for 1 tablet
Active ingredient: Dexamethasone 0.50 mg
Excipients: lactose monohydrate, pregelatinized starch, colloidal silicon dioxide, magnesium stearate
When prescribing dexamethasone for intercurrent infections, septic conditions and tuberculosis, it is necessary to simultaneously carry out specific antibacterial therapy when using the drug in patients with latent tuberculosis, lymphadenitis after BCG vaccination, poliomyelitis, with acute and chronic bacterial, parasitic infections; with specific therapy in patients with peptic ulcer of the stomach and / or intestine, osteoporosis.
With daily use for 5 months of treatment, atrophy of the adrenal cortex develops.
May mask some symptoms of infections; it is useless to carry out immunization during treatment.
With the sudden cancellation of corticosteroids, especially in the case of the previous use of high doses, there is a syndrome of "cancellation" of corticosteroids (not due to hypocorticism): loss of appetite, nausea, lethargy, generalized musculoskeletal pain, asthenia, as well as the occurrence of acute adrenal insufficiency (decrease Blood pressure, arrhythmia, increased sweating, weakness, oligoanuria, vomiting, abdominal pain, diarrhea, hallucinations, fainting, coma).
After cancellation, a relative insufficiency of the adrenal cortex remains for several months. If stressful situations arise during this period, prescribe (according to indications) for the time of GCS, if necessary in combination with mineralocorticosteroids.
The dose of dexamethasone must be temporarily increased in stressful situations during therapy (surgery, trauma). A temporary increase in the dose of the drug in stressful situations is necessary both before and after stress.
In children during long-term treatment, careful monitoring of the dynamics of growth and development is necessary. Children who were in contact with measles or chickenpox during the treatment period are given prophylactic immunoglobulins.
During treatment with dexamethasone (especially long-term), it is necessary to observe an ophthalmologist, monitor blood pressure and water-electrolyte balance, as well as pictures of peripheral blood and blood glucose concentration. In order to reduce side effects, you can prescribe anabolic steroids, antacids, as well as increase the intake of K + in the body (eating foods rich in potassium and calcium, or taking potassium, calcium, and vitamin D drugs). Food should be rich in protein, vitamins, low in fat, carbohydrates and salt.
In children, during the period of growth, corticosteroids should be used only according to absolute indications and under especially careful supervision of the attending physician.
When using dexamethasone, there is a risk of developing severe anaphylactic reactions, bradycardia.
Against the background of drug therapy, the risk of activation of strongyloidosis increases.
During drug therapy, careful monitoring of the condition of patients with heart failure, uncontrolled arterial hypertension, injuries and ulcerative lesions of the cornea, glaucoma is necessary.
May worsen the course of myasthenia gravis.
Against the background of the use of corticosteroids, sperm motility may change.
Taking the drug may mask the symptoms of "peritoneal irritation" in patients with perforation of the wall of the stomach or intestines.
The effect of the drug is enhanced in patients with cirrhosis. It should be borne in mind that in patients with hypothyroidism, dexamethasone clearance decreases, and in patients with thyrotoxicosis, it increases.
In patients with diabetes mellitus, the concentration of glucose in the blood should be monitored and, if necessary, correct doses of hypoglycemic drugs.
Perhaps the appearance of visual impairment with systemic and local application of corticosteroids. If blurred or other visual impairment occurs, an ophthalmologist should be consulted to rule out causes such as cataracts, glaucoma, or rare eye diseases, such as central serous chorioretinopathy, which have been reported after systemic and topical application of GCS.
During post-marketing observation, tumor lysis syndrome (TAS) was reported in patients with hematologic diseases after the use of dexamethasone in monotherapy or in combination with other chemotherapeutic agents. Patients with a high risk of SLO (patients with high proliferative activity of tumor cells, high tumor burden and high sensitivity to cytotoxic drugs) need careful monitoring and adherence to appropriate precautions.
Available data indicate long-term neurological adverse events after initiation of therapy (<96 hours) with starting doses of 0.25 mg / kg dexamethasone 2 times a day in premature infants with chronic lung diseases.
Special Information on Excipients
The drug Dexamethasone - KRKA contains lactose, therefore, it should not be used in the following conditions: lactose intolerance, lactase deficiency, glucose-galactose malabsorption syndrome.
Influence on the ability to drive vehicles, mechanisms
Considering possible side effects during the period of therapy with Dexamethasone - KRKA, caution must be exercised when driving vehicles and working with mechanisms, engaging in other activities that require an increased concentration of attention and speed of psychomotor reactions.
Dexamethasone increases the toxicity of cardiac glycosides (due to the occurrence of hypokalemia, the risk of developing arrhythmias increases).
It accelerates the excretion of acetylsalicylic acid, reduces its concentration in the blood (with dexamethasone withdrawal, the concentration of salicylates in the blood increases and the risk of side effects increases).
When used simultaneously with live antiviral vaccines and against the background of other types of immunization, it increases the risk of virus activation and the development of infections.
Increases the metabolism of isoniazid, mexiletine (especially in "fast acetylators"), which leads to a decrease in their plasma concentrations.
Increases the risk of hepatotoxic effects of paracetamol (induction of "liver" enzymes and the formation of a toxic metabolite of paracetamol).
Increases (with prolonged therapy) the content of folic acid.
Hypokalemia caused by corticosteroids can increase the severity and duration of muscle blockade against muscle relaxants.
In high doses, reduces the effect of somatropin.
Antacids reduce the absorption of corticosteroids.
Dexamethasone reduces the effect of hypoglycemic drugs, enhances the anticoagulant effect of coumarin derivatives.
It attenuates the effect of vitamin D on the absorption of Ca2 + in the intestinal lumen. Ergocalciferol and parathyroid hormone inhibit the development of osteopathy caused by corticosteroids. Reduces the concentration of praziquantel in the blood.
Cyclosporine (inhibits metabolism) and ketoconazole (reduces clearance) increase toxicity.
Thiazide diuretics, carbonic anhydrase inhibitors, other corticosteroids and amphotericin B increase the risk of hypokalemia, sodium-containing drugs - edema and increased blood pressure.
Nonsteroidal anti-inflammatory drugs (NSAIDs) and ethanol increase the risk of ulceration of the gastrointestinal mucosa, bleeding, in combination with NSAIDs for the treatment of arthritis, it is possible to reduce the dose of corticosteroids due to the summation of the therapeutic effect.
Indomethacin, displacing dexamethasone from its association with albumin, increases the risk of side effects.
Amphotericin B and carbonic anhydrase inhibitors increase the risk of osteoporosis. The therapeutic effect of GCS is reduced under the influence of phenytoin, barbiturates, ephedrine, theophylline, rifampicin and other inducers of “liver” microsomal enzymes (increase in metabolic rate).
Mitotan and other inhibitors of adrenal cortex function may necessitate an increase in the dose of corticosteroids.
GCS clearance increases against the background of thyroid hormones.
Immunosuppressants increase the risk of infections and lymphomas or other lymphoproliferative disorders associated with the Epstein-Barr virus.
Estrogens (including oral estrogen-containing contraceptives) reduce the clearance of corticosteroids, lengthen the half-life and their therapeutic and toxic effects. The appearance of hirsutism and acne is facilitated by the simultaneous use of other steroid hormonal drugs - androgens, estrogens, anabolic steroids, and oral contraceptives.
Tricyclic antidepressants can increase the severity of depression caused by dexamethasone (not indicated for the treatment of these side effects).
The risk of developing cataracts is increased when used against other GCS, antipsychotic drugs (antipsychotics), carbamide and azathioprine. The simultaneous use of m-anticholinergics (including antihistamines, tricyclic antidepressants), nitrates contributes to the development of increased intraocular pressure.
With simultaneous use with fluoroquinolones, the risk of tendonopathy (mainly the Achilles tendon) increases in elderly patients and in patients with tendon diseases.
Antimalarials (chloroquine, hydroxychloroquine, mefloquine) in combination with dexamethasone can increase the risk of myopathy, cardiomyopathy.
Inhibitors of an angiotensin-converting enzyme while using dexamethasone can alter the composition of peripheral blood.
The simultaneous use of inhibitors of the CYP3A isoenzyme, including drugs containing cobicistat, can lead to an increased risk of developing systemic side effects. Simultaneous use should be avoided unless the benefit of use exceeds the risk of developing systemic side effects of GCS, in which case patients should be monitored for the development of systemic side effects of GCS.
Dexamethasone - a synthetic glucocorticosteroid (GCS), a methylated derivative of fluoroprednisolone, inhibits the release of interleukin-1 and interleukin-2, interferon gamma from lymphocytes and macrophages. It has anti-inflammatory, anti-allergic, desensitizing, anti-shock, antitoxic and immunosuppressive effects. It inhibits the release of adrenocorticotropic hormone (ACTH) and beta-lipotropin by the pituitary gland, but does not reduce the content of circulating beta-endorphin. It inhibits the secretion of thyroid stimulating hormone (TSH) and follicle-stimulating hormone (FSH).
Increases the excitability of the central nervous system (CNS), reduces the number of lymphocytes and eosinophils, increases the number of red blood cells (stimulates the production of erythropoietins).
It interacts with specific cytoplasmic receptors, forms a complex that penetrates the cell nucleus, stimulates the synthesis of matrix ribonucleic acid (mRNA), which induces the formation of proteins, including lipocortin, which mediate cellular effects. Lipocortin inhibits phospholipase A2, inhibits the release of arachidonic acid and inhibits the synthesis of endoperoxides, prostaglandins (Pg), leukotrienes, which contribute to inflammation, allergies, etc.
Effect on protein metabolism: reduces the amount of protein in plasma (due to globulins) with an increase in the albumin / globulin coefficient, increases the synthesis of albumin in the liver and kidneys, and enhances protein catabolism in muscle tissue.
Effect on lipid metabolism: increases the synthesis of higher fatty acids and triglycerides (TG), 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, which leads to increased glucose from the liver to the blood, increases the activity of phosphoenolpyruvate carboxylase and the synthesis of aminotransferases, leading to activation of gluconeogenesis.
Effect on water-electrolyte metabolism: retains sodium ions (Na +) and water in the body, stimulates the excretion of potassium ions (K +) (mineralocorticosteroid (ISS) activity), reduces the absorption of calcium ions (Ca2 +) from the gastrointestinal tract, “leaches” Ca2 + from bones, increases the excretion of Ca2 + by the kidneys.
The anti-inflammatory effect is associated with inhibition of the release of inflammatory mediators by eosinophils, inducing the formation of lipocortin and a decrease in the number of mast cells producing hyaluronic acid, with a decrease in capillary permeability, stabilization of cell membranes and organelle membranes (especially lysosomal).
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, and a decrease in the number of T- and B-lymphocytes, mast cells , reducing the sensitivity of effector cells to allergy mediators, inhibition of antibody formation, changes in the body's immune response.
In chronic obstructive pulmonary disease (COPD), the action is mainly based on the inhibition of inflammatory processes, inhibition of the development or prevention of edema 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, and inhibition of erosion and mucosal desmosis . Increases the sensitivity of beta-adrenergic receptors of small and medium caliber 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 (BP) (due to an increase in the concentration of circulating catecholamines and restoration of the sensitivity of adrenoreceptors 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. It inhibits the synthesis and secretion of ACTH, and secondly, the synthesis of endogenous corticosteroids. It inhibits connective tissue reactions during the inflammatory process and reduces the possibility of scar tissue formation.
The peculiarity of the action is a significant inhibition of pituitary function and the almost complete absence of ISS activity. Doses of 1-1.5 mg / day inhibit the adrenal cortex, the biological half-life (T1 / 2) is 32-72 hours (the duration of inhibition of the hypothalamus-pituitary-cortical layer of the adrenal gland).
According to the strength of glucocorticosteroid activity, 0.5 mg of dexamethasone corresponds to approximately 3.5 mg of prednisone (or prednisolone), 15 mg of hydrocortisone or 17.5 mg of cortisone.
After oral administration, it is rapidly and completely absorbed, the maximum concentration of dexamethasone in blood plasma is 1-2 hours.
In plasma, it binds (60-70%) with a specific carrier protein - transcortin. It easily passes through histohematological barriers (including through the blood-brain and placental barriers).
It is metabolized in the liver (mainly by conjugation with glucuronic and sulfuric acids) to inactive metabolites.
It is excreted by the kidneys (a small amount of dexamethasone passes into breast milk). The elimination half-life is 3-5 hours.
Systemic diseases of the connective tissue (systemic lupus erythematosus, scleroderma, periarteritis nodosa, dermatomyositis, rheumatoid arthritis).
Acute and chronic inflammatory joint diseases: gouty and psoriatic arthritis, osteoarthritis (including post-traumatic), polyarthritis, periarthritis, ankylosing spondylitis (ankylosing spondylitis), juvenile arthritis, Still's syndrome in adults, bursitis, nonspecific epitonitis, sinusitis and synovitis.
Rheumatic fever, acute rheumatic heart disease.
Acute and chronic allergic diseases: allergic reactions to drugs and food products, serum sickness, urticaria, allergic rhinitis, angioedema, drug exanthema, hay fever.
Skin diseases: pemphigus, psoriasis, eczema, atopic dermatitis, diffuse neurodermatitis, contact dermatitis (with damage to a large surface of the skin), toxidermia, seborrheic dermatitis, exfoliative dermatitis, toxic epidermal necrolysis (Lyell syndrome), bullous herpetiform dermatitis, malignant dermatitis, malignant dermatitis, malignant Stevens-Johnson).
Cerebral edema (only after confirmation of the symptoms of increased intracranial pressure by magnetic resonance or computed tomography), due to a brain tumor and / or associated with surgical intervention, or radiation damage.
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 gland).
Congenital adrenal hyperplasia.
Autoimmune kidney disease (including acute glomerulonephritis), nephrotic syndrome.
Hematopoietic diseases: agranulocytosis, panmyelopathy, autoimmune hemolytic anemia, acute lymphoid and myeloid leukemia, lymphogranulomatosis, thrombocytopenic purpura, secondary thrombocytopenia in adults, erythroblastopenia (erythrocyte anemia).
Pulmonary diseases: acute alveolitis, pulmonary fibrosis, stage II-III sarcoidosis.
Bronchial asthma (with bronchial asthma, the drug is prescribed only in severe cases, inefficiency or inability to take inhaled GCS).
Tuberculous meningitis, pulmonary tuberculosis, aspiration pneumonia (in combination with specific chemotherapy).
Berylliosis, Leffler's syndrome (not amenable to other therapy).
Lung cancer (in combination with cytostatics).
Gastrointestinal diseases: ulcerative colitis, Crohn's disease, local enteritis.
Prevention of transplant rejection as part of complex therapy. Hypercalcemia on the background of cancer, nausea and vomiting during cytostatic therapy.
Conducting a test in the differential diagnosis of hyperplasia (hyperfunction) and tumors of the adrenal cortex.
For short-term use according to "vital" indications, the only contraindication is hypersensitivity to dexamethasone or auxiliary components of the drug; systemic mycosis; the period of breastfeeding; the use of live and attenuated vaccines with immunosuppressive doses of the drug.
The drug Dexamethasone - KRKA is contraindicated in patients with lactose intolerance, lactase deficiency and glucose-galactose malabsorption syndrome, because lactose is part of the drug Dexamethasone - KRKA.
Parasitic and infectious diseases of a viral, fungal or bacterial nature (currently or recently transferred, including recent contact with the patient) - herpes simplex, herpes zoster (viremic phase), chickenpox, measles; amoebiasis, strongyloidosis (established or suspected); active and latent tuberculosis. The use of the drug in severe infectious diseases is possible only against the background of specific antimicrobial therapy.
The pre- and post-vaccination period (8 weeks before and 2 weeks after vaccination), lymphadenitis after BCG vaccination, immunodeficiency states (including AIDS or HIV infection).
Gastrointestinal tract diseases: gastric and duodenal ulcer, esophagitis, gastritis, acute or latent peptic ulcer, recently created intestinal anastomosis, ulcerative colitis with the threat of perforation or abscess, diverticulitis.
Diseases of the cardiovascular system, including recently transferred myocardial infarction (in patients with acute and subacute myocardial infarction, the spread of the focus of necrosis is possible, the formation of scar tissue slows down and, as a result, rupture of the heart muscle), decompensated chronic heart failure (CHF), arterial hypertension, hyperlipidemia.
Endocrine diseases: diabetes mellitus (including impaired carbohydrate tolerance), thyrotoxicosis, hypothyroidism, Itsenko-Cushing's disease.
Severe chronic renal and / or liver failure, nephrourolithiasis, hypoalbuminemia and conditions predisposing to its occurrence, systemic osteoporosis, gravis myasthenia gravis, acute psychosis, severe affective disorders (including a history of), obesity (III-IV degree), poliomyelitis (except for the form of bulbar encephalitis), open-angle and angle-angle glaucoma, the use of the drug in elderly patients (due to the high risk of osteoporosis and hypertension), an infection of the eye due to herpes simplex virus (risk of corneal perforation) during pregnancy.
In children, during the period of growth, corticosteroids should be used only according to absolute indications and under especially careful supervision of the attending physician.
Use during pregnancy and during breastfeeding
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 a pregnancy, the use of the drug Dexamethasone - KRKA is shown only if the expected therapeutic effect exceeds the risk of a negative effect on the mother or fetus. GCS should be prescribed during pregnancy only by absolute indications. With prolonged therapy during pregnancy, the possibility of impaired fetal growth is not ruled out. 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.
The use of corticosteroids during pregnancy in animals can cause abnormalities in the development of the fetus, including cleavage of the palate, intrauterine growth retardation, and the effect on brain growth and development.
There is no evidence that the use of corticosteroids leads to an increase in the incidence of congenital abnormalities in humans, such as cleft palate / lips.
If it is necessary to carry out drug treatment during breastfeeding, breast-feeding should be discontinued.
Perhaps an increase in dose-dependent side effects, with the exception of allergic reactions. It is necessary to reduce the dose of dexamethasone.
The frequency of development and the severity of side effects depend on the duration of use, the size of the dose used and the ability to comply with the circadian rhythm of the appointment. Dexamethasone is generally well tolerated. It has low ISS activity, that is, its effect on water-electrolyte metabolism is small. As a rule, low and medium doses of dexamethasone do not cause a delay in Na and water in the body, increased K excretion. The following side effects are described:
Infectious and parasitic diseases: the development or exacerbation of infections (the use of immunosuppressants and vaccination at the same time contribute to this side effect), masking infections.
Disorders from the blood and lymphatic system: moderate leukocytosis, leukocyturia, lymphopenia, eosinopenia, polycythemia.
Disorders from the immune system: generalized (skin rash, skin itching, anaphylactic shock), local allergic reactions.
Disorders from the endocrine system: decreased glucose tolerance, “steroid” diabetes mellitus or manifestation of latent diabetes mellitus, inhibition of adrenal function, Itsenko-Cushing's syndrome (moon-shaped face, pituitary-type obesity, hirsutism, increased blood pressure, dysmenorrhea, amenorrhea, ), delayed sexual development in children.
Metabolic and nutritional disorders: hypercholesterolemia, increased Ca2 excretion, hypocalcemia, increased body weight, negative nitrogen balance (increased protein breakdown), increased sweating, epidural lipomatosis.
ISS-related activity is fluid retention and Na (peripheral edema), hypernatremia, hypokalemic syndrome (hypokalemia, arrhythmia, myalgia or muscle spasm, unusual weakness and fatigue).
Mental disorders: nervousness or anxiety, insomnia, emotional lability, delirium, disorientation, euphoria, hallucinations, manic-depressive psychosis, depression, paranoia, suicidal tendency.
Violations of the nervous system: increased intracranial pressure, pseudotumor of the cerebellum, headache, convulsions.
Disorders from the organ of vision: blurred vision, posterior subcapsular cataract, increased intraocular pressure with possible damage to the optic nerve, a tendency to develop secondary bacterial, fungal or viral infections of the eyes, trophic changes in the cornea, exophthalmos, perforation of the cornea, central serous chorioretinopathy.
Hearing disorders and labyrinth disorders: dizziness, vertigo.
Disorders from the heart and blood vessels: arrhythmias, bradycardia (up to cardiac arrest), development (in predisposed patients) or progression of heart failure, electrocardiographic changes characteristic of hypokalemia, increased blood pressure, hypercoagulation, thrombosis and thromboembolism, vasculitis, increased capillary fragility. In patients with acute and subacute myocardial infarction - the spread of the focus of necrosis, slowing the formation of scar tissue, which can lead to rupture of the heart muscle.
Digestive disorders: nausea, vomiting, abdominal pain, discomfort in the epigastric region, pancreatitis, “steroid” ulcer of the stomach and duodenum, erosive esophagitis, bleeding and perforation of the stomach and intestines, increased or decreased appetite, flatulence hiccups. In rare cases, an increase in the activity of hepatic transaminases and alkaline phosphatase.
Disorders from the musculoskeletal and connective tissue: growth retardation and processes of ossification in children (premature closure of the pineal gland), osteoporosis (very rarely pathological bone fractures, aseptic necrosis of the head of the humerus and femur), muscle tendon rupture, "steroid" myopathy, decreased muscle mass (atrophy).
Disorders of the skin and subcutaneous tissues: delayed healing of wounds, petechiae, ecchymosis, thinning of the skin, atrophy of the skin and subcutaneous tissue, hyper- or hypopigmentation, steroid acne, striae, tendency to develop pyoderma and candidiasis, impaired skin pigmentation (hypo- or hyperpigmentation), telangiectasia.
General disorders and disorders at the injection site: "withdrawal" syndrome.
Ways of application:
Inside, in individually selected doses, the value of which is determined by the type of disease, the degree of its activity and the nature of the patient's response.
The average daily dose is 0.75-9 mg. In severe cases, large doses can be used, divided into 3-4 doses. The maximum daily dose is usually 15 mg. After achieving a therapeutic effect, the dose is gradually reduced (usually by 0.5 mg in 3 days) to a maintenance dose of 2-4.5 mg / day. The minimum effective dose is 0.5-1 mg / day. Children (depending on age) are prescribed 83.3-333.3 mcg / kg or 2.5-10 mg / m2 / day in 3-4 doses.
The duration of the use of dexamethasone depends on the nature of the pathological process and the effectiveness of treatment and ranges from several days to several months or more. Treatment is stopped gradually (at the end, several injections of corticotropin are prescribed).
With bronchial asthma, rheumatoid arthritis, ulcerative colitis - 1.5-3 mg / day; with systemic lupus erythematosus - 2-4.5 mg / day; with oncohematological diseases - 7.5-10 mg.
For the treatment of acute allergic diseases, it is advisable to combine parenteral and oral administration: 1 day - 4-8 mg parenterally; 2 day - inside, 4 mg 3 times a day; 3, 4 day - inside, 4 mg 2 times a day; 5, 6 day - 4 mg / day, inside; 7 day - drug withdrawal.
A test with dexamethasone (Liddle's test) is carried out in the form of small and large tests. With a small test, dexamethasone is given to the patient at 0.5 mg every 6 hours during the day (that is, at 8 a.m., at 2 p.m., 8 p.m. and 2 a.m.). Urine for the determination of 17-hydroxycorticosteroids or free cortisol is collected from 8 a.m. to 8 a.m. 2 days before the appointment of dexamethasone and also 2 days at the same time intervals after taking the indicated doses of dexamethasone. These doses of dexamethasone inhibit the formation of corticosteroids in almost all healthy individuals. 6 hours after the last dose of dexamethasone, the plasma cortisol content is below 135-138 nmol / L (less than 4.5-5 μg / 100 ml). A decrease in the excretion of 17-hydroxycorticosteroids below 3 mg / day, and free cortisol below 54-55 nmol / day (below 19-20 μg / day) excludes hyperfunction of the adrenal cortex. In persons suffering from a disease or Itsenko-Cushing's syndrome, during a small test, changes in the secretion of corticosteroids are not observed.
When conducting a large test, dexamethasone is prescribed 2 mg every 6 hours for 2 days (that is, 8 mg of dexamethasone per day). Urine is also collected to determine 17-hydroxycorticosteroids or free cortisol (if necessary, free plasma cortisol is determined). With Itsenko-Cushing's disease, the excretion of 17-hydroxycorticosteroids or free cortisol is reduced by 50% or more, while with adrenal tumors or adrenocorticotropic-ectopic (or corticoliberin-ectopic) syndrome, excretion of corticosteroids does not change. In some patients with adrenocorticotropic-ectopic syndrome, a decrease in corticosteroid excretion is not detected even after taking dexamethasone at a dose of 32 mg / day.
|Pills in 1 package||10|
|Expiration Date (in months)||60|
|Country of origin||Russia|