Prednisolone with edema

Form of release, composition and packaging

Tablets with a diameter of 6.5 mm, with a squeezed out symbol on one side. 1 tab. prednisolone 5 mg. Excipients: lactose, potato starch, gelatin, magnesium stearate.

Clinico-pharmacological group: GCS for oral administration.

Synthetic GCS. Has a pronounced anti-inflammatory effect. It is believed that the anti-inflammatory effect of 5 mg of prednisolone is equivalent to the action of 4 mg of methylprednisolone or triamcinolone, 0.75 mg of dexamethasone, 0.6 mg of betamethasone and 20 mg of hydrocortisone. Mineralocorticoid activity of prednisolone is about 60% of hydrocortisone. The drug inhibits the development of symptoms of inflammation.

It inhibits the accumulation of macrophages, leukocytes andother cells in the inflammation zone. Inhibits phagocytosis, the release of microsomal enzymes, as well as the synthesis and release of inflammatory mediators. It causes a decrease in the permeability of capillaries, inhibition of migration of leukocytes.

Enhances the synthesis of lipomodulin, an inhibitorphospholipase A2, releasing arachidonic acid from phospholipid membranes with simultaneous inhibition of its synthesis. The mechanism of immunosuppressive action of prednisolone is not fully understood. The drug reduces the number of T-lymphocytes, monocytes and acidophilic granulocytes, as well as the binding of immunoglobulins to receptors on the cell surface, inhibits the synthesis or release of interleukins by reducing the blastogenesis of T lymphocytes; reduces early immunological response.

It also inhibits the penetration of immunologicalcomplexes through membranes and reduces the concentration of components of complement and immunoglobulins. Prednisolone acts on the distal part of the renal tubules, enhancing the reabsorption of sodium and water, as well as an increase in the release of potassium and hydrogen ions.

Prednisolone inhibits the secretion of ACTH by the pituitary gland,which leads to a decrease in the production of corticosteroids and androgens by the adrenal cortex. After long-term use of the drug in high doses, the function of the adrenal glands can be restored within a year, and in some cases, a persistent suppression of their function develops.

Prednisolone enhances protein catabolism andinduces enzymes involved in the metabolism of amino acids. It inhibits synthesis and enhances catabolism of proteins in lymphatic, connective, muscle tissue. With prolonged use, it is possible to develop atrophy of these tissues (as well as skin).

Increases the concentration of glucose in the blood byinduction of enzymes of gluconeogenesis in the liver, stimulation of protein catabolism (which increases the number of amino acids for gluconeogenesis) and a decrease in glucose consumption in peripheral tissues. This leads to the accumulation of glycogen in the liver, increased blood glucose concentration and increased insulin resistance. With prolonged use of the drug, a redistribution of adipose tissue is possible.

Oppresses the formation of bone tissue and strengthens itresorption, reducing the concentration of calcium in the blood serum, which leads to secondary hyperfunction of parathyroid glands and simultaneous stimulation of osteoclasts and inhibition of osteoblasts. These effects, together with a secondary decrease in the amount of protein components due to protein catabolism, can lead to suppression of bone growth in children and adolescents and to the development of osteoporosis in children of all ages. Strengthens the action of endo- and exogenous catecholamines.

Endocrine diseases:
insufficiency of the adrenal cortex: primary (Addison's disease) and secondary;
adrenogenital syndrome (congenital adrenal hyperplasia);
acute insufficiency of the adrenal cortex;
before surgical interventions and in severe diseases and injuries in patients with adrenal insufficiency;
subacute thyroiditis.

Severe allergic diseases resistant to other therapies:
contact dermatitis;
atopic dermatitis;
serum sickness;
reactions of hypersensitivity to medicines;
permanent or seasonal allergic rhinitis;
anaphylactic reaction;

Rheumatic diseases:
rheumatoid arthritis, juvenile rheumatoid arthritis (in cases resistant to other methods of treatment);
psoriatic arthritis;
ankylosing spondylitis;
acute gouty arthritis;
acute rheumatic fever;
myocarditis (including rheumatic);
systemic lupus erythematosus;
mesoarteritis granulomatous giant cell;
systemic scleroderma;
nodular periarteritis;
recurrent polychondritis;
Rheumatic polymyalgia (Horton's disease);
systemic vasculitis.

Dermatological diseases:
exfoliative dermatitis;
herpetiform bullous dermatitis;
severe seborrheic dermatitis;
severe erythema multiforme (Stevens-Johnson syndrome);
mushroom mycosis;
severe psoriasis;
severe forms of eczema;

Hematological diseases:
acquired autoimmune hemolytic anemia;
congenital aplastic anemia;
idiopathic thrombocytopenic purpura (Verlhof's disease) in adults;

Liver diseases:
alcoholic hepatitis with encephalopathy;
chronic active hepatitis.

Hypercalcemia in malignant neoplasms or sarcoidosis.

Inflammatory diseases of the joints:
acute and subacute bursitis;
acute tendovaginitis;
posttraumatic osteoarthritis.

Oncological diseases:
acute and chronic leukemia;
mammary cancer;
prostate cancer;
multiple myeloma.

Neurological diseases:
tuberculous meningitis with a subarachnoid block;
Multiple sclerosis in the phase of exacerbation;
myasthenia gravis.

Diseases of the eyes (severe acute and chronic allergic and inflammatory processes):
severe sluggish anterior and posterior uveitis;
optic neuritis;
sympathetic ophthalmia. Pericarditis.

Diseases of the respiratory system:
bronchial asthma;
Leffler's syndrome;
symptomatic sarcoidosis;
fulminant or disseminated pulmonary tuberculosis (in combination with antituberculous chemotherapy);
chronic pulmonary emphysema (resistant to aminophylline and beta-adrenomimetics).

When transplanting organs and tissues to prevent and treat the reaction of graft rejection (in combination with other immunosuppressive drugs).

The dosage regimen is set individually independing on the indications, the effectiveness of therapy and the patient's condition. In accordance with the daily rhythm of the secretion of endogenous glucocorticoids, the drug is recommended to be taken 1 time / day in the morning. In some cases, more frequent drug intake is required. After achieving the desired therapeutic effect, a gradual dose reduction to a minimally effective dose is recommended. The average recommended dose for adults is 5-60 mg / day, the maximum daily dose is 200 mg.

With multiple sclerosis during the exacerbation of the drug is prescribed at a dose of 200 mg / day for 7 days, then 80 mg / day for a month.

Children dose set at 0.14 mg / kg body weight / day. in 3-4 reception. In case of missing the dose, the drug should be taken as soon as possible or, if the next appointment is approaching, the missed dose should not be taken. Do not take a double dose at a time.

With short-term use of prednisolone (asand other SCS), side effects are rare. With the use of prednisolone for a long time, the following side effects may develop.
From the water-electrolyte balance: a delay in the body of sodium and liquid, hypokalemia, hypokalemic alkalosis, increased blood pressure, circulatory insufficiency.
From the musculoskeletal system: muscle weakness, steroid myopathy, loss of muscle mass, osteoporosis, compression fracture of the spine, aseptic necrosis of femoral and humerus head, pathological fractures of long tubular bones.
From the digestive system: steroid ulcer with possible perforation and bleeding, pancreatitis, flatulence, ulcerative esophagitis, digestive disorders, nausea, increased appetite. Dermatological reactions: skin atrophy, striae, acne, delayed wound healing, thinning of the skin, petechiae, hematoma, erythema, increased sweating, allergic dermatitis, urticaria, angioedema.
From the side of the central nervous system and the peripheral nervous system: increased intracranial pressure with the syndrome of the congestive nipple of the optic nerve (occurs most often in children, after too rapid reduction of the dose, symptoms - headache, deterioration of visual acuity, double vision); convulsions, dizziness, headache, sleep disturbances.
On the part of the endocrine status: secondary adrenal and hypothalamic-pituitary insufficiency (especially during stressful situations: illness, trauma, surgical operation); Cushing's syndrome, growth inhibition in children, menstrual irregularities, hyperglycemia, glucosuria, decreased tolerance to carbohydrates, manifestation of latent diabetes mellitus, and increased need for insulin or oral hypoglycemic drugs in patients with diabetes mellitus, hirsutism.
From the side of the organ of vision: posterior subcapsular cataract, increased intraocular pressure, glaucoma, exophthalmos.
From the psychic sphere: most often occur during the first 2 weeks of therapy, the symptoms can mimic schizophrenia, mania, delirious syndrome; The most susceptible to the development of mental disorders are women and patients with systemic lupus erythematosus.
From the side of metabolism: negative nitrogen balance (as a result of protein catabolism).
From the laboratory indicators: an increase in the number of white blood cells (20,000 / μl), a decrease in the number of lymphocytes and monocytes, an increase or decrease in the number of platelets, an increase in the concentration of calcium in the blood and urine, an increase in total cholesterol, LDL, triglycerides in the serum, an increase in the concentration of 17-hydroxycorticosteroids and 17 -ketosteroid in the urine, a decrease in the capture of labeled technetium with bone tissue and tissue of brain tumors, a decrease in the capture of the labeled iodine by the thyroid gland; weakened reaction in skin allergic tests and tuberculin test. Other: anaphylactic reactions, hypersensitivity reactions; obliterating arteritis, weight gain, fainting.

systemic fungal infections;
hypersensitivity to the components of the drug.

Controlled clinical trialssafety of use of the drug during pregnancy was not conducted. In experimental studies, it was established that GCS caused an increase in the incidence of cleft palate, miscarriage, placental insufficiency, and delayed fetal development.

In clinical practice, the teratogenic effect is notconfirmed, but there are data indicating an increase in the risk of placental insufficiency, birth and fetal death in women who received SCS during pregnancy. The appointment of GCS in pregnancy and women of childbearing age is permissible only in cases where the intended benefit to the mother exceeds the potential risk to the fetus.

Women of childbearing age should bewere informed of the potential risk of HA therapy for the fetus. Prednisolone is excreted in breast milk and can cause unsuccessful effects in a breastfed infant (growth retardation or inhibition of the production of endogenous hormones in the adrenal cortex). If it is necessary to use the drug during lactation, breastfeeding should be stopped.

Prednisolone is contraindicated in patients with systemicfungal infections due to the risk of increased infection. The drug in some cases used in the treatment of fungal infections amphotericin B to reduce the side effects of the antifungal drug, but this combination can lead to the development of circulatory insufficiency and myocardial hypertrophy of the left ventricle of the heart, as well as the occurrence of severe hypokalemia.

In case of stressful situations,patients receiving Prednisolone, recommended parenteral administration of GCS. Sudden abolition of GCS can cause the development of acute adrenocortical insufficiency, so the dose of Prednisolone should be reduced gradually. Prednisolone can mask the symptoms of infection, reduce the resistance of the body to infections, and also reduce the body's ability to localize the infection process. Against the background of the use of the drug, clinical manifestations of latent amoebiasis are possible.

For persons arriving from tropical countries, orpatients with dysentery of unknown etiology, dysenteric amoebiasis should be excluded before Prednisolone is used. Prolonged use of prednisolone increases the risk of developing secondary fungal or viral infections. Against the background of long-term use of GCS, the development of cataracts, glaucoma (including with optic nerve damage) is possible.

When using prednisolone in high dosesshould monitor blood pressure (the possible development of hypertension), the body weight of patients (possibly the occurrence of peripheral edema). Periodically monitor the concentration of electrolytes in the serum. In some cases, it may be necessary to limit sodium intake and increase potassium intake. Prednisolone also causes an increase in calcium excretion.

Patients receiving SCS should notvaccinate with live viral vaccines (due to the possible replication of viruses and the development of viral diseases), and there may also be a decrease in the production of antibodies. The introduction of an inactivated viral or bacterial vaccine may not produce the expected increase in the number of antibodies. It is possible to vaccinate patients who receive SCS as a substitution therapy, for example, with Addison's disease.

In addition, in patients taking GCS,there is an increased risk of developing neurological complications. The appointment of SCS to patients with active tuberculosis is possible only in cases of disseminated or fulminant tuberculosis and only in combination with anti-tuberculosis therapy. Patients with latent tuberculosis or positive tuberculin test taking Prednisolone should be monitored because of the high risk of activation of the tuberculosis process. With prolonged use of GCS, this category of patients should receive chemoprophylaxis. The use of the drug can mask the symptoms of infectious diseases.

With the sudden reversal of prednisolone (especially afterprolonged use) may develop withdrawal syndrome (manifested by anorexia, increased body temperature, myalgia and arthralgia, general weakness). Symptoms can occur even when there is no evidence of adrenocortical insufficiency. In patients with hypothyroidism or cirrhosis, the effect of prednisolone is enhanced.

When Prednisolone is used, it is possible to developmental disorders (euphoria, insomnia, sudden mood changes, personality changes, severe depression, symptoms of psychosis). The emotional instability or psychotic tendencies that existed earlier may be amplified against the background of SCS therapy. When using GCS in patients with hypoprothrombinemia, caution should be given to acetylsalicylic acid.

With caution appoint a drug whennonspecific ulcerative colitis due to the risk of intestinal perforation, abscess or other purulent infections; with diverticulosis of the intestine, fresh intestinal anastomoses, erosive and ulcerative gastrointestinal lesions, with renal insufficiency, arterial hypertension, osteoporosis, myasthenia gravis, diabetes mellitus, impaired liver function, glaucoma, viral infections, hyperlipidemia, hypoalbuminemia. With the development of gastrointestinal perforation against the background of the use of GCS, the symptoms of peritonitis can be expressed slightly or absent altogether.

At some patients on a background of therapy GKSthe amount and mobility of spermatozoa varies. Taking the drug during meals can reduce the likelihood of side effects from the gastrointestinal tract. The effectiveness of antacid drugs in preventing the formation of ulcers, bleeding from the gastrointestinal tract or intestinal perforation is not confirmed.
With the development of steroid myopathy and impossibilityabolition of therapy with GCS replacement of prednisolone on another GCS can alleviate symptoms. The risk of developing osteoporosis associated with prolonged use of GCS can be reduced by taking vitamin D and calcium preparations or, if the patient's condition allows, by performing appropriate physical exercises.
When psychosis or depression occurs, it should be possible to reduce the dose or stop taking the drug.
If necessary, you can use phenothiazine orlithium preparations. The use of tricyclic antidepressants is contraindicated. In order to mitigate some manifestations of withdrawal syndrome, it is possible to prescribe acetylsalicylic acid or other NSAIDs.

When prescribing a drug, children need to monitor their growth and development.

The risk of overdose increases withprolonged use of prednisone, especially in high doses. Symptoms: increased blood pressure, peripheral edema; In addition, there may be an increase in side effects. Treatment: temporarily stop taking the drug or reduce the dose.

Drug Interactions
When combined with cardiacglycosides increases the risk of heart rhythm disorders and glycosides toxicity associated with hypokalemia. Barbiturates, anticonvulsants (phenytoin, carbamazepine), rifampicin, glutetimide accelerate the metabolism of GCS (by induction of microsomal enzymes), weaken their action.
When combined, histamine H1 receptor blockers weaken the action of prednisolone.
With the combined use of prednisolone with amphotericin B, carbonic anhydrase inhibitors may develop hypokalemia, left ventricular myocardial hypertrophy, circulatory insufficiency.
When combined with paracetamolpossibly the development of hypernatremia, peripheral edema, increased excretion of calcium, increases the risk of hypocalcemia and osteoporosis, as well as hepatotoxic reactions associated with paracetamol.
When combined with anabolicsteroids, androgens increases the risk of developing peripheral edema, acne (this combination requires caution, especially in the case of concomitant diseases of the heart and liver).
When used simultaneously with oralcontraceptives containing estrogens, it is possible to increase the concentration of globulins that bind steroids in the blood serum, slow the metabolism, increase T1 / 2 and increase the action of prednisolone.
When combined with holinoblokatorami (atropine) may increase intraocular pressure.
When combined with anticoagulants(coumarin derivatives, indadion, heparin), streptokinase, urokinase, there may be a decrease (in some patients - an increase) in effectiveness, ulceration and bleeding from the gastrointestinal tract may occur; the dose should be determined based on prothrombin time.
When combined with tricyclicantidepressants may increase the mental disorder associated with taking prednisolone (the use of tricyclic antidepressants for the correction of mental disorders on the background of taking GCS is not recommended).
When combined with prednisolonepossibly reducing the hypoglycemic effect of insulin and oral hypoglycemic agents, possibly increasing the level of glucose (which may require correction of the dose of antidiabetic drugs).
When combined with prednisolone,a dose adjustment or discontinuation of antithyroid drugs or thyroid hormones is required; it is possible to change the indices of thyroid function.
When combined with prednisolone, the effect of potassium-sparing diuretics, hypokalemia, is possible.
When combined with prednisolone, laxative agents and the development of hypokalemia may be weakened.
When combined, ephedrine can accelerate the metabolism of GCS (prednisolone dose adjustment may be required).
With the combined use of prednisolone with other immunosuppressive drugs, the risk of infection, lymphomas and other lymphoproliferative diseases increases.
With simultaneous use with prednisolone, a decrease in the concentration of isoniazid in the blood plasma (mainly in individuals with rapid acetylation), a dose adjustment of prednisolone may be required.
With simultaneous use with prednisolone, accelerated metabolism of mexiletine and a decrease in its concentration in plasma are noted.
When combined with depolarizingmuscle relaxants, it should be taken into account that hypocalcemia associated with the use of prednisolone may enhance the blockade of synapses, leading to an increase in the duration of the neuromuscular blockade. Acetylsalicylic acid and other NSAIDs, ethanol weaken the action of prednisolone, increase the risk of developing peptic ulcer and bleeding from the digestive tract.

Drugs and food containing sodium, withsimultaneous application with prednisolone increase the likelihood of developing arterial hypertension and peripheral edema. Against the background of the use of GCS, the need for folic acid is increasing.

Terms and conditions of storage

The drug should be stored in a dry place, protected from light and inaccessible to children. Shelf life - 3 years.