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Alfacort is a glucocorticosteroid. Alfacort inhibits the function of leukocytes and tissue macrophages. The migration of leukocytes in the area of inflammation. Impair the capacity of macrophages to phagocytosis and the formation of interleukin-1. Contributes to the stabilization of lysosomal membranes, thereby reducing the concentration of proteolytic enzymes in the field of inflammation. Decreases capillary permeability due to histamine release. Inhibits activity of fibroblasts and collagen formation.
Alfacort inhibits the activity of phospholipase A2 which leads to suppression of the synthesis of prostaglandins and leukotrienes. Suppresses the release of COX (mainly COX-2), which also helps to reduce production of prostaglandins.
Reduces the number of circulating lymphocytes (T-and B-cells), monocytes, eosinophils and basophils as a result of their displacement from the vascular bed to lymphoid tissue, suppresses the formation of antibodies.
Alfacort suppresses the release of pituitary ACTH and beta-lipotropin but does not reduce the level of circulating beta-endorphin. Inhibits the secretion of TSH and FSH.
With direct application of the receptacles has a vasoconstrictor effect.
Alfacort has a pronounced dose-dependent effect on the metabolism of carbohydrates, proteins and fats. Stimulates gluconeogenesis, promotes the capture of amino acids by the liver and kidneys and increases the activity of enzymes of gluconeogenesis. In the liver of Alfacort increases glycogen deposition by stimulating the activity of glycogen synthase and synthesis of glucose from the products of protein metabolism. Increased blood glucose activates the secretion of insulin.
Alfacort suppresses the seizure of glucose by fat cells that leads to activation of lipolysis. However, due to increased secretion of insulin is stimulation of lipogenesis which leads to the accumulation of fat.
Alfacort has catabolic effect in lymphoid and connective tissue, muscle, adipose tissue, skin, bone tissue; to a lesser extent than the mineralocorticoid affects the processes of water and electrolyte metabolism: promotes the excretion of potassium ions and calcium, delay in the body of sodium and water. Osteoporosis and Itsenko-Cushing's syndrome are the main factors limiting the long-term therapy of GCS. As a result of catabolic actions may suppress growth in children.
In high doses Alfacort may increase the excitability of brain tissue and contributes to lowering the threshold of convulsive readiness. It stimulates the excessive production of hydrochloric acid and pepsin in the stomach that promotes the development of peptic ulcers.
For systems use therapeutic activity of Alfacort caused by anti-inflammatory, anti-allergic, immunosuppressive and antiproliferative action. When external and local application the therapeutic activity of Alfacort is due to anti-inflammatory, anti-allergic and antiexudative (due to vasoconstrictor effect) action. For anti-inflammatory activity this medicine is 4 times weaker than prednisolone, at mineralocorticoid activity is superior to other GCS.
Binding to plasma proteins - 40-90%. Metabolised mainly in the liver. T1/2 is 80-120 min. It is withdrawed by the kidneys mainly as metabolites.
Why is Alfacort prescribed?
For parenteral use of Alfacort: acute adrenal insufficiency, allergic reactions of immediate type, asthmatic status, prevention and treatment of shock, myocardial infarction complicated by cardiogenic shock, thyrotoxic crisis, thyroiditis, congenital adrenal hyperplasia, hypercalcemia due to tumor disease, short or additional therapy in acute rheumatic diseases, collagen diseases, pemphigus, bullous Dermatitis herpetiformis (Duhring disease), polymorphic bullous erythema, exfoliative dermatitis, granulosarcoid, severe forms of psoriasis and seborrheic dermatitis, severe acute and chronic allergic and inflammatory processes with eyes involvement, symptomatic sarcoidosis, Loeffler syndrome if not amenable to other forms of therapy, berylliosis, focal or disseminated form of tuberculosis during anti tuberculosis chemotherapy, aspiration pneumonitis, adult idiopathic thrombocytopenic purpura (only IV), adult secondary thrombocytopenia, acquired (autoimmune) hemolytic anemia, erythroblastopenia, congenital (erythroid) anemotrophy, palliative therapy in leukemia and lymphoma adults with acute leukemia in children, to enhance diuresis and to reduce proteinuria in nephrotic syndrome without uremia, with nephrotic syndrome of idiopathic type or lupus erythematosus, in a critical stage of ulcerative colitis, and regional enteritis (as a systemic treatment), tuberculous meningitis with subarachnoid block or the development of its stake (in conjunction with antituberculosis chemotherapy), trichinosis with nervous system or myocardium, bronchial asthma, diseases of the joints.
For local use: inflammation of the anterior eyeball in intact epithelium of the cornea and after injury and surgery on the eyeball.
For external use: allergic dermatitis, seborrhea, various forms of eczema, atopic dermatitis, psoriasis, pruritus, red flat verrucous zoster.
Dosage and administration
For parenteral use. Dosage and administration of Alfacort is individual. Applied IV as jet, IV as drip, rarely - IM. For emergency treatment is recommended IV injections. The initial dose is 100 mg (to be entered for 30 seconds) - 500 mg (to be entered for 10 min), then repeat every 2-6 hours, depending on the clinical situation. High doses should be used only to stabilize the patient's condition, but usually not more than 48-72 hours, because possible development of hypernatraemia. For children - not less than 25 mg / kg / day. In the form of depot-entry form intra or periarticular in a dose of 5-50 mg single with an interval of 1-3 weeks. IM - 125-250 mg / day.
In ophthalmology apply 2-3 times / day.
Topically - 1-3 times / day.
Alfacort side effects, adverse reactions
Endocrine system: reduction of glucose tolerance, diabetes mellitus, steroid or manifestation of latent diabetes mellitus, adrenal suppression, Itsenko-Cushing's syndrome (including moon face, obesity, pituitary type, hirsutism, increased blood pressure, dysmenorrhea, amenorrhea, myasthenia gravis, striae), delayed sexual development in children.
Metabolism: increased excretion of calcium, hypocalcemia, increased body weight, negative nitrogen balance (increased breakdown of proteins), increased sweating, fluid retention and sodium ions (peripheral edema), hypernatremia, kaliopenia syndrome (including hypokalemia, arrhythmia, myalgia or muscle spasm, unusual weakness, and fatigue).
Cardiovascular system: arrhythmia, bradycardia (up to heart failure), development (in predisposed patients) or increased severity of chronic heart failure, ECG changes typical for hypokalemia, increased blood pressure, hypercoagulation, thrombosis. In patients with acute and subacute myocardial infarction - the spread foci of necrosis, slowing the formation of scar tissue that may lead to rupture of the heart muscle, with intracranial introduction - nosebleeds.
Digestive system: nausea, vomiting, pancreatitis, steroid ulcer and duodenal ulcers, erosive esophagitis, bleeding and perforation of the gastrointestinal tract, increased or decreased appetite, flatulence, hiccups, rarely - increased activity of hepatic transaminases and alkaline phosphatase.
Senses: a sudden loss of view (for parenteral administration in the head, neck, nasal turbinate, the scalp may be the deposition of crystals of the drug in the vessels of eyes), posterior subcapsular cataracts, increased intraocular pressure with possible damage to the optic nerve, the propensity to develop secondary bacterial, fungal or viral eye infections, trophic changes of the cornea, exophthalmos.
Musculoskeletal system: slowing growth and ossification processes in children (premature closure of epiphyseal growth zones), osteoporosis (very rarely - pathological fractures, aseptic necrosis of head of humerus and femur), rupture of tendons of muscles, steroid myopathy, reduced muscle mass (atrophy); with intraarticular injection - increased pain in the joint.
Dermatological reactions: delayed wound healing, petechiae, ecchymosis, skin thinning, hyper- or hypopigmentation, steroid acne, striae, susceptibility to the development of pyoderma and candidiasis.
Effects due to the immunosuppressive effect: the development or exacerbation of infection (the appearance of this side effect contribute jointly used immunosuppressive drugs and vaccination).
Local reactions: with a parenteral - burning, numbness, pain, paresthesia, and infection at the injection site, rarely - necrosis of surrounding tissue, scarring at the injection site, with i / m administration (particularly in the deltoid muscle) - atrophy of the skin and subcutaneous tissue.
Other: pyuria, withdrawal syndrome.
For IV administration - arrhythmias, rush of blood to the face, convulsions.
For exterior use: rarely - itching, hyperemia, burning, dryness, folliculitis, acne, hypopigmentation, perioral dermatitis, allergic dermatitis, maceration of the skin, secondary infection, skin atrophy, striae, miliaria. With prolonged use or application on large areas of skin may develop systemic side effects characteristic of SCS.
For short-term use of Alfacort according to the life - hypersensitivity to hydrocortisone. For intraarticular administration and injection directly into the lesion: previous arthroplasty, abnormal bleeding (endogenous or caused by the use of anticoagulants), intra-articular fracture, infection (septic) inflammatory process in joints and periarticular infections (including history), and also general infectious disease marked juxta-articular osteoporosis, lack of signs of inflammation in the joint ("dry" joint, such as osteoarthrosis without synovitis), marked bone destruction and deformity of joints (sharp narrowing of joint space, ankylosis), instability of the joint as a result of arthritis, aseptic necrosis of the epiphyses of bones forming the joint.
For external use: bacterial, viral, fungal skin diseases, tuberculosis, skin, cutaneous manifestations of syphilis, tumors of the skin, post-vaccination period, violation of the integrity of the skin (ulcers, wounds), children's age (up to 2 years, with itching in the anal area - up to 12 years), rosacea, acne vulgaris, perioral dermatitis.
For use in ophthalmology: bacterial, viral, fungal eye diseases, tuberculosis eye disease, trachoma, violation of the integrity of the eye epithelium.
Alfacort using during pregnancy and breastfeeding
Application of pregnancy is only possible when the intended benefits to the mother outweighs the potential risk to the fetus, it is recommended to use the minimum dose and short-term therapy. Children whose mothers during pregnancy were receiving Alfacort are subject to careful monitoring for signs of adrenal insufficiency.
If necessary, use during lactation should decide on the termination of breastfeeding.
In experimental studies have shown that GCS can cause malformations of the fetus. Currently there is no clear evidence of these data in humans.
With caution use in parasitic and infectious diseases of viral, fungal or bacterial origin (currently or recently transferred, including the recent contact with a patient) - herpes simplex, herpes zoster (viremic phase), chickenpox, measles, amoebiasis, strongyloidiasis (set or suspected), systemic mycosis, active and latent tuberculosis. Application for serious infectious diseases is permissible only against the background of specific therapy.
Precautions to apply for 8 weeks before and 2 weeks after vaccination, with lymphadenitis after BCG, with immunodeficiency (including AIDS or HIV infection).
Precautions to apply for gastrointestinal diseases: gastric ulcer and duodenal ulcer, esophagitis, gastritis, acute or latent peptic ulcer, the newly formed anastomosis of the intestine, ulcerative colitis with perforation or abscess formation threat, diverticulitis.
With caution used in diseases of the cardiovascular system, including after recent myocardial infarction (in patients with acute and subacute myocardial necrosis may spread the fire, slowing the formation of scar tissue and therefore break the heart muscle), with decompensated chronic heart failure, hypertension, hyperlipidemia) and endocrine diseases - diabetes mellitus (including breach of tolerance to carbohydrates), thyrotoxicosis, hypothyroidism, Itsenko-Cushing disease, with severe chronic renal and / or hepatic failure, nefrourolitiaze, with hypoalbuminemia and conditions that predispose to its occurrence, with systemic osteoporosis, myasthenia gravis, acute psychosis, obesity (III-IV degree), and polio (except bulbar form of encephalitis), open-and angle-closure glaucoma, pregnancy, lactation.
If necessary of intraarticular injection use with caution to patients with severe general condition, failure (or brevity) of the 2 previous injections (based on the individual properties used GCS).
For lack of effectiveness of Alfacort in 48-72 hours and the need for more long-term therapy should be replaced by Alfacort at different glucocorticoid preparation does not cause sodium retention in the body. During treatment with Alfacort should appoint a diet with restriction of sodium and high potassium content. Alfacort caused a relative adrenal insufficiency may persist for several months after its cancellation. Given this under stressful situations that arise during the period, hormone therapy resume with simultaneous appointment of salts and / or mineral corticoids.
Patients with active tuberculosis Alfacort should be used in conjunction with the appropriate anti tuberculosis therapy. In latent tuberculosis or during superelevation tuberculin tests should carefully monitor the status of the patient, and if necessary to chemoprophylaxis.
Alfacort drug interactions
With simultaneous use of Alfacort increases the toxicity of cardiac glycosides (because of the emerging hypokalemia increases the risk of arrhythmias); with acetylsalicylic acid - accelerates its excretion and reduces its concentration in blood plasma (with the abolition of Alfacort concentration of salicylates in the blood increases, and increases the risk of side effects); with paracetamol - increased risk of hepatotoxic action of paracetamol (induction of hepatic enzymes and formation of a toxic metabolite of paracetamol); with cyclosporine - increased side effects of Alfacort as a result of inhibition of its metabolism; with ketoconazole - increased side effects of Alfacort as a result of reduction of its clearance.
Alfacort reduces the effectiveness of hypoglycemic; intensifies the effect of indirect anticoagulants of coumarin derivatives.
Alfacort reduces the effect of vitamin D on the absorption of calcium ions into the lumen of the intestine. Ergocalciferol and parathyroid hormone hinder the development of osteopathy caused by GCS.
Alfacort increases the metabolism of isoniazid, meksiletina (especially in "fast acetylators"), which leads to a decrease in their plasma concentrations; increases (with prolonged therapy) the content of folic acid reduces the concentration of praziquantel in blood.
Alfacort in high doses reduces the effect somatropina.
Hypokalemia caused by GCS, may increase the severity and duration of muscle blockade on the background of muscle relaxants.
Antacids reduce the absorption of the GCS.
At simultaneous application with SCS thiazides, carbonic anhydrase inhibitors, other GCS, amphotericin B increase the risk of hypokalemia, drugs containing sodium ions - swelling and increase blood pressure.
NSAIDs and ethanol increases the risk of gastrointestinal ulcerations and bleeding, in combination with NSAIDs to treat arthritis may reduce the dose of GCS due to summation of therapeutic effect. Indomethacin displacing the SCS from its association with albumin, increases the risk of its side effects.
Amphotericin B and carbonic anhydrase inhibitors increase the risk of osteoporosis.
The therapeutic effect of GCS is reduced under the influence of inducers of microsomal liver enzymes (including phenytoin, barbiturates, ephedrine, theophylline, rifampin) due to increased rate of metabolism of these substances.
Inhibitors of the function of the adrenal cortex (including mitotan) may necessitate higher doses of GCS.
Clearance GCS increased against the background of preparations of thyroid hormones.
Immunosuppressants increase the risk of infection and lymphoma or other lymphoproliferative disorders associated with Epstein-Barr virus.
Estrogens (including oral contraceptives containing estrogen) reduce the clearance of GKS, lengthens T1/2 and their therapeutic and toxic effects. The appearance of hirsutism and acne promotes the simultaneous use of other steroid hormone funds - androgens, estrogens, anabolic steroids, oral contraceptives.
Tricyclic antidepressants may increase the severity of depression caused by GCS (not shown for the treatment of these side effects).
The risk of developing cataracts increases with the application against other GCS antipsychotic funds (neuroleptics), carbutamide and azathioprine. Simultaneous of Alfacort with the appointment of m-cholinoblockers, as well as with means having m-anticholinergic action (including antihistamines, tricyclic antidepressants), with nitrates improves the intraocular pressure.
With simultaneous application of SCS with live vaccines and antiviral compared to other types of immunization increases the risk of activation of viruses and development of infections.
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