Dexamethasone | Lekhim
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on the medical use of the medicinal product
active substance: dexamethasone sodium phosphate;
solution contains 4 mg of dexamethasone sodium phosphate on a dry basis
excipients: propylene glycol, glycerin, disodium edetate, phosphate buffer solution
pH 7.5, methylparaben (E 218), propylparaben (E 216), water for
Dosage form. Solution
Basic physical and chemical
Pharmacotherapeutic group. Corticosteroids for systemic
ATX code Н02А B02.
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
Impact on energy metabolism and
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
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
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.
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).
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
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.
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.
The biological half-life of dexamethasone is 24-72 hours.
Predominantly excreted in urine.
intravenously or intramuscularly in urgent cases and if impossible
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
– 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
– 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.
(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.
– 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.
(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).
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:
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.
– 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).
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
– cerebral edema
due to a primary or metastatic brain tumor, trepanation
skull and traumatic brain injury.
– 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
– 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;
sensitivity to the active substance or to any other ingredient
bacterial or systemic fungal infections (unless appropriate
breastfeeding (except in urgent cases).
administration is contraindicated in patients with severe blood clotting diseases.
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.
other drugs and other types of interactions.
Parallel use of dexamethasone and non-steroidal
anti-inflammatory drugs increase the risk of gastrointestinal bleeding and
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,
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
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
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.
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
for the prevention of nausea and vomiting caused by cisplatin chemotherapy,
cyclophosphamide, methotrexate, fluorouracil.
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
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.
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.
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.
dexamethasone or natural glucocorticoids may mask symptoms
existing or new infection, as well as symptoms of intestinal perforation.
may exacerbate systemic fungal infection, latent amebiasis, and tuberculosis
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
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.
during treatment, there may be an exacerbation of diabetes or a transition from latent
phases to clinical manifestations of diabetes.
long-term treatment should monitor serum potassium levels.
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
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.
exercise caution in patients who recover from surgery or
bone fracture, as dexamethasone can slow wound healing and
glucocorticoids are increased in patients with liver cirrhosis or hypothyroidism.
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administration of corticosteroids can lead to local and systemic effects. Frequent
application may cause cartilage damage or bone necrosis.
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.
should be advised to avoid physical exertion on the affected
joints until the inflammation is cured.
avoid injecting the drug into unstable joints.
may skew the results of allergy skin tests.
Special warnings regarding
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
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
The ability to influence the reaction rate when driving or
Dexamethasone does not affect
on the ability to drive a car and other mechanical means.
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%
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.
Dexamethasone should be administered parenterally in emergencies,
in cases where oral therapy is not possible, and in the cases specified in
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
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
2-6 injectable sustanon 250 for sale mg.
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
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.
isolated reports of acute overdose or death due to acute
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
Side effects with short-term treatment
side of the immune system: hypersensitivity reactions.
side of the endocrine system: transient suppression of the function of the adrenal glands.
side of metabolism and nutrition: decreased tolerance to carbohydrates, increased
appetite and weight gain, hypertriglyceridemia.
side of the psyche: mental disorders.
sides of the gastrointestinal tract: peptic ulcer and acute pancreatitis.
Side effects with long-term treatment
side of the immune system: a decrease in the immune response and an increase
susceptibility to infections.
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
metabolic and nutritional aspects: obesity.
sides of the organs of vision: cataract, glaucoma.
vascular sides: hypertension; telangiectasia.
sides of the skin and subcutaneous tissue: thinning of the skin.
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:
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
sides of the immune system: rash, bronchospasm, anaphylactic reactions,
development of opportunistic infections, hypersensitivity reactions.
sides of the heart: multifocal extrasystole of the ventricle, temporary bradycardia,
heart failure, cardiac arrest, myocardial perforation due to
suffered myocardial infarction.
vascular side: hypertensive encephalopathy.
sides of the respiratory system, organs of the chest and mediastinum: relapse of inactive
side of the nervous system: edema of the optic nerve and increased intracranial
pressure (benign intracranial hypertension) after discontinuation
treatment; dizziness; vertigo, headache, convulsions.
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.
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.
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;
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).
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).
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.
sides of the organs of vision: increased intraocular pressure; exophthalmos; aggravation
bacterial, fungal, or viral eye infections, thinning of the cornea.
sides of the genitals and mammary gland: impotence, amenorrhea.
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.
Keep out of the reach of children.
original packaging at a temperature not exceeding 25 ° С.
The drug should not be mixed with others
drugs other than the following: 0.9% sodium chloride solution or 5%
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
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
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.
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”.
manufacturer and address of the place of business.
Ukraine, 61115, Kharkiv region, Kharkiv city, Severin Pototskogo street, house 36.