Prednisolone tablets 5mg, No. 60

• Systemic connective tissue diseases (systemic lupus erythematosus, scleroderma, periarteritis nodosa, dermatomyositis, rheumatoid arthritis);

• acute and chronic inflammatory diseases of the joints - gouty and psoriatic arthritis, osteoarthritis (including post-traumatic), polyarthritis, periarthritis of the shoulder scapula, ankylosing spondyloarthritis (ankylosing spondylitis), juvenile arthritis, Still's syndrome in adults, bursitis, nonspecific tendonitis and sinusitis ;

• rheumatic fever, acute rheumatic heart disease;

• bronchial asthma, asthmatic status;

• acute and chronic allergic diseases - incl. allergic reactions to drugs and food, serum sickness, urticaria, allergic rhinitis, Quincke's edema, drug exanthema, hay fever, etc.;

• skin diseases - pemphigus, psoriasis, eczema, atopic dermatitis (widespread neurodermatitis), contact dermatitis (with lesions of a large surface of the skin), toxidermia, seborrheic dermatitis, exfoliative dermatitis, toxic epidermal necrolysis (Lyell's syndrome), bullous herpetiform dermatitis, Stevens-Jones syndrome ;

• cerebral edema (including against the background of a brain tumor or associated with surgery, radiation therapy or head injury) after prior parenteral administration;

• allergic eye diseases: 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 glands);

• congenital adrenal hyperplasia;

• kidney disease of autoimmune genesis (including acute glomerulonephritis); nephrotic syndrome (including against the background of lipoid nephrosis);

• subacute thyroiditis;

• diseases of the blood and hematopoietic system - agranulocytosis, panmyelopathy, autoimmune hemolytic anemia, lympho- and myeloid leukemia, lymphogranulomatosis, thrombocytopenic purpura, secondary thrombocytopenia in adults, erythroblastopenia (erythrocytic anemia), congenital anemia;

• interstitial lung diseases - acute alveolitis, pulmonary fibrosis, stage II-III sarcoidosis;

• tuberculous meningitis, pulmonary tuberculosis, aspiration pneumonia (in combination with specific chemotherapy);

• beryllium disease, Loeffler's syndrome (not amenable to other therapy); lung cancer (in combination with cytostatics);

• multiple sclerosis;

• gastrointestinal diseases - ulcerative colitis, Crohn's disease, local enteritis;

• hepatitis;

• prevention of the graft rejection reaction during organ transplantation;

• hypercalcemia against the background of oncological diseases;

• multiple myeloma.

The dose of the drug and the duration of treatment are set by the doctor individually, depending on the indications and severity of the disease.

It is recommended to take the entire daily dose of the drug once or twice a daily dose - every other day, taking into account the circadian rhythm of endogenous secretion of glucocorticosteroids in the interval from 6 to 8 am. The high daily dose can be divided into 2-4 doses, with a large dose taken in the morning. The tablets should be taken orally during or immediately after a meal with a small amount of liquid.

In acute conditions and as replacement therapy, adults are prescribed an initial dose of 20-30 mg / day, the maintenance dose is 5-10 mg / day. If necessary, the initial dose may be 15-100 mg / day, the maintenance dose is 5-15 mg / day. For children from 3 years of age and older, the initial dose is 1-2 mg / kg of body weight per day in 4-6 doses, the maintenance dose is 0.3-0.6 mg / kg / day.

When a therapeutic effect is obtained, the dose is gradually reduced - 5 mg each, then 2.5 mg at intervals of 3-5 days, canceling the later doses first. With prolonged use of the drug, the daily dose should be reduced gradually. Long-term therapy should not be stopped suddenly! Withdrawal of the maintenance dose is carried out the slower, the longer glucocorticosteroid therapy has been used.

Under stressful influences (infection, allergic reaction, trauma, surgery, nervous stress), in order to avoid exacerbation of the underlying disease, the dose of Prednisolone should be temporarily increased (by 1.5-3, and in severe cases - by 5-10 times).

Tablets of white color of a flat-cylindrical shape with a beveled and scored.

1 tab.

prednisolone 5 mg

Excipients: sucrose (refined sugar) 37.5 mg, lactose monohydrate (milk sugar) 105 mg, gelatin 1 mg, calcium stearate monohydrate 2.5 mg, potato starch sufficient to obtain a tablet weighing 250 mg.

For short-term use for health reasons, a contraindication is

• hypersensitivity to Prednisolone or drug components;

• lactase deficiency, lactose intolerance, sucrase / isomaltase deficiency, fructose intolerance, glucose-galactose malabsorption;

• children's age up to 3 years.

The drug should be used with caution in the following diseases and conditions:

• gastrointestinal diseases - gastric ulcer and duodenal ulcer, esophagitis, gastritis, acute or latent peptic ulcer, recently created intestinal anastomosis, ulcerative colitis with the threat of perforation or abscess formation, diverticulitis;

• parasitic and infectious diseases of a viral, fungal or bacterial nature (ongoing or recently transferred, including recent contact with a patient) - herpes simplex, herpes zoster (viremic phase), chickenpox, measles; amebiasis, strongyloidosis; systemic mycosis; active and latent tuberculosis. Application for severe infectious diseases is permissible only against the background of specific therapy;

• pre- and post-vaccination period (8 weeks before and 2 weeks after vaccination), lymphadenitis after BCG vaccination. Immunodeficiency states (including AIDS or HIV infection).

• diseases of the cardiovascular system, incl. decompensated chronic heart failure, arterial hypertension, hyperlipidemia;

• endocrine diseases - diabetes mellitus (including impaired carbohydrate tolerance), thyrotoxicosis, hypothyroidism, Itsenko-Cushing's disease, obesity (III-IV stage);

• severe chronic renal and / or hepatic failure, nephrourolithiasis;

• hypoalbuminemia and conditions predisposing to its occurrence (cirrhosis of the liver, nephrotic syndrome);

• systemic osteoporosis, myasthenia gravis, acute psychosis, poliomyelitis (except for the form of bulbar encephalitis), open and closed angle glaucoma;

• pregnancy.

In children, during the growth period, glucocorticosteroids should be used only for absolute indications and under the particularly careful supervision of the attending physician.

pharmachologic effect

Prednisolone is a synthetic glucocorticosteroid drug, a dehydrated analogue of hydrocortisone. It has anti-inflammatory, anti-allergic, immunosuppressive effects, anti-shock effects, increases the sensitivity of beta-adrenergic receptors to endogenous catecholamines.

Interacts with specific cytoplasmic receptors (receptors for glucocorticosteroids (GCS) are present in all tissues, especially in the liver) to form a complex that induces the formation of proteins (including enzymes that regulate vital processes in cells).

The anti-inflammatory effect is associated with inhibition of the release of inflammatory mediators by eosinophils and mast cells; inducing the formation of lipocortins and reducing the number of mast cells that produce hyaluronic acid; with a decrease in capillary permeability; stabilization of cell membranes (especially lysosomal) and organelle membranes. Acts at all stages of the inflammatory process: inhibits the synthesis of prostaglandins (Pg) at the level of arachidonic acid (lipocortin inhibits phospholipase A2, inhibits the liberation of arachidonic acid and inhibits the biosynthesis of endoperoxides, leukotrienes that promote inflammation, allergies, etc.), synthesis of 'pro-inflammatory' interleukin 1, tumor necrosis factor alpha, etc.); increases the resistance of the cell membrane to the action of various damaging factors.

Protein metabolism: reduces the amount of globulins in the plasma, increases the synthesis of albumin in the liver and kidneys (with an increase in the albumin / globulin ratio), reduces the synthesis and enhances the catabolism of protein in muscle tissue.

Lipid metabolism: increases the synthesis of higher fatty acids and triglycerides, redistributes fat (fat accumulation occurs mainly in the shoulder girdle, face, abdomen), leads to the development of hypercholesterolemia.

Carbohydrate metabolism: increases the absorption of carbohydrates from the gastrointestinal tract; increases the activity of glucose-6-phosphatase (increasing the flow of glucose from the liver into the blood); increases the activity of phosphoenolpyruvate carboxykinase and the synthesis of aminotransferases (activation of gluconeogenesis); promotes the development of hyperglycemia.

Water-electrolyte metabolism: detains sodium ions (Na +) and water in the body, stimulates the excretion of potassium ions (K +) (mineralocorticosteroid activity), reduces the absorption of calcium ions (Ca2 +) from the gastrointestinal tract, causes the 'washout' of calcium ions from the bones and increasing its renal excretion, reduces bone mineralization.

The immunosuppressive effect is caused by the involution of lymphoid tissue caused by the inhibition of the proliferation of lymphocytes (especially T-lymphocytes), suppression of the migration of B-cells and the interaction of T- and B-lymphocytes, inhibition of the release of cytokines (interleukin-1, 2; gamma-interferon) from lymphocytes and macrophages and a decrease in the formation of antibodies.

The antiallergic effect develops as a result of a decrease in 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, a decrease in the number of T- and B-lymphocytes, mast cells , decrease in the sensitivity of effector cells to allergy mediators, inhibition of antibody production, changes in the body's immune response.

In obstructive respiratory diseases, the action is mainly due to the inhibition of inflammatory processes, the prevention or reduction of the severity of edema of the mucous membranes, a decrease in eosinophilic infiltration of the submucous layer of the bronchial epithelium and the deposition of circulating immune complexes in the bronchial mucosa, as well as inhibition of erosion and desquamation of the mucous membrane. Increases the sensitivity of the beta-adrenergic receptors of the bronchi of small and medium caliber to endogenous catecholamines and exogenous sympathomimetics, reduces the viscosity of mucus by reducing its production.

Suppresses the synthesis and secretion of ACTH and, secondarily, the synthesis of endogenous GCS.

Pharmacokinetics

When taken orally, prednisolone is well absorbed from the gastrointestinal tract. Cmax in the blood is reached within 1-1.5 hours after oral administration. Up to 90% of the drug binds to plasma proteins: transcortin (cortisol-binding globulin) and albumin.

Prednisolone is metabolized in the liver, partly in the kidneys and other tissues, mainly by conjugation with glucuronic and sulfuric acids. The metabolites are inactive.

It is excreted in the bile and kidneys by glomerular filtration and is 80-90% reabsorbed by the tubules. 20% of the dose is excreted by the kidneys unchanged. T1 / 2 from plasma after oral administration is 2-4 hours.

Side effect

The frequency of development and the severity of side effects depends on the duration of use, the size of the dose used and the possibility of observing the circadian rhythm of the appointment of Prednisolone.

When using Prednisolone, there may be:

From the endocrine system: decreased glucose tolerance, 'steroid' diabetes mellitus or manifestation of latent diabetes mellitus, suppression of adrenal function, Itsenko-Cushing's syndrome (moon face, pituitary obesity, hirsutism, increased blood pressure, dysmenorrhea, amenorrhea, muscle striae), delayed sexual development in children.

On the part of the digestive system: nausea, vomiting, pancreatitis, 'steroid' stomach and duodenal ulcer, erosive esophagitis, gastrointestinal bleeding and perforation of the gastrointestinal tract wall, increased or decreased appetite, indigestion, flatulence, hiccups, increased activity of liver transplant and alkaline phosphatase.

From the side of the cardiovascular system: arrhythmias, bradycardia (up to cardiac arrest); development (in predisposed patients) or increased severity of heart failure, ECG changes characteristic of hypokalemia, increased blood pressure, hypercoagulation, thrombosis. In patients with acute and sub-acute myocardial infarction, the spread of the focus of necrosis, slowing of the formation of scar tissue, which can lead to rupture of the heart muscle.

From the nervous system: delirium, disorientation, euphoria, hallucinations, manic-depressive psychosis, depression, paranoia, increased intracranial pressure, nervousness or anxiety, insomnia, dizziness, vertigo, cerebellar pseudotumor, headache, convulsions.

From the senses: posterior subcapsular cataract, increased intraocular pressure with possible damage to the optic nerve, a tendency to develop secondary bacterial, fungal or viral eye infections, trophic changes in the cornea, exophthalmos.

From the side of metabolism: increased excretion of calcium ions, hypocalcemia, increased body weight, negative nitrogen balance (increased protein breakdown), increased sweating.

Due to mineralocorticosteroid activity - fluid and sodium ion retention in the body (peripheral edema), hypernatremia, hypokalemic syndrome (hypokalemia, arrhythmia, myalgia or muscle spasm, unusual weakness and fatigue).

On the part of the musculoskeletal system: growth retardation and ossification processes in children (premature closure of the epiphyseal growth zones), osteoporosis (pathological bone fractures, aseptic necrosis of the humerus and femur head), muscle tendon rupture, 'steroid' myopathy, decreased muscle mass ( atrophy).

On the part of the skin and mucous membranes: delayed wound healing, petechiae, ecchymosis, thinning of the skin, hyper- or hypopigmentation, acne, striae, a tendency to develop pyoderma and candidiasis.

Allergic reactions: skin rash, itching, anaphylactic shock.

Others: the development or exacerbation of infections (the occurrence of this side effect is facilitated by jointly used immunosuppressants and vaccinations), leukocyturia, withdrawal syndrome, frequent nighttime urination, urolithiasis.

Application during pregnancy and lactation

During pregnancy in the I and II trimester, it is used only for health reasons. With prolonged therapy during pregnancy, fetal growth is impaired. In the third trimester of pregnancy, there is a risk of atrophy of the adrenal cortex in the fetus, which may require replacement therapy for the newborn.

Since glucocorticosteroids pass into breast milk, if it is necessary to use the drug during breastfeeding, it is recommended to stop breastfeeding.

Application for violations of liver function

Contraindicated in severe chronic liver failure

Application for impaired renal function

Contraindicated in severe chronic renal failure

Application in children

Contraindicated in children under 3 years of age. In children, during the growth period, glucocorticosteroids should be used only for absolute indications and under the particularly careful supervision of the attending physician.

special instructions

Before starting treatment (if it is impossible due to the urgency of the condition - during treatment), the patient should be examined to identify possible contraindications. Clinical examination should include examination of the cardiovascular system, X-ray examination of the lungs, examination of the stomach and duodenum, urinary system, organs of vision; control of blood count, glucose and electrolytes in blood plasma.

During treatment with Prednisolone (especially long-term), it is necessary to observe an ophthalmologist, control blood pressure, the state of water and electrolyte balance, as well as a picture of peripheral blood and blood glucose concentration.

In order to reduce side effects, antacids can be used, as well as to increase the flow of potassium ions (K +) into the body (diet, potassium preparations). Food should be rich in proteins, vitamins, with limited content of fats, carbohydrates and table salt.

The effect of the drug is enhanced in patients with hypothyroidism and liver cirrhosis.

The drug can exacerbate existing emotional instability or psychotic disturbances. If a history of psychosis is indicated, Prednisolone in high doses is used under the strict supervision of a physician.

In stressful situations during supportive treatment (for example, surgery, trauma or infectious diseases), the dose of the drug should be adjusted due to the increased need for glucocorticosteroids. Patients should be carefully monitored for a year after the end of long-term therapy with Prednisolone due to the possible development of relative adrenal insufficiency in stressful situations.

With a sudden cancellation, especially in the case of previous use of high doses, it is possible to develop a withdrawal syndrome (anorexia, nausea, lethargy, generalized musculoskeletal pain, general weakness), as well as exacerbation of the disease for which Prednisolone was prescribed.

During treatment with Prednisolone, vaccination should not be carried out due to a decrease in its effectiveness (immune response).

Applying Prednisolone for intercurrent infections, septic conditions and tuberculosis, it is necessary to simultaneously treat with antibiotics with bactericidal action.

In children, during long-term treatment with Prednisolone, careful monitoring of the dynamics of growth and development is necessary. Children who, during the period of treatment, were in contact with patients with measles or chickenpox, prophylactically use specific immunoglobulins.

Due to the weak mineralocorticosteroid effect for replacement therapy for adrenal insufficiency, Prednisolone is used in combination with mineralocorticosteroids.

In patients with diabetes mellitus, blood glucose should be monitored and, if necessary, therapy should be corrected.

X-ray control of the osteoarticular system is shown (images of the spine, hand).

ѕреднизолон у больных с латентными инфекционными заболевани¤ми почек и мочевыво-д¤щих путей способен вызвать лейкоцитурию, что может иметь диагностическое значение.

ѕреднизолон повышает содержание метаболитов 11- и 17-оксикетокортикостероидов.

¬ли¤ние на способность к вождению автотранспорта и управлению механизмами

¬ период применени¤ необходимо воздержатьс¤ от управлени¤ автотранспортом и зан¤тий потенциально опасными видами де¤тельности, требующими повышенной концентрации внимани¤ и быстроты психомоторных реакций.

ѕередозировка

¬озможно усиление дозозависимых побочных ¤влений.

Ќеобходимо уменьшить дозу ѕреднизолона. Ћечение симптоматическое.

Ћекарственное взаимодействие

ќдновременное применение преднизолона с:

индукторами 'печеночных' микросомальных ферментов (фенобарбитал, рифампицин, фенитоин, теофиллин, эфедрин) приводит к снижению его концентрации;

диуретиками (особенно 'тиазидными' и ингибиторами карбоангидразы) и амфотерицином ¬ может привести к усилению выведени¤ из организма ионов  +;

натрийсодержащими препаратами - к развитию отеков и повышению артериального давлени¤;

амфотерицином ¬ - увеличиваетс¤ риск развити¤ сердечной недостаточности;

сердечными гликозидами - ухудшаетс¤ их переносимость и повышаетс¤ веро¤тность развити¤ желудочковой экстрасистолии (из-за вызываемой гипокалиемии);

непр¤мыми антикоагул¤нтами - ослабл¤ет (реже усиливает) их действие (требуетс¤ коррекци¤ дозы);

антикоагул¤нтами и тромболитиками - повышаетс¤ риск развити¤ кровотечений из ¤зв в желудочно-кишечном тракте;

этанолом и нестероидными противовоспалительными препаратами (Ќѕ¬ѕ) - усиливаетс¤ риск возникновени¤ эрозивно-¤звенных поражений в желудочно-кишечном тракте и развити¤ кровотечений (в комбинации с Ќѕ¬ѕ при лечении артритов возможно снижение дозы глюкокортикостероидов из-за суммации терапевтического эффекта);

парацетамолом - возрастает риск развити¤ гепатотоксичности (индукци¤ 'печеночных' ферментов и образовани¤ токсичного метаболита парацетамола);

ацетилсалициловой кислотой - ускор¤ет ее выведение и снижает концентрацию в крови (при отмене преднизолона уровень салицилатов в крови увеличиваетс¤ и возрастает риск развити¤ побочных ¤влений);

инсулином и пероральными гипогликемическими препаратами, гипотензивными средствами - уменьшаетс¤ их эффективность;

витамином D - снижаетс¤ его вли¤ние на всасывание ионов кальци¤ (—а2+) в кишечнике;

соматотропным гормоном Ч снижает эффективность последнего, а с празиквантелом - его концентрацию;

ћ-холиноблокаторами (включа¤ антигистаминные препараты и трициклические антидепрессанты с м-холиноблокирующей активностью) и нитратами - способствует повышению внутриглазного давлени¤;

изониазидом и мексилетином - увеличивает их метаболизм (особенно у 'медленных' ацетил¤торов), что приводит к снижению их плазменных концентраций.

»нгибиторы карбоангидразы и 'петлевые' диуретики могут увеличивать риск развити¤ остеопороза.

»ндометацин, вытесн¤¤ преднизолон из св¤зи с альбуминами, увеличивает риск развити¤ его побочных эффектов.

јдренокортикотропный гормон (ј “v) усиливает действие преднизолона.

Ёргокальциферол и паратгормон преп¤тствуют развитию остеопатии, вызываемой преднизолоном.

?иклоспорин и кетоконазол, замед뤤 метаболизм преднизолона, могут в р¤де случаев увеличивать его токсичность.

ќдновременное применение андрогенов и стероидных анаболических препаратов с преднизолоном способствует развитию периферических отеков и гирсутизма, по¤влению угрей.

Ёстрогены и пероральные эстрогенсодержащие контрацептивы снижают клиренс преднизолона, что может сопровождатьс¤ усилением выраженности его действи¤.

ћитотан и другие ингибиторы функции коры надпочечников могут обусловливать необходимость повышени¤ дозы преднизолона.

ѕри одновременном применении с живыми противовирусными вакцинами и на фоне других видов иммунизации - увеличивает риск активации вирусов и развити¤ инфекций.

јнтипсихотические средства (нейролептики) и азатиоприн повышают риск развити¤ катаракты при применении преднизолона.

Immunosuppressants increase the risk of Epstein-Barr virus infections and lymphoma or other lymphoproliferative disorders.

The simultaneous use of antacids reduces the absorption of prednisolone.

With simultaneous use with antithyroid drugs, it decreases, and with thyroid hormones, the clearance of prednisolone increases.