Diseases of the endocrine system: primary adrenal insufficiency (Addison's disease) and secondary (the drugs of choice are Hydrocortisone and Cortisone, synthetic derivatives can be used with mineralocorticoids), congenital adrenal hyperplasia, hypercalcaemia associated with cancer; Thyroiditis (non-dermatitis).Allergic diseases with a severe course, resistant to other methods of treatment: contact dermatitis, atopic dermatitis, serum sickness, hypersensitivity reactions to medications, year-round or seasonal allergic rhinitis.Collagenosis (during periods of exacerbation or in some cases as maintenance treatment): acute rheumatic myocarditis, dermatomyositis (in children, glucocorticoids may be the drug of choice), systemic lupus erythematosus.Diseases of the skin and mucous membranes: exfoliative dermatitis, herpetic bullous dermatitis, severe seborrheic dermatitis, severe erythema multiforme (Stevens-Johnson syndrome), mycosis fungoides, pemphigus, severe psoriasis.Diseases of the gastrointestinal tract (during periods of exacerbation, long-term treatment is not recommended): ulcerative colitis, Leśniowski-Crohn's disease.Haematopoietic system diseases: acquired (autoimmune) haemolytic anemia, congenital aplastic anemia, anemia due to selective red cell hypoplastic system, secondary thrombocytopenia in adults, idiopathic thrombocytopenic purpura (Werlhof's disease) in adults.Cancer diseases (as palliative treatment, including appropriate anticancer treatment): leukemia and lymphomas in adults, acute leukemia in children.Nephrotic syndrome - glucocorticosteroids are indicated for the purpose of causing diuresis or remission in the case of albuminuria in idiopathic nephrotic syndrome without uremia or to improve renal function in patients with lupus erythematosus; in idiopathic nephrotic syndrome, long-term treatment may be necessary to prevent frequent relapse.Neurological diseases: multiple sclerosis during periods of exacerbation.Eye diseases (severe, acute and chronic allergic and inflammatory processes): iritis, iritis and ciliary inflammation, choroidal and retinal inflammation, diffuse uveitis of the posterior segment of the eye, optic neuritis, sympathetic choroiditis, anterior segment of the eye, allergic conjunctivitis, keratitis (unrelated to herpes infection or infection) fungal), allergic marginal ulceration.Respiratory system diseases: berylliosis, Loffler's syndrome, aspiration pneumonia, symptomatic sarcoidosis, fulminant or disseminated pulmonary tuberculosis (with concomitant anti-tuberculosis treatment), bronchial asthma.Rheumatic diseases (as supportive treatment in conditions of exacerbation): ankylosing spondylitis, psoriatic arthritis, rheumatoid arthritis, juvenile rheumatoid arthritis (in cases refractory to other treatments).Other, non-rheumatic inflammations of the osteoarticular system: acute and subacute bursitis, acute gouty arthritis, acute non-specific inflammation of the tendon sheath, post-traumatic osteoarthritis, synovitis in patients with osteoarthritis, epicondylitis.Other: tuberculous meningitis with subarachnoid block (simultaneously with anti-tuberculosis treatment), trichinosis with involvement of the myocardium or nervous system.
Synthetic glucocorticoid, a derivative of cortisol. Clinical significance is the prednisone metabolite formed in the liver - Prednisolone, a glucocorticosteroid with a strong anti-inflammatory effect. Prednisolone inhibits the development of inflammation symptoms without affecting its cause. It inhibits the accumulation of macrophages, leukocytes and other cells in the region of the inflammatory focus. It inhibits phagocytosis, the release of lysosomal enzymes and the synthesis and release of chemical mediators of inflammation.It reduces the expansion and permeability of capillaries, reduces the adhesion of leukocytes to the endothelium of the capillaries, which leads to both inhibition of leukocyte migration and formation of edema. It intensifies the synthesis of lipomodulin, a phospholipase A inhibitor2 releasing arachidonic acid from the phospholipid membrane, while inhibiting its synthesis. Mechanisms of the immunosuppressive action of the drug are not completely understood, but prednisolone may prevent or inhibit cellular immune responses as well as specific mechanisms associated with immune response. It reduces the number of T lymphocytes, monocytes and eosinophils. It also reduces the binding of immunoglobulins to receptors on the cell surface and inhibits the synthesis or release of interleukins by reducing T-cell blastogenesis and reducing the severity of the early immune response. It can also inhibit the penetration of immune complexes through basement membranes and reduce the concentration of complement components and immunoglobulins. Prednisone, through the action on the coil, further intensifies sodium reabsorption, potassium and hydrogen ions excretion and water retention. To a lesser extent it affects the excretion of water and electrolytes through the large intestine, sweat and salivary glands. Prednisolone inhibits the hypothalamic-pituitary axis in the negative feedback mechanism. The development of adrenocortical insufficiency and its recovery time depend primarily on the duration of treatment and to a lesser extent on the dose, time and frequency of administration of the drug as well as on the half-life. After long-term use of high doses, the adrenal function may return after about 1 year, and in some patients never. It intensifies the catabolism of proteins and induces enzymes involved in the metabolism of amino acids. It inhibits the synthesis and causes the degradation of proteins in lymphoid, connective, muscular and skin tissue. After long-term use, these tissues may disappear. Prednisolone increases the availability of Glucose by inducing hepatic gluconeogenesis enzymes, reducing glucose consumption in peripheral tissues, leading to increased glycogen accumulation in the liver, increased blood glucose and increased insulin resistance. The drug intensifies lipolysis and the release of fatty acids from the adipose tissue, which increases the concentration of fatty acids in the plasma. Long-term treatment may lead to incorrect distribution of fat tissue. Prednisolone disturbs bone formation and intensifies their resorption. It reduces the concentration of Calcium in the plasma, which leads to secondary hyperparathyroidism and simultaneous stimulation of osteoclasts and osteoblast inhibition. These effects, together with a reduction in the amount of protein components secondary to catabolism of proteins, may lead to inhibition of bone growth in children and adolescents and the development of osteoporosis at any age. Prednisolone increases the effects of endo- and exogenous catecholamines. The bioavailability of the drug after oral administration is 70-90%. The highest concentration of the drug in plasma occurs after 1-2 h. T0,5 prednisolone in plasma is 3.4-3.8 h, in tissues 18-36 h. The duration of action is 1.25-1.5 days. Prednisone is 70-73% bound to plasma proteins and 90-95% prednisolone at concentrations below 200 ng / ml, while at concentrations above 1 mg / ml it is about 70%. Prednisone is mainly metabolised in the liver, and to a lesser extent in the kidneys. It is excreted mainly in the bile, in 1-5% in the urine in the form of inactive metabolites and in 10-20% as prednisolone. Prednisone and prednisolone penetrate the placental barrier. Less than 1% of the prednisone and prednisolone doses are excreted into breast milk.
Contraindications:
Hypersensitivity to prednisone or to any of the excipients. Systemic fungal infections (risk of aggravation of infection).
Precautions:
During the treatment, adrenal function, electrolytes and glucose concentration in the blood should be monitored, the prothrombin time (in patients receiving anticoagulants from the coumarin group), ophthalmologic examinations and faecal occult blood tests should be performed. Children treated for a long time should be observed to detect the occurrence of growth and development disorders. The drug should be used in the smallest effective doses; if it is possible to reduce the dose, it should be reduced gradually. In patients with hypothyroidism or cirrhosis, the drug has a stronger effect.Prednisone should be used with caution in: nonspecific ulcerative colitis if there is a risk of perforation, abscesses or other purulent infections, bowel disease, fresh intestinal anatomy, active or latent peptic ulcer, oesophagitis, gastritis, hyperthyroidism, renal insufficiency, hypertension , osteoporosis, myasthenia gravis, diabetes, impaired liver function, heart disease, congestive heart failure, recent heart attack, glaucoma, fungal or viral infections, hyperlipidemia, hypoalbuminemia. Caution should be exercised in combination therapy with Acetylsalicylic acid and prednisone in patients with hypoprotrombinemia. Prolonged use of prednisone may cause cataracts, glaucoma with possible damage to the optic nerves, as well as increase the risk of secondary fungal or viral infections. Prednisone administered in medium and high doses may cause increased blood pressure, water and sodium retention and increased potassium excretion; it may be necessary to limit sodium in the diet and potassium supplementation. Prednisone also causes increased calcium excretion. In the case of perforation in the gastrointestinal tract in patients treated with high doses of prednisone, the symptoms of peritonitis may be slight or not at all. Prednisone can mask the symptoms of infection, reduce resistance to infection and the ability to locate it. People treated with corticosteroids should avoid exposure to chickenpox and measles, because in the case of infection with these diseases, their course is much heavier (even fatal). Prednisone may reveal latent ameba; if you come from tropical countries or patients with diarrhea of unknown cause, you should exclude infestation with dysentery before dying with glucocorticosteroids. Patients treated with prednisone should not be vaccinated with live virus vaccines. Administration of an inactivated viral or bacterial vaccine may not result in the expected increase in antibody unless vaccination is used in patients receiving glucocorticosteroids as a substitution treatment, e.g. in Addison's disease. Administration of prednisone to patients with active tuberculosis should be limited to cases of disseminated or fulminant tuberculosis and only with concomitant anti-tuberculosis treatment. Patients with latent tuberculosis or a positive tuberculin test receiving prednisone should be monitored to detect the development of tuberculosis; in the case of long-term use of glucocorticoids should receive prophylactic anti-tuberculosis drugs. In fungal infections treated with amphotericin B, prednisone may sometimes be used to reduce its side effects, but in these cases it may cause congestive heart failure and enlargement of the heart and severe hypokalemia. In the case of herpes zoster, use with caution, due to the risk of corneal perforation. Mental disorders may occur while using prednisone; pre-existing emotional instability or psychotic tendencies may increase during treatment. In patients treated with corticosteroids, in an increased stress situation, an increased dose of fast acting glucocorticoid may be required. Abrupt cessation of treatment may result in adrenal insufficiency, therefore the prednisone dose should be reduced gradually. The schedule for dose reduction depends on the type of disease, duration of treatment, dose size used, and patient response. Discontinuation of treatment after long-term use may result in symptoms of glucocorticoid withdrawal syndrome. These symptoms can occur even when there is no evidence of adrenocortical insufficiency. Due to the lactose content, the drug should not be used in patients with rare hereditary galactose intolerance, Lapp lactase deficiency or malabsorption of glucose-galactose.
Pregnancy and lactation:
The use of corticosteroids in pregnant women is permissible only if the benefit of the medicine outweighs the potential risk to the fetus (there is a risk of placental insufficiency, low birth weight and death of the fetus). The use of a breast-feeding mother with prednisone up to 5 mg / day does not cause adverse reactions in the child; use of higher doses may cause the child to stop growth or stop the secretion of endogenous adrenocortical hormones.If it is necessary to use higher doses of the drug in women during lactation, it is advisable to stop breastfeeding. In some patients, glucocorticoids may increase or decrease motility and sperm count.
Side effects:
The short-term use of prednisone, like other corticosteroids, only exceptionally leads to side effects. The risk of adverse reactions affects patients who receive prednisone for a long time. The following may occur: muscle weakness, steroidal myopathy (more common in women, usually starting with the muscles of the iliac girdle and widening to the proximal muscles of the shoulder and arm, rarely affecting the respiratory muscles), loss of muscle mass in the case of steroidal myopathy, if not possible discontinue the glucocorticosteroid, replacing it with another medicine can relieve symptoms; osteoporosis, compression spinal fractures, aseptic necrosis of the femoral and humerus head, pathological fracture of long bones - the risk of osteoporosis associated with long-term use of glucocorticoids can be reduced by administering calcium and vitamin D or by appropriate physical exercises; peptic ulcer and its consequences (perforations, bleeding), perforations of the large or small intestine (especially in patients with intestinal inflammation), pancreatitis, bloating, ulcerative esophagitis, digestive disorders - prednisone administration during meals can reduce digestive disorders and irritation of the gastrointestinal tract; dermatoses, acne, impaired wound healing, ecchymosis and haemorrhage, erythema, increased sweating, allergic dermatitis, urticaria, angioneurotic edema, increased intracranial pressure with congestive disc (brain tumor - usually in children, usually after too rapid dose reduction, symptoms are headache, blurred or double vision), convulsions, dizziness, headache, secondary adrenal insufficiency and pituitary (in patients treated with doses above 5 mg daily, especially in stressful situations such as illness, trauma, surgery), Cushing's syndrome, growth inhibition in children, menstrual cycle disorders, reduced carbohydrate tolerance, diabetes mellitus, increased need for insulin and oral hypoglycaemic agents in patients with overt diabetes, hirsutism, posterior subcapsular cataract (2.5 to 60% of patients, most often according to many reports only in children, it can go back after treatment discontinuation or surgical treatment may be necessary), increase in intraocular pressure, glaucoma (usually after treatment lasting at least 1 year), exophthalmos, symptoms of schizophrenia, mania or delirium (occur in 15 to 50% of patients; they are dose-dependent, most often in patients treated with 40 mg prednisone per day; the most susceptible to occurrence of symptoms are women and patients with lupus erythematosus) - if psychosis or depression should occur, if possible, reduce the dose or discontinue prednisone, if necessary, use phenothiazine or lithium compounds, do not use TLPD, because they may exacerbate the disorder psychiatric induced by glucocorticoids; negative nitrogen balance - due to the increased catabolism of proteins, a greater supply of protein in the diet may be indicated during long-term treatment; hyperglycemia, glucosuria, weight gain, increased appetite, thromboembolic syndromes, anaphylactic reactions and hypersensitivity, nausea, malaise, sleep disorders, sodium retention, fluid retention, congestive heart failure, potassium loss, hypertension, hypokalemiemic alkalosis, withdrawal symptoms ( including fever, muscle and joint pain, unwellness) - to reduce some symptoms of glucocorticoid withdrawal (without inhibition of the hypothalamo-pituitary-adrenal axis) you can administer acetylsalicylic acid or other non-steroidal anti-inflammatory drugs.
Dosage:
Orally. The dose should be determined individually, depending on the type of disease and response to treatment. After obtaining the desired therapeutic effect, it is advisable to gradually reduce the dose to the lowest effective dose. The dose should also be reduced gradually before the planned discontinuation. In the case of long-term treatment with high doses, discontinuation of the drug can be started with a dose reduction of 1 mg per month, in the case of a short treatment period of 2-5 mg every 2-7 days. Prednisone administered at a dose of up to 40 mg per day for less than 7 days can be discontinued without the risk of suppression of the pituitary-adrenal axis.In order to reduce the risk of inhibition of the hypothalamic-pituitary-adrenal axis, it is recommended to administer the drug once a day in the morning, because the morning is the highest secretion of endogenous corticosteroids. However, in some cases it may be necessary to give prednisone more frequently.The average dose is used. Adults and adolescents: 5-60 mg daily as a single dose or in divided doses, up to a maximum of 250 mg daily. Children: 2 mg / kg daily in divided doses every 6-8 h or in a single dose.Multiple sclerosis during periods of exacerbation: adults - 200 mg per day for 7 days, then 80 mg every other day for 1 month.Nephrotic syndrome: children up to 18 months of age: the dose has not been determined; children from 18 months up to 4 years - initially 7-10 mg 4 times a day; children aged 4-10 - initially 15 mg 4 times a day; children> 10 years - initially 20 mg 4 times a day.Rheumatic heart disease, leukemia, cancer: children - for the first 2 or 3 weeks, 0.5 mg / kg or 15 mg / m2 pc. 4 times a day, then 0.375 mg / kg. or 11.25 mg / m2 pc. 4 times a day for 4-6 weeksTuberculosis (with simultaneous anti-tuberculosis treatment): children - 0.5 mg / kg or 15 mg / m2 pc. 4 times a day for 2 months.Way of giving. The drug should be administered during a meal. The tablets should not be divided.
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