Dexamethasone | Lekhim

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INSTRUCTION

on the medical use of the medicinal product

DEXAMETHAZONE

(DEXAMETHASONE)

Structure:

active substance: dexamethasone sodium phosphate;

1 ml

solution contains 4 mg of dexamethasone sodium phosphate on a dry basis

substance;

excipients: propylene glycol, glycerin, disodium edetate, phosphate buffer solution

pH 7.5, methylparaben (E 218), propylparaben (E 216), water for

injections.

Dosage form. Solution

for injection.

Basic physical and chemical

properties: transparent

colorless liquid.

Pharmacotherapeutic group. Corticosteroids for systemic

application.

ATX code Н02А B02.

Pharmacological properties.

Pharmacodynamics.

Dexamethasone is a semi-synthetic adrenal hormone

(corticosteroid) with glucocorticoid activity. Renders

anti-inflammatory and immunosuppressive action, and also affects

energy metabolism, glucose metabolism and (through negative feedback) on

secretion of the activation factor of the hypothalamus and trophic hormone of the adenohypophysis.

The mechanism of action of glucocorticoids is still not fully understood. Now

there are enough messages about the mechanism of action

glucocorticoids to confirm that they act at the cellular level. IN

the cytoplasm of cells, there are two well-established receptor systems. because of

binding to glucocorticoid receptors, corticoids have anti-inflammatory

and immunosuppressive action and regulate glucose metabolism, and due to

binding to mineralocorticoid receptors they regulate sodium metabolism,

potassium and water-electrolyte balance.

Glucocorticoids dissolve in lipids and easily enter target cells

through the cell membrane. The binding of the hormone to the receptor leads to a change

the conformation of the receptor, which enhances its affinity with DNA. Complex

the hormone / receptor enters the cell nucleus and binds to the regulatory center of the molecule

DNA, also called glucocorticoid response element (GRE).

Activated receptor associated with GRE or specific genes,

regulates mRNA transcription, which can be increased or decreased.

The newly formed mRNA is transported to the ribosomes, after which there is

the formation of new proteins. Depending on target cells and processes,

occurring in cells, protein synthesis can be enhanced (for example

formation of tyrosine transaminase in liver cells) or decreased (for example

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

body cells.

Impact on energy metabolism and

glucose homeostasis.

Dexamethasone, together with insulin, glucagon and catecholamines, regulate the retention of

and energy consumption. The production of glucose from pyruvate increases in the liver

or amino acids and the formation of glycogen. In peripheral tissues, especially in

muscle, decreases glucose intake and mobilization of amino acids (from proteins),

which are substrates for gluconeogenesis in the liver. Direct influence on

fat metabolism is the central distribution of adipose tissue and an increase

lipolytic direction to catecholamines.

Dexamethasone via receptors in the renal proximal tubule

increases renal blood flow and glomerular filtration, inhibits the formation and

secretion of vasopressin, improves the ability of the kidneys to excrete from the body

acid.

Due to an increase in the number of β-adrenergic receptors and an affinity for

β-adrenergic receptors, which transmit a positive inotropic effect

catecholamines, dexamethasone directly increases contractile function

heart and peripheral vascular tone.

When using high doses, dexamethasone inhibits fibroblastic

collagen production of type I and type III and formation of glycosaminoglycans.

Thus, due to the inhibition of the formation of extracellular collagen and

matrix, delayed wound healing occurs. Long-term administration of high doses

induces, indirectly, progressive bone resorption and

reduces osteogenesis by direct action (increased secretion

parathyroid hormone and a decrease in the secretion of calcitonin), and is also

cause a negative calcium balance due to a decrease in calcium

absorption in the intestine and an increase in its excretion in the urine. This usually results in

secondary hyperparathyroidism and phosphaturia.

Impact on the pituitary gland and

hypothalamus.

Dexamethasone is 30 times more potent than cortisol. So

Thus, it is a more potent inhibitor of corticotropin-releasing factor

(CRF) and secretion of adrenocorticotropic hormone (ACTH) versus endogenous

cortisol. This leads to a decrease in the secretion of cortisol and after prolonged

suppression of CRF and ACTH secretion – to adrenal atrophy. Failure

the adrenal cortex may occur already on the 5th and 7th day of administration

dexamethasone at a dose equivalent

20-30 mg prednisone daily, or after 30 days of low-dose therapy.

After discontinuation of short-term therapy (up to 5 days) with high doses, function

the adrenal cortex should recover within 1 week; after

long-term therapy, normalization occurs later, usually up to 1 year. Have

some patients may develop irreversible adrenal atrophy.

Anti-inflammatory and

the immunosuppressive effect of glucocorticoids is based on their molecular and biochemical

impact. Molecular anti-inflammatory action results from

binding to glucocorticoid receptors and from changes in the expression of a number

genes that regulate the formation of various information molecules, proteins

and enzymes involved in the inflammatory response. Biochemical

anti-inflammatory effect of glucocorticoids – the result of blocking

the formation and functioning of humoral inflammatory mediators:

prostaglandins, thoromboxanes, cytokines and leukotrienes. Dexamethasone

reduces the formation of leukotrienes by decreasing the release of arachidonic

acids from cellular phospholipids, which is caused by inhibition of activity

phospholipase A2. The effect on phospholipases is not achieved directly

exposure, and as a result of an increase in the concentration of lipocortin (macrocortin),

which is an inhibitor of phospholipase A2. Dexamethasone slows down

the formation of prostaglandins and thromboxane by reducing the formation

specific mDNA and thereby reduces the formation of cyclooxygenase.

Dexamethasone also reduces the production of platelet activating factor (PAF)

by increasing the concentration of lipocortin. Other biochemical

anti-inflammatory effects include reduction in necrosis factor formation

tumors (TNF) and interleukin (IL-1).

Pharmacokinetics.

Absorption.

Dexamethasone reaches its peak plasma concentration within the first 5 minutes

with intravenous administration and within 1 hour with intramuscular administration.

After local administration to the joint or soft tissue (inflammation focus), absorption

occurs more slowly than in the case of intramuscular injection. Intravenous

the onset of action is instantaneous, after intramuscular administration

the clinical effect occurs after 8 hours. The action lasts 17-28 days

after intramuscular injection and from 3 days to 3 weeks after local

introduction.

Distribution.

In blood plasma and synovial fluid, the conversion of dexamethasone phosphate

a dexamethasone occurs very rapidly. In blood plasma approximately 77%

dexamethasone bind to plasma proteins, mainly albumin. Only

a small amount of dexamethasone binds to other proteins. Dexamethasone

is fat-soluble, so it freely penetrates into cells and intercellular

space. In the central nervous system (hypothalamus, pituitary gland), it

binds and acts through membrane receptors. In peripheral tissues

binds and acts via cytoplasmic receptors.

Biotransformation.

The destruction of dexamethasone occurs at the site of action, that is, in the very

cage. Dexamethasone is primarily metabolized in the liver, also,

possibly in the kidneys and other tissues.

Withdrawal.

The biological half-life of dexamethasone is 24-72 hours.

Predominantly excreted in urine.

Clinical characteristics.

Indications.

Dexamethasone inject

intravenously or intramuscularly in urgent cases and if impossible

oral administration.

Endocrine system diseases:

– substitution therapy

primary or secondary (pituitary) adrenal insufficiency (except

acute adrenal insufficiency, in which hydrocortisone or

cortisone are more appropriate given their more pronounced hormonal

the effect);

– acute adrenal insufficiency (hydrocortisone or cortisone

are the drugs of choice; it may be necessary to

use with mineralocorticoids, especially in the case of synthetic

analogs);

– before operations and in cases

serious injury or illness in patients with established adrenal

insufficiency or with an undefined adrenocortical reserve;

– shock resistant to traditional

therapy, with existing or suspected adrenal insufficiency;

– congenital adrenal hyperplasia;

– non-suppurative inflammation of the thyroid

glands and severe forms of radiation thyroiditis.

Rheumatological diseases

(as an adjunct therapy in the period when the basic therapy is not

worked, that is, in patients who have anesthetic and

anti-inflammatory effect of NSAIDs was unsatisfactory):

– rheumatoid arthritis, including juvenile rheumatoid arthritis and

extra-articular manifestations of rheumatoid arthritis (rheumatic lungs, changes

heart, eyes, cutaneous vasculitis);

– synovitis in osteoarthritis, post-traumatic osteoarthritis;

epicondylitis, acute nonspecific tendosynovitis; acute gouty arthritis;

psoriatic arthritis; ankylosing spondylitis; systemic diseases

connective tissue; vasculitis.

Skin diseases:

– pemphigus; severe erythema multiforme (Stevens-Johnson syndrome);

exfoliative dermatitis; bullous dermatitis herpetiformis; severe forms

exudative erythema; erythema nodosum; severe forms of seborrheic dermatitis;

severe psoriasis; hives that do not respond to standard treatment

fungoid mycosis; dermatomyositis.

Allergic diseases

(not amenable to traditional treatment)

– bronchial asthma; contact dermatitis; atopic dermatitis;

serum sickness; chronic or seasonal allergic rhinitis; allergy to

medicines; urticaria after blood transfusion.

Diseases of the organs of vision:

– inflammatory diseases of the eyes (acute central choroiditis,

optic neuritis); allergic diseases (conjunctivitis, uveitis,

sclerites, keratitis, iritis); systemic immune diseases (sarcoidosis, temporal

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

pseudotumor); immunosuppressive therapy for corneal transplant.

The solution can be administered systemically or locally (administration under the conjunctiva and

retrobulbar or parabulbar administration).

Gastrointestinal diseases:

to remove the patient from

critical state at:

– ulcerative colitis (severe

development); Crohn’s disease (severe development); chronic autoimmune hepatitis;

liver transplant rejection reaction.

Respiratory tract diseases:

– symptomatic

sarcoidosis (symptomatic); acute toxic bronchiolitis; chronic bronchitis and

asthma (with exacerbation); focal or disseminated pulmonary tuberculosis

(along with appropriate anti-tuberculosis therapy); beryllium disease

(granulomatous inflammation); radiation or aspiration pneumonitis.

Hematological diseases:

– acquired or

congenital chronic aplastic anemia; autoimmune hemolytic

anemia; secondary thrombocytopenia in adults; erythroblastopenia; sharp

lymphoblastoma leukemia (induction therapy); idiopathic

thrombocytopenic purpura in adults (intravenous only – intramuscular

introduction is contraindicated).

Renal diseases:

– immunosuppressive

kidney transplant therapy; stimulating urine output or decreasing

proteinuria in idiopathic nephrotic syndrome (without uremia) and impairment

renal function in systemic lupus erythematosus.

Malignant oncological diseases:

– palliative care

leukemia and lymphoma in adults; acute leukemia in children; hypercalcemia with

malignant diseases.

Cerebral edema:

– cerebral edema

due to a primary or metastatic brain tumor, trepanation

skull and traumatic brain injury.

Shock:

– shock that defies standard

treatment; shock in patients with adrenal insufficiency;

anaphylactic shock (intravenously after administration of adrenaline), before surgery

to prevent shock if there is suspicion or established deficiency

adrenal cortex.

Other indications:

– tuberculous meningitis

with subarachnoid blockade (along with proper anti-tuberculosis

therapy); trichinosis with neurological symptoms or myocardial trichinosis;

cystic swelling of the aponeurosis or tendon (ganglion).

Indications for intra-articular or soft tissue injection:

– rheumatoid arthritis

(severe inflammation of an individual joint); ankylosing spondylitis (when

inflamed joints do not respond to traditional treatment); psoriatic arthritis

(oligoarticular form and tendovaginitis); monoarthritis (after evacuation

synovial fluid); osteoarthritis of the joints (only in the case of synovitis and

exudation); extra-articular rheumatism (epicondylitis, tendovaginitis, bursitis); acute

and gouty arthritis.

Local administration (introduction to the lesion site):

– keloid lesions;

hypertrophic, inflammatory and infiltrated lesions with lichen,

psoriasis, annular granuloma, sclerosing folliculitis, discoid

lupus and cutaneous sarcoidosis; disc lichen lichen planus; Urbach-Oppenheim disease;

localized alopecia.

Contraindications.

Increased

sensitivity to the active substance or to any other ingredient

drug.

Acute viral,

bacterial or systemic fungal infections (unless appropriate

therapy).

Cushing’s syndrome.

Live vaccination

vaccine.

Feeding period

breastfeeding (except in urgent cases).

Intramuscular

administration is contraindicated in patients with severe blood clotting diseases.

Local introduction

contraindicated in bacteremia, systemic fungal infections, in patients with

unstable joints, infections at the site of application, including septic

arthritis due to gonorrhea or tuberculosis.

Interaction

other drugs and other types of interactions.

Parallel use of dexamethasone and non-steroidal

anti-inflammatory drugs increase the risk of gastrointestinal bleeding and

ulceration.

The effect of dexamethasone decreases with simultaneous

the use of drugs that activate the CYP 3A4 enzyme (phenytoin,

phenobarbital, carbamazepine, primidone, rifabutin, rifampicin) or increase metabolic

clearance of glucocorticoids (ephedrine and aminoglutethimide). In these cases, the dose

dexamethasone should be increased. Interaction between dexamethasone and

all of the aforementioned drugs may distort the test results

suppression of dexamethasone. This must be taken into account when evaluating test results..

Combined use of dexamethasone and drugs,

inhibiting the activity of the enzyme CYP 3A4 (ketoconazole, macrolides), may

cause an increase in serum dexamethasone concentration. Dexamethasone

is a moderate inducer of CYP 3A4. Combined use with

drugs that are metabolized by CYP 3A4 (indinavir, erythromycin),

can increase their clearance, which leads to a decrease in serum concentration.

By inhibiting the enzymatic action of CYP 3A4

ketoconazole may increase serum dexamethasone concentration. With another

hand, ketoconazole can suppress adrenal glucocorticoid synthesis,

thus, due to a decrease in the concentration of dexamethasone,

adrenal insufficiency.

Dexamethasone reduces the therapeutic effect of drugs against

diabetes, hypertension, praziquantel and natriuretics (therefore, the dose

these drugs should be increased), but increases the activity of heparin,

albendazole and potassium uretics (the dose of these drugs should be reduced if

necessary).

Dexamethasone can alter the action of coumarins

anticoagulants, therefore, when using this combination of drugs, you should

control prothrombin time more often.

Parallel use of high doses of glucocorticoids and

β2-adrenergic receptor agonists increases the risk

development of hypokalemia. In patients with hypokalemia, cardiac glycosides

more conducive to rhythm disturbance and are more toxic.

Dexamethasone reduces the therapeutic effect

anticholinesterase agents used for myasthenia gravis.

Antacids reduce the absorption of dexamethasone in the stomach.

The effect of dexamethasone when taken simultaneously with food and alcohol is not

researched, however, the simultaneous use of drugs and food with high

sodium content is not recommended. Smoking does not affect pharmacokinetics

dexamethasone.

Glucocorticoids increase renal clearance of salicylates,

therefore, it is sometimes difficult to obtain therapeutic serum concentrations. It is necessary

exercise caution in patients who gradually reduce the dose

corticosteroids, as this may increase the concentration

serum salicylates buy tren injection this trenbolone and trenbolone and intoxication.

If you use oral contraceptives in parallel,

the half-life of glucocorticoids can be lengthened, which increases their

biological effect and increases the risk of side effects.

Concomitant use of ritordine and dexamethasone

contraindicated during childbirth, as this can lead to fatal

outcome for a woman in labor due to pulmonary edema. Fatalities reported

in a woman in labor due to the development of such a condition.

The simultaneous use of dexamethasone and thalidomide can

cause toxic epidermal necrolysis.

Views

interactions that have therapeutic benefits: parallel administration

dexamethasone and metoclopramide, diphenhydramide, prochlorperazine, or

antagonists of 5-HT3 receptors (serotonin receptors or

5-hydroxytryptamine, type 3, such as ondansetron or granisetron) effectively

glucose solution

for the prevention of nausea and vomiting caused by cisplatin chemotherapy,

cyclophosphamide, methotrexate, fluorouracil.

Application features.

In

during parenteral treatment with corticoids, reactions may occur occasionally

hypersensitivity, therefore appropriate measures must be taken before starting

treatment with dexamethasone, given the possibility of allergic reactions (especially in

patients with allergic reactions to any drugs in

anamnesis).

Heavy

mental reactions may accompany systemic use of corticosteroids.

Symptoms usually appear several days or weeks after onset

treatment. The risk of developing these symptoms increases with high doses..

Most reactions resolve with dose reduction or drug withdrawal. Need to watch

and timely identify changes in mental status, especially

depressive mood, suicidal thoughts and intentions. With a special

corticosteroids should be used with caution in patients with affective

a history of disorders, especially in patients with allergic

a history of reactions to any other medications, including a family history

anamnesis. The appearance of unwanted effects can be avoided by applying minimal

effective doses for a short period or using the required daily

dose of the drug once in the morning.

Have

patients who have been treated with dexamethasone for a long time, in case

discontinuation of treatment, a withdrawal syndrome may occur (no visible signs

adrenal insufficiency) with symptoms: fever,

runny nose, conjunctival redness, headache, dizziness, drowsiness, or

irritability, muscle and joint pain, vomiting, weight loss,

general weakness, often convulsions. Therefore, the dose of dexamethasone should be reduced.

gradually. Sudden discontinuation of the drug can be fatal. If

the patient is under severe stress (due to injury, surgery, or

severe illness) during therapy, the dose of dexamethasone should be increased,

if this occurs during discontinuation of treatment, it should be used

hydrocortisone or cortisone.

For patients,

who have been injected with dexamethasone for a long time and who are experiencing severe

stress after discontinuation of therapy, use should be reinstated

dexamethasone, because adrenal insufficiency caused by it can

last for several months after stopping treatment.

Treatment

dexamethasone or natural glucocorticoids may mask symptoms

existing or new infection, as well as symptoms of intestinal perforation.

Dexamethasone

may exacerbate systemic fungal infection, latent amebiasis, and tuberculosis

lungs.

The patients

with active pulmonary tuberculosis should receive dexamethasone (together with

anti-tuberculosis drugs) only for fleeting or highly disseminated tuberculosis

lungs. Patients with inactive pulmonary tuberculosis who are being treated

dexamethasone, or patients who respond to tuberculin should receive

chemical prophylaxis.

Caution

and medical supervision are recommended for patients with osteoporosis, arterial

hypertension, heart failure, tuberculosis, glaucoma, hepatic

or renal failure, diabetes, active peptic ulcer, with recent

intestinal anastomosis, ulcerative colitis and epilepsy. Need special care

patients during the first weeks after myocardial infarction, patients with

thromboembolism, myasthenia gravis, glaucoma, hypothyroidism, psychosis, or

psychoneurosis, as well as elderly patients.

In

during treatment, there may be an exacerbation of diabetes or a transition from latent

phases to clinical manifestations of diabetes.

When

long-term treatment should monitor serum potassium levels.

Vaccination

live vaccine is contraindicated in treatment with dexamethasone. Vaccination inanimate

a viral or bacterial vaccine does not lead to the expected synthesis of antibodies and does not

has the expected protective effect. Dexamethasone is usually not prescribed for

8 weeks before vaccination and do not start using earlier than 2 weeks

after vaccination.

The patients,

who have been treated with high doses of dexamethasone for a long time and have never

have had measles, should avoid contact with infected persons; at random

contact recommended preventive treatment with immunoglobulin.

Recommended

exercise caution in patients who recover from surgery or

bone fracture, as dexamethasone can slow wound healing and

bone formation.

Act

glucocorticoids are increased in patients with liver cirrhosis or hypothyroidism.

Intra-articular

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administration of corticosteroids can lead to local and systemic effects. Frequent

application may cause cartilage damage or bone necrosis.

Front

intra-articular injection should remove synovial fluid from the joint and

examine it (check for infection). The introduction of

corticoids into infected joints. If a joint infection develops after

injection, proper antibiotic therapy should be initiated.

For patients

should be advised to avoid physical exertion on the affected

joints until the inflammation is cured.

Should

avoid injecting the drug into unstable joints.

Corticoids

may skew the results of allergy skin tests.

Special warnings regarding

excipients.

A drug

contains less than 1 mmol (23 mg) sodium per dose, which is

extremely small amount.

Application during pregnancy or lactation.

Pregnancy. Harmful effects on the fetus and newborn

a child cannot be excluded. The drug suppresses

intrauterine development of the child. Dexamethasone can be administered to pregnant women

women only in isolated emergency cases, when the expected benefit for

the mother outweighs the potential risk to the fetus. Extra caution

recommended for preeclampsia. According to general recommendations, during treatment during

during pregnancy with glucocorticoids, the minimum effective

dose to control the underlying disease. Children born to mothers who

prescribed glucocorticoids during pregnancy, should be carefully checked for

adrenal insufficiency.

Glucocorticoids cross the placenta and reach high concentrations in

the fetus. Dexamethasone is less actively metabolized in the placenta than, for example,

prednisone. Based on this, in the blood serum of the embryo can be observed

high concentrations of dexamethasone. According to some reports, even pharmacological

doses of glucocorticoids may increase the risk of placental insufficiency,

oligohydramnios, retarded fetal development or intrauterine death,

an increase in the number of leukocytes (neutrophils) in the fetus and failure

adrenal glands. There is no evidence to support the teratogenic effect of glucocorticosteroids.

It is recommended to use additional doses of glucocorticosteroids during

childbirth to women who took glucocorticosteroids during pregnancy. IN

in case of prolonged labor or if a cesarean section is planned, it is recommended

intravenous administration of 100 mg hydrocortisone every 8 hours.

Lactation. Application during breastfeeding

contraindicated (except in urgent cases).

Small amounts of glucocorticoids pass into breast milk, so

mothers receiving dexamethasone are not advised to breastfeed,

especially when it is used in excess of physiological norms (about 1 mg). it

can lead to a slowdown in the growth of the child and a decrease in the secretion of endogenous

corticosteroids.

The ability to influence the reaction rate when driving or

other mechanisms.

Dexamethasone does not affect

on the ability to drive a car and other mechanical means.

Way

applications and doses.

Dexamethasone injection solution for adults and

children from birth.

The solution for injection can be administered intravenously (with

by injection or infusion with glucose solution or sodium chloride solution),

intramuscularly or topically (by injection into the joint or injection into the site

lesions on the skin or in the infiltration into soft tissues). As a solvent for

intravenous infusion apply 0.9% sodium chloride solution or 5%

glucose solution.

Solutions intended for intravenous administration or

further dissolution of the drug, should not contain preservatives when

use for babies, especially premature babies.

Mix the drug with a solvent for infusion should be

sterile conditions. The mixture should be applied within 24 hours, as

infusion solutions usually do not contain preservatives. Preparations for

parenteral administration should be visually inspected for foreign

inclusions and color changes each time before the introduction.

The dose should be determined individually in accordance with

disease of a particular patient, provided for the period of treatment,

tolerance of corticosteroids and body response.

Parenteral

introduction.

Dexamethasone should be administered parenterally in emergencies,

in cases where oral therapy is not possible, and in the cases specified in

section “Indications”.

Solution for injection is intended for administration

intravenously, intramuscularly or by infusion (with glucose solution or

sodium chloride solution).

Recommended average starting daily dose for

intravenous or intramuscular injection – 0.5-9 mg per day, if necessary, the dose can be increased. Initial

the dose of the drug should be used until a clinical reaction appears, and then the dose

should be gradually reduced to the lowest clinically effective dose.

If high doses are prescribed over several days, the dose

decrease gradually over the next few days or longer

period.

Local application.

For injection into the joint, doses from 0.4 mg are recommended

up to 4 mg. The dose depends on the size of the affected joint. Usually give 2-4 mg

in large joints and 0.8-1 mg in small ones. Re-introduction into the joint

possibly after 3-4 months. The introduction can be done three or four

once in one joint throughout life and no more than 2 joints

at the same time. More frequent intra-articular injection can damage the articular

cartilage and cause bone necrosis.

The dose of dexamethasone that is injected into the synovial

a bag, usually 2-3 mg, in the tendon sheath – 0.4-1 mg, in the ganglion

– from 1 to 2 mg.

The dose of dexamethasone that is injected into the injury site,

equated to the intra-articular dose. Dexamethasone can be administered simultaneously

in no more than two places of damage.

Doses for injection into soft tissues (around the joint) are

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Doses for children.

When administered intramuscularly, the recommended dose for

replacement therapy is 0.02 mg / kg body weight or 0.67 mg / m2

body surface area, divided into 3 doses, which is administered every third

day, or 0.008-0.01 mg / kg body weight or 0.2-0.3 mg / m2

body surface area per day.

For all other indications, the recommended dose is

0.02-0.1 mg / kg body weight or 0.8-5 mg / m2 area

body surfaces every 12-24 hours.

Equivalent doses of corticosteroids:

Dexamethasone 0.75 mg

Prednisone 5 mg

Cortisone 25 mg

Methylprednisolone 4 mg

Hydrocortisone 20 mg

Triamcinolone 4 mg

Prednisolone 5 mg

Betamezon 0.75 mg

Children.

Apply to children from the neonatal period, but only in case of extreme

necessity. Close supervision is necessary during dexamethasone treatment

for the growth and development of children and adolescents.

Overdose.

Exists

isolated reports of acute overdose or death due to acute

overdose.

Overdose

usually occurs only after several weeks of administration. Overdose can

cause most of the undesirable effects listed in the section “Side

reactions ”, especially Cushing’s syndrome. There is no specific antidote.

Overdose treatment should be supportive and symptomatic. Hemodialysis

is not an effective method of accelerated elimination of dexamethasone from

organism.

Side

reactions.

Side effects with short-term treatment

dexamethasone:

Co

side of the immune system: hypersensitivity reactions.

Co

side of the endocrine system: transient suppression of the function of the adrenal glands.

Co

side of metabolism and nutrition: decreased tolerance to carbohydrates, increased

appetite and weight gain, hypertriglyceridemia.

Co

side of the psyche: mental disorders.

Co

sides of the gastrointestinal tract: peptic ulcer and acute pancreatitis.

Side effects with long-term treatment

dexamethasone:

Co

side of the immune system: a decrease in the immune response and an increase

susceptibility to infections.

Co

side of the endocrine system: permanent suppression of the function of the adrenal glands,

growth retardation in children and adolescents, premature closure of the epiphyseal zones

growth.

Co

metabolic and nutritional aspects: obesity.

Co

sides of the organs of vision: cataract, glaucoma.

Co

vascular sides: hypertension; telangiectasia.

Co

sides of the skin and subcutaneous tissue: thinning of the skin.

Co

sides of musculoskeletal and connective tissue: muscle atrophy,

osteoporosis, aseptic bone necrosis, long bone fractures.

Side effects that can also occur

in individual organs and systems during treatment with dexamethasone:

Co

sides of the blood and lymphatic system: thromboembolic complications; decrease

the number of monocytes and / or lymphocytes; leukocytosis; eosinophilia (as with

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the use of other glucocorticosteroids); thrombocytopenia and non-thrombocytopenic

purpura.

Co

sides of the immune system: rash, bronchospasm, anaphylactic reactions,

development of opportunistic infections, hypersensitivity reactions.

Co

sides of the heart: multifocal extrasystole of the ventricle, temporary bradycardia,

heart failure, cardiac arrest, myocardial perforation due to

suffered myocardial infarction.

high doses

Co

vascular side: hypertensive encephalopathy.

Co

sides of the respiratory system, organs of the chest and mediastinum: relapse of inactive

tuberculosis.

Co

side of the nervous system: edema of the optic nerve and increased intracranial

pressure (benign intracranial hypertension) after discontinuation

treatment; dizziness; vertigo, headache, convulsions.

Co

sides of the psyche: changes in personality and behavior often manifest themselves in the form of euphoria;

insomnia, irritability, hyperkinesis, depression, nervousness,

anxiety, manic-depressive psychosis, delirium, disorientation,

hallucinations, paranoia, mood lability, suicidal thoughts, psychosis,

sleep disturbances, confusion, amnesia, worsening of schizophrenia,

worsening of the course of epilepsy.

Co

side of the endocrine system: suppression of the function of the adrenal glands and atrophy of the adrenal glands (decreased response to stress), syndrome

Cushing’s, menstrual irregularities, hirsutism.

Co

aspects of metabolism and nutrition: the transition from latent to clinical

manifestations of diabetes; increased need for insulin and oral

antidiabetic drugs in patients with diabetes mellitus;

sodium and water retention; increased potassium consumption; hypokalemic alkalosis;

negative nitrogen balance due to protein catabolism;

hypocalcemia.

Co

sides of the gastrointestinal tract: dyspepsia, nausea, vomiting, hiccups, peptic

stomach or duodenal ulcer, esophagitis, perforation and bleeding

in the gastrointestinal tract (vomiting with blood, melena), pancreatitis,

gallbladder perforation and intestinal perforation (especially in patients with

inflammatory bowel disease).

Co

sides of the musculoskeletal and connective tissue: muscle weakness,

steroid myopathy (muscle weakness due to muscle catabolism),

fractures of the spine with compression, tendon ruptures (especially with

simultaneous use with some quinolines), damage to the articular cartilage

and bone necrosis (with frequent injections into the joint).

Co

sides of the skin and subcutaneous tissues: delayed healing of wounds, striae, petechiae and

bruising, increased sweating, acne, a suppressed reaction to skin tests,

Quincke’s edema, allergic dermatitis, urticaria, itchy skin.

Co

sides of the organs of vision: increased intraocular pressure; exophthalmos; aggravation

bacterial, fungal, or viral eye infections, thinning of the cornea.

Co

sides of the genitals and mammary gland: impotence, amenorrhea.

Are common

disorders and disorders at the injection site: a transient burning sensation and tingling sensation in

perineum when administered intravenously or when high doses are administered; edema, hyper-

or hypopigmentation of the skin, atrophy of the skin and subcutaneous tissue, sterile abscess, and

redness of the skin.

Signs of glucocorticoid withdrawal syndrome.

In patients who have been treated for a long time

dexamethasone, during a too rapid dose reduction may occur

withdrawal syndrome, as a result of which cases of adrenal insufficiency are possible

glands, arterial hypotension or death. In some cases

withdrawal symptoms may be similar to those of worsening or relapse

disease for which the patient was treated. If severe unwanted

reactions, treatment must be discontinued.

Shelf life. 2 years.

Storage conditions.

Keep out of the reach of children.

original packaging at a temperature not exceeding 25 ° С.

Incompatibility.

The drug should not be mixed with others

drugs other than the following: 0.9% sodium chloride solution or 5%

glucose solution.

When mixing dexamethasone with

chlorpromazine, diphenhydramine, doxapram, doxorubicin, daunorubicin,

idarubicin, hydromorphone, ondansetron, prochlorperazine, potassium nitrate and

vancomycin forms a precipitate.

Approximately 16% of dexamethasone is degraded

in 2.5% glucose solution and 0.9% sodium chloride solution with

amikacin.

Certain medicines such as

lorazepam should be mixed with dexamethasone in glass vials, not in

plastic bags (the concentration of lorazepam is reduced to values ​​below 90%

for 3-4 hours of storage in PVC bags at room temperature

temperature).

With some medications such as

metaraminol, the so-called incompatibility develops, which develops

slowly after 24 hours when mixed with dexamethasone.

Dexamethasone and glycopyrollate: pH value over the counter what happened when methenolone enanthate in

the final solution is 6.4, which is outside the stability range.

Packaging.

1 ml in an ampoule; 5 or 100 ampoules per

a pack or 5 ampoules in a blister, 1 blister in a pack.

Vacation category. On prescription.

Manufacturer. Private Joint Stock Company “Lekhim-Kharkov”.

Location

manufacturer and address of the place of business.

Ukraine, 61115, Kharkiv region, Kharkiv city, Severin Pototskogo street, house 36.