dexamethasone suppress the formation of corticosteroids in almost all healthy volunteers. 6 hours after the last dose of dexamethasone, the plasma cortisol content is less than 135–138 nmol/l (4.5–5 μg/100 ml). A decrease in the excretion of 17-hydroxycorticosteroid less than 3 mg/day and free cortisol less than 54–55 nmol/day (19–20 μg/day) excludes adrenal hyperfunction. In individuals with Itsenko-Cushing's disease or syndrome, corticosteroid excretion is not altered when performing a small test.

During a major test, dexamethasone is administered at a dose of 2 mg every 6 hours for 48 hours (i.e., 8 mg of dexamethasone per day). Urine is also collected to determine 17-hydroxycorticosteroid or free cortisol (if necessary, free cortisol in plasma is determined). In Itsenko-Cushing's disease, a decrease in the excretion of 17-hydroxycorticosteroid or free cortisol by 50% or more is observed, while in adrenal tumors or ACTH-ectopic (or corticoliberin-ectopic) syndrome, corticosteroid excretion does not change. In some patients with ACTH-ectopic syndrome, a decrease in corticosteroid excretion is not detected even after taking dexamethasone at a dose of 32 mg/day.

Equivalent doses of corticosteroids

These dosage ratios apply only to oral or intravenous administration of these drugs. When these drugs or their derivatives are administered intramuscularly or intraarticularly, their relative properties may change significantly.

Children.

Use in children from birth only if clearly needed. During treatment with dexamethasone, careful monitoring of the growth and development of children and adolescents is necessary. Premature infants: available data indicate long-term neurological side effects after early treatment (up to 96 hours) of premature infants with chronic lung disease when using an initial dose of 0.25 mg/kg 2 times a day.

Overdose

There have been isolated reports of acute overdose or fatal outcome due to acute overdose.

Overdose, usually only after several weeks of excessive doses, can cause most of the undesirable effects mentioned in the "Adverse reactions" section, primarily Cushing's syndrome.

A single intake of a large number of tablets does not lead to clinically significant intoxication. There is no specific antidote. Treatment of overdose should be supportive and symptomatic. Hemodialysis is not an effective method of accelerating the removal of dexamethasone from the body.

Side effects

Side effects of short-term dexamethasone treatment

Immune system disorders: hypersensitivity reactions.

On the part of the endocrine system: transient suppression of adrenal function.

Metabolism and nutrition: decreased carbohydrate tolerance, increased appetite and weight gain, hypertriglyceridemia.

From the psyche: mental disorders.

Gastrointestinal: peptic ulcer and acute pancreatitis.

Side effects of long-term treatment with dexamethasone

On the part of the immune system: decreased immune response and increased susceptibility to infections.

On the part of the endocrine system: persistent suppression of adrenal function, growth retardation in children and adolescents, premature closure of epiphyseal growth zones.

Metabolism and nutrition disorders: obesity.

From the organs of vision: cataract, glaucoma, chorioretinopathy.

Vascular: hypertension; telangiectasia.

Skin and subcutaneous tissue disorders: thinning of the skin.

Musculoskeletal and connective tissue disorders: muscle atrophy, osteoporosis, aseptic bone necrosis, long bone fractures.

Side effects that may also occur in individual organs and systems during treatment with dexamethasone:

Blood and lymphatic system disorders: thromboembolic complications; decreased monocytes and/or lymphocytes; leukocytosis; eosinophilia (as with other glucocorticosteroids); thrombocytopenia and nonthrombocytopenic purpura.

On the part of the immune system: rash, bronchospasm, anaphylactic reactions, development of opportunistic infections.

Cardiac: multifocal ventricular extrasystole, transient bradycardia, heart failure, cardiac arrest, myocardial perforation due to previous myocardial infarction.

Vascular disorders: hypertensive encephalopathy.

Respiratory, thoracic and mediastinal disorders: relapse of inactive tuberculosis.

On the part of the psyche: personality and behavioral changes are more often manifested in the form of euphoria; insomnia, irritability, hyperkinesia, depression, nervousness, restlessness, manic-depressive psychosis, delirium, disorientation, hallucinations, paranoia, mood lability, suicidal thoughts, psychosis, sleep disorders, confusion, amnesia, worsening of schizophrenia, worsening of epilepsy.

On the part of the endocrine system: suppression of adrenal function and adrenal atrophy (decreased response to stress), Cushing's syndrome, menstrual disorders, hirsutism.

Metabolism and nutrition: transition from latent form to clinical manifestations of diabetes; increased need for insulin and oral antidiabetic drugs in patients with diabetes; sodium and water retention; increased potassium expenditure; hypokalemic alkalosis; negative nitrogen balance due to protein catabolism; hypocalcemia.

Gastrointestinal: dyspepsia, vomiting, nausea, hiccups, peptic ulcer of the stomach or duodenum, esophagitis, perforations and bleeding in the gastrointestinal tract (vomiting with blood, melena), pancreatitis, perforation of the gallbladder and intestinal perforation (especially in patients with inflammatory bowel disease).

Musculoskeletal and connective tissue disorders: muscle weakness, steroid myopathy (muscle weakness caused by muscle catabolism), spinal compression fractures, tendon ruptures (especially when used simultaneously with some quinolines), damage to articular cartilage and bone necrosis (with frequent injections into the joint).

Skin and subcutaneous tissue disorders: delayed wound healing, striae, petechiae and bruises, increased sweating, acne, suppression of skin tests, angioedema, allergic dermatitis, urticaria, skin itching.

On the part of the organs of vision: increased intraocular pressure; exophthalmos; exacerbation of bacterial, fungal or viral eye infections; thinning of the cornea, blurred vision.

From the genitals and mammary glands: impotence, amenorrhea.

General disorders and administration site conditions: transient burning and tingling sensation in the perineum with intravenous administration or with high doses; edema, hyper- or hypopigmentation of the skin, atrophy of the skin and subcutaneous tissue, sterile abscess and skin redness.

Signs of glucocorticoid withdrawal syndrome

In patients who have been treated with dexamethasone for a long time, a withdrawal syndrome may occur when the dose is reduced too rapidly, resulting in adrenal insufficiency, hypotension, or death. In some cases, the signs of withdrawal syndrome may be similar to those of worsening or relapse of the disease for which the patient was being treated. In the event of severe adverse reactions, treatment should be discontinued.

Expiration date

3 years.

Storage conditions

Store in the original package in order to protect from light and moisture. This medicinal product does not require any special temperature storage conditions.

Keep out of reach of children.

Packaging

10 tablets in a blister of aluminum foil / OPA/Al/PVC film, 1 or 2, or 3, or 5, or 6, or 9, or 10 blisters with or without perforation in a cardboard box.

Vacation category

According to the recipe.

Producer

KRKA, dd, Novo mesto/KRKA, dd, Novo mesto.

Address

Smarjeska cesta 6, 8501 Novo mesto, Slovenia.