Glucocorticoids are steroid hormones synthesized by the adrenal cortex. Natural glucocorticoids and their synthetic analogues are used in medicine for adrenal insufficiency. In addition, in some diseases, anti-inflammatory, immunosuppressive, antiallergic, anti-shock and other properties of these drugs are used.
The beginning of the use of glucocorticoids as medicines (drugs) dates back to the 40s. XX century. Back in the late 30s. of the last century, it was shown that hormonal compounds of a steroid nature are formed in the adrenal cortex. In 1937, the mineralocorticoid deoxycorticosterone was isolated from the adrenal cortex, in the 40s. – glucocorticoids cortisone and hydrocortisone. The wide range of pharmacological effects of hydrocortisone and cortisone predetermined the possibility of their use as drugs. Their synthesis was soon carried out.
The main and most active glucocorticoid formed in the human body is hydrocortisone (cortisol), others, less active, are represented by cortisone, corticosterone, 11-deoxycortisol, 11-dehydrocorticosterone.
Systemic glucocorticoids can be divided into several groups.
By origin, they are divided into:

  • natural (hydrocortisone, cortisone);
  • synthetic (prednisone, methylprednisolone, prednisone, triamcinolone, dexamethasone, betamethasone).

According to the duration of action, glucocorticoids for systemic use can be divided into three groups (in brackets – biological (from tissues) half-life (T1/2 biol.):

  • short-acting glucocorticoids (T1/2 biol. – 8-12 hours): hydrocortisone, cortisone;
  • medium-acting glucocorticoids (T1/2 biol. – 18–36 h): prednisolone, prednisone, methylprednisolone;
  • long-acting glucocorticoids (T1/2 biol. – 36-54 hours): triamcinolone, dexamethasone, betamethasone.
  • The duration of action of glucocorticoids depends on the route / site of administration, the solubility of the dosage form (mazipredon is a water-soluble form of prednisolone), and the dose administered. After oral administration or intravenous administration, the duration of action depends on T1/2 biol., with i / m administration – from the solubility of the dosage form and T1/2 biol., after local injections – from the solubility of the dosage form and the specific route / site of administration.
    When taken orally, glucocorticoids are rapidly and almost completely absorbed from the gastrointestinal tract. WITHmax in the blood is noted after 0.5-1.5 hours. Glucocorticoids bind in the blood with transcortin (corticosteroid-binding alphaone-globulin) and albumin, and natural glucocorticoids bind to proteins by 90–97%, synthetic ones by 40–60%. Glucocorticoids penetrate well through histohematogenous barriers, incl. through the BBB, pass through the placenta. Fluorinated derivatives (including dexamethasone, betamethasone, triamcinolone) pass through the histohematogenous barriers worse. Glucocorticoids undergo biotransformation in the liver with the formation of inactive metabolites (glucuronides or sulfates), which are excreted mainly by the kidneys. Natural drugs are metabolized faster than synthetic drugs and have a shorter half-life.
    Modern glucocorticoids are a group of drugs that are widely used in clinical practice, incl. in rheumatology, pulmonology, endocrinology, dermatology, ophthalmology, otorhinolaryngology.
    The main indications for the use of glucocorticoids are collagenoses, rheumatism, rheumatoid arthritis, bronchial asthma, acute lymphoblastic and myeloid leukemia, infectious mononucleosis, eczema and other skin diseases, various allergic diseases. For the treatment of atopic, autoimmune diseases, glucocorticoids are the basic pathogenetic agents. Glucocorticoids are also used for hemolytic anemia, glomerulonephritis, acute pancreatitis, viral hepatitis and respiratory diseases (COPD in the acute phase, acute respiratory distress syndrome, etc.). Due to the anti-shock effect, glucocorticoids are prescribed for the prevention and treatment of shock (post-traumatic, operational, toxic, anaphylactic, burn, cardiogenic, etc.).
    The immunosuppressive effect of glucocorticoids allows them to be used in organ and tissue transplantation to suppress the rejection reaction, as well as in various autoimmune diseases.
    The main principle of glucocorticoid therapy is to achieve the maximum therapeutic effect with minimal doses. The dosage regimen is selected strictly individually, to a greater extent depending on the nature of the disease, the patient’s condition and response to the treatment, than on age or body weight.
    When prescribing glucocorticoids, it is necessary to take into account their equivalent doses: according to the anti-inflammatory effect, 5 mg of prednisolone corresponds to 25 mg of cortisone, 20 mg of hydrocortisone, 4 mg of methylprednisolone, 4 mg of triamcinolone, 0.75 mg of dexamethasone, 0.75 mg of betamethasone.
    There are 3 types of glucocorticoid therapy: substitutional, suppressive, pharmacodynamic.
    Substitution therapy glucocorticoids are necessary for adrenal insufficiency. With this type of therapy, physiological doses of glucocorticoids are used, in stressful situations (for example, surgery, trauma, acute illness), the doses are increased by 2-5 times. When prescribing, one should take into account the circadian rhythm of endogenous secretion of glucocorticoids: at 6-8 am, most (or all) of the dose is prescribed. For chronic adrenal insufficiency (Addison’s disease), glucocorticoids can be used throughout life.
    Suppressive therapy glucocorticoids are used for adrenogenital syndrome – congenital dysfunction of the adrenal cortex in children. In this case, glucocorticoids are used in pharmacological (supraphysiological) doses, which leads to the suppression of ACTH secretion by the pituitary gland and a subsequent decrease in the increased secretion of androgens by the adrenal glands. Most (2/3) of the dose is prescribed at night to, according to the principle of negative feedback, prevent a peak in ACTH release.
    Pharmacodynamic therapy used most often, incl. in the treatment of inflammatory and allergic diseases.
    There are several types of pharmacodynamic therapy: intensive, limiting, long-term.
    Intensive pharmacodynamic therapy: used in acute, life-threatening conditions, glucocorticoids are administered intravenously, starting with large doses (5 mg / kg – day); after the patient leaves the acute state (1-2 days), glucocorticoids are canceled immediately, simultaneously.
    Limiting pharmacodynamic therapy: prescribed for subacute and chronic processes, incl. inflammatory (systemic lupus erythematosus, systemic scleroderma, polymyalgia rheumatica, severe bronchial asthma, hemolytic anemia, acute leukemia, etc.). The duration of therapy is, as a rule, several months, glucocorticoids are used in doses exceeding physiological (2-5 mg / kg / day), taking into account the circadian rhythm.
    To reduce the inhibitory effect of glucocorticoids on the hypothalamic-pituitary-adrenal system, various schemes of intermittent glucocorticoid administration have been proposed:

  • alternating therapy – use glucocorticoids of short / medium duration of action (prednisolone, methylprednisolone), once, in the morning (about 8 hours), every 48 hours;
  • intermittent circuit – glucocorticoids are prescribed in short courses (3-4 days) with 4-day breaks between courses;
  • pulse therapy – rapid intravenous administration of a large dose of the drug (at least 1 g) – for emergency therapy. The drug of choice for pulse therapy is methylprednisolone (it enters inflamed tissues better than others and causes side effects less often).
  • Long-term pharmacodynamic therapy: used in the treatment of diseases with a chronic course. Glucocorticoids are prescribed orally, doses exceed physiological (2.5-10 mg / day), therapy is prescribed for several years, the withdrawal of glucocorticoids with this type of therapy is very slow.
    Dexamethasone and betamethasone are not used for long-term therapy, because with the strongest and most prolonged, in comparison with other glucocorticoids, anti-inflammatory action, they also cause the most pronounced side effects, incl. inhibitory effect on lymphoid tissue and corticotropic function of the pituitary gland.
    During treatment, it is possible to switch from one type of therapy to another.
    Glucocorticoids are used orally, parenterally, intra- and periarticular, inhalation, intranasal, retro- and parabulbar, in the form of eye and ear drops, externally in the form of ointments, creams, lotions, etc.
    For example, in rheumatic diseases, glucocorticoids are used for systemic, local or local (intra-articular, peri-articular, external) therapy. In case of broncho-obstructive diseases, inhaled glucocorticoids are of particular importance.
    Glucocorticoids are effective therapeutic agents in many cases. However, it must be borne in mind that they can cause a number of side effects, including the Itsenko-Cushing symptom complex (sodium and water retention in the body with the possible appearance of edema, loss of potassium, increased blood pressure), hyperglycemia up to diabetes mellitus (steroid diabetes), slowing down the processes of tissue regeneration, exacerbation of gastric ulcer and duodenal ulcer, ulceration of the digestive tract, perforation of an unrecognized ulcer, hemorrhagic pancreatitis, a decrease in the body’s resistance to infections, hypercoagulability with a risk of thrombosis, the appearance of acne, a lunate menstrual cycle, obesity, and other disorders. taking glucocorticoids, there is an increased excretion of calcium and osteoporosis (with prolonged use of glucocorticoids at doses of more than 7.5 mg / day – in the equivalent of prednisolone – the development of osteoporosis of long bones is possible). Prevention of steroidal osteoporosis is carried out with calcium and vitamin D preparations from the moment you start taking glucocorticoids. The most pronounced changes in the musculoskeletal system are observed in the first 6 months of treatment. One of the dangerous complications is aseptic bone necrosis, therefore it is necessary to warn patients about the possibility of its development and when “new” pains appear, especially in the shoulder, hip and knee joints, it is necessary to exclude aseptic bone necrosis. Glucocorticoids cause changes in the blood: lymphopenia, monocytopenia, eosinopenia, a decrease in the number of basophils in the peripheral blood, the development of neutrophilic leukocytosis, an increase in the content of erythrocytes. Nervous and mental disorders are also possible: insomnia, agitation (with the development of psychosis in some cases), epileptiform seizures, euphoria.
    With prolonged use of glucocorticoids, one should take into account the probable suppression of the function of the adrenal cortex (atrophy is not excluded) with suppression of the biosynthesis of hormones. Administration of corticotropin simultaneously with glucocorticoids prevents adrenal atrophy.
    The frequency and severity of side effects caused by glucocorticoids can be expressed to varying degrees. Side effects, as a rule, are a manifestation of the actual glucocorticoid effect of these drugs, but to an extent that exceeds the physiological norm. With the correct selection of the dose, the observance of the necessary precautions, constant monitoring of the course of treatment, the incidence of side effects can be significantly reduced.
    To prevent undesirable effects associated with the use of glucocorticoids, it is necessary, especially with long-term treatment, to carefully monitor the dynamics of growth and development in children, periodically conduct an ophthalmological examination (to detect glaucoma, cataracts, etc.), regularly monitor the function of the hypothalamic-pituitary-adrenal systems, glucose in blood and urine (especially in patients with diabetes mellitus), monitor blood pressure, ECG, blood electrolyte composition, monitor the state of the gastrointestinal tract, musculoskeletal system, monitor the development of infectious complications, etc.
    Most of the complications of glucocorticoid treatment are treatable and disappear after drug withdrawal. Irreversible side effects of glucocorticoids include growth retardation in children (occurs with glucocorticoid treatment for more than 1.5 years), subcapsular cataract (develops in the presence of a family predisposition), steroid diabetes.
    Abrupt withdrawal of glucocorticoids can cause an exacerbation of the process – withdrawal syndrome, especially when long-term therapy is stopped. In this regard, treatment should end with a gradual dose reduction. The severity of the withdrawal syndrome depends on the degree of preservation of the function of the adrenal cortex. In mild cases, the withdrawal syndrome is manifested by an increase in body temperature, myalgia, arthralgia, and malaise. In severe cases, especially with severe stress, an addison crisis (accompanied by vomiting, collapse, convulsions) may develop.
    Due to side effects, glucocorticoids are used only if there are clear indications and under close medical supervision. Contraindications for the administration of glucocorticoids are relative. In emergency situations, the only contraindication for short-term systemic use of glucocorticoids is hypersensitivity. In other cases, when planning long-term therapy, contraindications should be taken into account.
    Glucocorticoids are contraindicated in severe arterial hypertension, Itsenko-Cushing’s disease, pregnancy (suppression of the development of the adrenal glands in the fetus is possible), stage III circulatory failure, acute endocarditis, psychosis, nephritis, osteoporosis, gastric ulcer and duodenal ulcer, after recent syphilis , active forms of tuberculosis (in the absence of specific treatment), with diabetes mellitus, allergic reactions to glucocorticoids (including history). The use of systemic glucocorticoids in children is possible only for absolute indications (growth retardation is possible). Preparations containing glucocorticoids (ointments, drops) should not be used for viral diseases of the eyes and skin, since in connection with the suppression of regeneration processes, the formation of common ulcers is possible (in eye practice, up to corneal perforation). In case of fungal and parasitic skin lesions, ointments containing glucocorticoids should also not be used unless antifungal or antiparasitic agents are added to them.
    The therapeutic and toxic effects of glucocorticoids reduce – inducers of microsomal liver enzymes, increase – estrogens and oral contraceptives. Digitalis glycosides, diuretics (causing potassium deficiency), amphotericin B, carbonic anhydrase inhibitors increase the likelihood of arrhythmias and hypokalemia. Alcohol and NSAIDs increase the risk of ulcerative lesions or gastrointestinal bleeding. Immunosuppressants increase the likelihood of developing infections. Glucocorticoids weaken the hypoglycemic activity of antidiabetic agents and insulin, natriuretic and diuretic – diuretics, anticoagulant and fibrinolytic – coumarin and indandione derivatives, heparin, streptokinase and urokinase, vaccine activity (due to a decrease in the production of antibodies), reduce the concentration of saliciletin in the blood. With the use of prednisolone and paracetamol, the risk of hepatotoxicity increases.
    There are five known drugs that suppress the secretion of corticosteroids by the adrenal cortex. (inhibitors of the synthesis and action of corticosteroids): mitotane, metirapone, aminoglutethimide, ketoconazole, trilostane. Aminoglutethimide, metirapone and ketoconazole suppress the synthesis of steroid hormones due to inhibition of hydroxylases (cytochrome P450 isoenzymes) involved in biosynthesis. All three drugs are specific because act on different hydroxylases. These drugs can cause acute adrenal insufficiency, so they should be used in strictly defined doses and with careful monitoring of the patient’s hypothalamic-pituitary-adrenal system.
    Aminoglutethimide inhibits 20,22-desmolase, which catalyzes the initial (limiting) stage of steroidogenesis – the conversion of cholesterol into pregnenolone. As a result, the production of all steroid hormones is disrupted. In addition, aminoglutethimide inhibits 11-beta-hydroxylase as well as aromatase. Aminoglutethimide is used in Cushing’s syndrome caused by unregulated excessive secretion of cortisol by adrenal cortex tumors or ectopic ACTH production. The ability of aminoglutethimide to inhibit aromatase is used in the treatment of hormone-dependent tumors such as prostate cancer, breast cancer.
    Ketoconazole is used primarily as an antifungal agent. However, at higher doses, it inhibits several cytochrome P450 enzymes involved in steroidogenesis, incl. 17-alpha-hydroxylase, as well as 20,22-desmolase, and thus blocks steroidogenesis in all tissues. According to some reports, ketoconazole is the most effective inhibitor of steroidogenesis in Cushing’s disease. However, the feasibility of using ketoconazole in case of excessive production of steroid hormones requires further research.
    Aminoglutethimide, ketoconazole, and metirapone are used to diagnose and treat adrenal hyperplasia.
    TO antagonists of glucocorticoid receptors refers to mifepristone. Mifepristone is an antagonist of progesterone receptors, in large doses it blocks glucocorticoid receptors, prevents the suppression of the hypothalamic-pituitary-adrenal system (by the mechanism of negative feedback) and leads to a secondary increase in the secretion of ACTH and cortisol.
    One of the most important areas of clinical use of glucocorticoids is the pathology of various parts of the respiratory tract.
    Indications for appointment systemic glucocorticoids in diseases of the respiratory system are bronchial asthma, COPD in the acute phase, severe pneumonia, interstitial lung disease, acute respiratory distress syndrome.
    After systemic glucocorticoids (oral and injectable forms) were synthesized at the end of the 40s of the 20th century, they immediately began to be used to treat severe bronchial asthma. Despite the good therapeutic effect, the use of glucocorticoids in bronchial asthma was limited to the development of complications – steroid vasculitis, systemic osteoporosis, diabetes mellitus (steroid diabetes). Local forms of glucocorticoids began to be used in clinical practice only after some time – in the 70s. XX century. The publication on the successful use of the first topical glucocorticoid – beclomethasone (beclomethasone dipropionate) – for the treatment of allergic rhinitis dates back to 1971. In 1972, a report appeared on the use of the topical form of beclomethasone for the treatment of bronchial asthma.
    Inhaled glucocorticoids are basic drugs in the treatment of all pathogenetic variants of persistent bronchial asthma, are used for moderate and severe COPD (with spirographically confirmed response to treatment).
    Inhaled glucocorticoids include beclomethasone, budesonide, fluticasone, mometasone, triamcinolone. Inhaled glucocorticoids differ from systemic ones in pharmacological properties: high affinity for HA receptors (act in minimal doses), strong local anti-inflammatory effect, low systemic bioavailability (oral, pulmonary), rapid inactivation, short T1/2 from blood. Inhaled glucocorticoids inhibit all phases of inflammation in the bronchi and reduce their increased reactivity. Their ability to reduce bronchial secretion (reduce the volume of tracheobronchial secretion) and potentiate the action of beta is very important.2-adrenergic agonists. The use of inhaled forms of glucocorticoids reduces the need for tableted glucocorticoids. An important characteristic of inhaled glucocorticoids is the therapeutic index – the ratio of local anti-inflammatory activity and systemic action. Of the inhaled glucocorticoids, budesonide has the most favorable therapeutic index.
    One of the factors that determine the effectiveness and safety of inhaled glucocorticoids are the systems for their delivery into the respiratory tract. Currently, metered-dose and powder inhalers (turbuhaler, etc.), nebulizers are used for this purpose.
    With the correct choice of the system and inhalation technique, the systemic side effects of inhaled glucocorticoids are insignificant due to the low bioavailability and rapid metabolic activation of these drugs in the liver. It should be borne in mind that all existing inhaled glucocorticoids are absorbed in the lungs to one degree or another. Local side effects of inhaled glucocorticoids, especially with prolonged use, are the occurrence of oropharyngeal candidiasis (in 5-25% of patients), less often – esophageal candidiasis, dysphonia (in 30-58% of patients), cough.
    It has been shown that inhaled glucocorticoids and long-acting beta-adrenergic agonists (salmeterol, formoterol) have a synergistic effect. This is due to the stimulation of the biosynthesis of beta2-adrenergic receptors and an increase in their sensitivity to agonists under the influence of glucocorticoids. In this regard, in the treatment of bronchial asthma, combined drugs are effective for long-term therapy, but not for the relief of attacks – for example, a fixed combination of salmeterol / fluticasone or formoterol / budesonide.
    Inhalation with glucocorticoids is contraindicated for fungal infections of the respiratory tract, tuberculosis, pregnancy.
    Currently for intranasal clinical applications use beclomethasone dipropionate, budesonide, fluticasone, mometasone furoate. In addition, dosage forms in the form of nasal aerosols exist for flunisolide and triamcinolone, but they are not currently used in Russia.
    Nasal forms of glucocorticoids are effective in the treatment of non-infectious inflammatory processes in the nasal cavity, rhinitis, incl. medication, professional, seasonal (intermittent) and year-round (persistent) allergic rhinitis, to prevent recurrence of the formation of polyps in the nasal cavity after their removal. Topical glucocorticoids are characterized by a relatively late onset of action (12-24 hours), a slow development of the effect – manifests itself by the 3rd day, reaches a maximum on the 5th-7th day, sometimes after several weeks. Mometasone begins to act most rapidly (12 hours).
    Modern intranasal glucocorticoids are well tolerated; when used in recommended doses, systemic ones (part of the dose is absorbed from the nasal mucosa and enters the systemic circulation), the effects are minimal. Among the local side effects in 2-10% of patients at the beginning of treatment are nosebleeds, dry and burning in the nose, sneezing and itching. It is possible that these side effects are due to the irritating effect of the propellant. Described isolated cases of perforation of the nasal septum with the use of intranasal glucocorticoids.
    Intranasal use of glucocorticoids is contraindicated in hemorrhagic diathesis, as well as with a history of repeated nosebleeds.
    Thus, glucocorticoids (systemic, inhalation, nasal) are widely used in pulmonology and otorhinolaryngology. This is due to the ability of glucocorticoids to stop the main symptoms of diseases of the ENT organs and respiratory organs, and with a persistent course of the process, to significantly prolong the interictal period. The obvious advantage of using topical dosage forms of glucocorticoids is the ability to minimize systemic side effects, thereby increasing the effectiveness and safety of therapy.
    In 1952, Sulzberger and Witten first reported the successful use of 2.5% hydrocortisone ointment for the topical treatment of cutaneous dermatosis. Natural hydrocortisone is historically the first glucocorticoid used in dermatological practice, later it became the standard for comparing the strength of different glucocorticoids. Hydrocortisone, however, is not effective enough, especially in severe dermatoses, due to relatively weak binding to steroid receptors of skin cells and slow penetration through the epidermis.
    Later, glucocorticoids were widely used in dermatology for the treatment of various skin diseases of a non-infectious nature: atopic dermatitis, psoriasis, eczema, lichen planus and other dermatoses. They have a local anti-inflammatory, anti-allergic effect, eliminate itching (use for itching is justified only if it is caused by an inflammatory process).
    Topical glucocorticoids differ from each other in chemical structure, as well as in the strength of local anti-inflammatory action.
    The creation of halogenated compounds (the inclusion of fluorine or chlorine in the halogen molecule) made it possible to increase the anti-inflammatory effect and reduce systemic side effects when applied topically due to the lower absorption of drugs. Compounds containing two fluorine atoms in their structure – flumethasone, fluocinolone acetonide, etc., are characterized by the lowest absorption when applied to the skin.
    According to the European classification (Niedner, Schopf, 1993), 4 classes are distinguished according to the potential activity of local steroids:
    – weak (class I) – hydrocortisone 0.1–1%, prednisolone 0.5%, fluocinolone acetonide 0.0025%;
    – medium strength (class II) – alclomethasone 0.05%, betamethasone valerate 0.025%, triamcinolone acetonide 0.02%, 0.05%, fluocinolone acetonide 0.00625%, etc.;
    – strong (class III) – betamethasone valerate 0.1%, betamethasone dipropionate 0.025%, 0.05%, hydrocortisone butyrate 0.1%, methylprednisolone aceponate 0.1%, mometasone furoate 0.1%, triamcinolone acetonide 0.025%, 0 , 1%, fluticasone 0.05%, fluocinolone acetonide 0.025%, etc.
    – very strong (class III) – clobetasol propionate 0.05%, etc.
    Along with an increase in the therapeutic effect when using fluorinated glucocorticoids, the incidence of side effects also increases. The most common local side effects when using strong glucocorticoids are skin atrophy, telangiectasias, steroid acne, striae, and skin infections. The likelihood of developing both local and systemic side effects increases with application to large surfaces and prolonged use of glucocorticoids. Due to the development of side effects, the use of fluorine-containing glucocorticoids is limited if long-term use is necessary, as well as in pediatric practice.
    In recent years, by modifying the steroid molecule, new generation local glucocorticoids have been obtained that do not contain fluorine atoms, but at the same time are characterized by high efficacy and a good safety profile (for example, mometasone in the form of furoate, a synthetic steroid that began to be produced in 1987 in the USA, methylprednisolone aceponate, which has been used in practice since 1994).
    The therapeutic effect of topical glucocorticoids also depends on the dosage form used. Glucocorticoids for topical use in dermatology are produced in the form of ointments, creams, gels, emulsions, lotions, etc. The ability to penetrate the skin (penetration depth) decreases in the following order: oily ointment>ointment>cream>lotion (emulsion). With chronic dry skin, the penetration of glucocorticoids into the epidermis and dermis is difficult, therefore, with dermatoses, accompanied by increased dryness and peeling of the skin, lichenization is more advisable to use ointments, because moisturizing the stratum corneum of the epidermis with an ointment base several times increases the penetration of drugs into the skin. In acute processes with pronounced weeping, it is more advisable to prescribe lotions, emulsions.
    Since glucocorticoids for topical use reduce the resistance of the skin and mucous membranes, which can lead to the development of superinfection, in case of secondary infection, it is advisable to combine a glucocorticoid with an antibiotic in one dosage form, for example, Diprogen cream and ointment (betamethasone + gentamicin), Oxycort aerosols (hydrocortisone + oxytetracycline) and Polcortolone TS (triamcinolone + tetracycline), etc., or with an antibacterial and antifungal agent, for example, Akriderm GK (betamethasone + clotrimazole + gentamicin).
    Topical glucocorticoids are used in the treatment of complications of chronic venous insufficiency (CVI) such as trophic skin disorders, varicose eczema, hemosiderosis, contact dermatitis, etc. Their use is due to the suppression of inflammatory and toxic-allergic reactions in soft tissues that occur in severe CVI. In some cases, local glucocorticoids are used to suppress vascular reactions that occur during phlebosclerosing treatment. Most often, ointments and gels containing hydrocortisone, prednisolone, betamethasone, triamcinolone, fluocinolone acetonide, mometasone furoate, etc. are used for this.
    The use of glucocorticoids in ophthalmology based on their local anti-inflammatory, anti-allergic, antipruritic action. Indications for the appointment of glucocorticoids are inflammatory eye diseases of non-infectious etiology, incl. after injuries and operations – iritis, iridocyclitis, scleritis, keratitis, uveitis, etc. For this purpose are used: hydrocortisone, betamethasone, desonide, triamcinolone, etc. The most preferable use of local forms (eye drops or suspension, ointments), in severe cases – subconjunctival injections. With systemic (parenteral, oral) use of glucocorticoids in ophthalmology, it should be remembered that there is a high probability (75%) of developing steroid cataracts with daily use for several months of prednisolone at a dose of more than 15 mg (as well as equivalent doses of other drugs), while the risk increases with increasing the duration of treatment.
    Glucocorticoids are contraindicated in acute infectious eye diseases. If necessary, for example, for bacterial infections, combined preparations containing antibiotics are used, such as eye / ear drops Garazon (betamethasone + gentamicin) or Sofradex (dexamethasone + framycetin + gramicidin), etc. and antibiotics are widely used in ophthalmic and otorhinolaryngological practice. In ophthalmology – for the treatment of inflammatory and allergic eye diseases in the presence of concomitant or suspected bacterial infection, for example, in some types of conjunctivitis, in the postoperative period. In otorhinolaryngology – with otitis externa; rhinitis complicated by a secondary infection, etc. It should be borne in mind that the same vial of the drug is not recommended for the treatment of otitis media, rhinitis and eye diseases in order to avoid the spread of infection.
    Below is a list of glucocorticosteroids:

  • Fluticasone furoate
  • Mometasone
  • Methylprednisolone aceponate
  • Triamcinolone
  • Hydrocortisone
  • Betamethasone
  • Cyclesonide
  • Beclomethasone
  • Budesonide
  • Alclomethasone
  • Betamethasone + Neomycin
  • Dexamethasone
  • Prednisolone
  • Mazipredon
  • Methylprednisolone
  • Prednikarbat
  • Clobetasol
  • Flunisolide
  • Cortisone
  • Fludrocortisone
  • Fluticasone
  • Flumethasone
  • Mometasone furoate (Mometasonum)
  • Desonide
  • Prednisone
  • Fluocinolone acetonide
  • Fluocortolone