Indications and contraindications for the use of Hydrocortisone
As a component of systemic and replacement therapy, the drug is indicated for the following conditions: adrenal insufficiency, shock of various origins, hepatic coma, allergic laryngeal edema, status asthmaticus, exacerbation of Crohn's disease and ulcerative colitis, gouty, rheumatoid and psoriatic arthritis, SLE, dermatomyositis.
Local use of the drug is indicated for eczema, various dermatitis, psoriasis, scabies, and insect bites.
Eye ointment is used to treat chronic or allergic blepharoconjunctivitis, acute keratitis, anterior and posterior uveitis, and burns of the ocular surface.
Contraindications to the systemic administration of Hydrocortisone are a history of allergic reactions, epilepsy, hypertensive crisis, Itsenko-Cushing syndrome and disease, osteoporosis, peptic ulcer and duodenal ulcer, diabetes mellitus type 1 and 2, HIV infection, pregnancy, lactation, and childhood.
Skin ointment should not be used for malignant neoplasms, syphilis, tuberculosis, viral, fungal and bacterial local infections.
The ophthalmic form of Hydrocortisone should not be prescribed for violations of the integrity of the cornea, infectious diseases, or trachoma.
Hydrocortisone, 1%, ointment, 10 g, 1 pc.
From the endocrine system: decreased glucose tolerance, steroid diabetes mellitus or manifestation of latent diabetes mellitus, suppression of adrenal function, Itsenko-Cushing syndrome (including moon face, pituitary type obesity, hirsutism, increased blood pressure, dysmenorrhea, amenorrhea, myasthenia gravis , striae), delayed sexual development in children.
Metabolism: increased excretion of calcium ions, hypocalcemia, increased body weight, negative nitrogen balance (increased protein breakdown), increased sweating, fluid and sodium ion retention (peripheral edema), hypernatremia, hypokalemic syndrome (including hypokalemia, arrhythmia, myalgia or muscle spasm, unusual weakness and fatigue).
From the central nervous system: delirium, disorientation, euphoria, hallucinations, manic-depressive psychosis, depression, paranoia, increased intracranial pressure, nervousness or anxiety, insomnia, dizziness, vertigo, pseudotumor of the cerebellum, headache, convulsions.
From the cardiovascular system: arrhythmias, bradycardia (up to cardiac arrest); development (in predisposed patients) or increased severity of chronic heart failure, ECG changes characteristic of hypokalemia, increased blood pressure, hypercoagulation, thrombosis. In patients with acute and subacute myocardial infarction - the spread of necrosis, slowing down the formation of scar tissue, which can lead to rupture of the heart muscle; with intracranial administration - nosebleeds.
From the digestive system: nausea, vomiting, pancreatitis, steroid ulcer of the stomach and duodenum, erosive esophagitis, bleeding and perforation of the gastrointestinal tract, increased or decreased appetite, flatulence, hiccups; rarely - increased activity of liver transaminases and alkaline phosphatase.
From the senses: sudden loss of vision (with parenteral administration in the head, neck, nasal turbinates, scalp, deposition of drug crystals in the vessels of the eye is possible), posterior subcapsular cataract, increased intraocular pressure with possible damage to the optic nerve, tendency to develop secondary bacterial , fungal or viral eye infections, trophic changes in the cornea, exophthalmos.
From the musculoskeletal system: slower growth and ossification processes in children (premature closure of the epiphyseal growth plates), osteoporosis (very rarely - pathological bone fractures, aseptic necrosis of the head of the humerus and femur), rupture of muscle tendons, steroid myopathy, decreased muscle mass (atrophy); with intra-articular administration - increased pain in the joint.
Dermatological reactions: delayed wound healing, petechiae, ecchymosis, skin thinning, hyper- or hypopigmentation, steroid acne, stretch marks, tendency to develop pyoderma and candidiasis.
Allergic reactions: generalized (including skin rash, skin itching, anaphylactic shock), local allergic reactions.
Effects due to immunosuppressive effects: development or exacerbation of infections (the appearance of this side effect is facilitated by jointly used immunosuppressants and vaccination).
Local reactions: with parenteral administration - burning, numbness, pain, paresthesia and infection at the injection site; rarely - necrosis of surrounding tissues, scar formation at the injection site; with intramuscular injection (especially into the deltoid muscle) - atrophy of the skin and subcutaneous tissue.
Other: leukocyturia, withdrawal syndrome.
With intravenous administration - blood flow to the face, convulsions.
For external use: rarely - itching, hyperemia, burning, dryness, folliculitis, acne, hypopigmentation, perioral dermatitis, allergic dermatitis, skin maceration, secondary infection, skin atrophy, stretch marks, prickly heat. With prolonged use or application to large areas of skin, systemic side effects characteristic of GCS may develop.
Side effects and symptoms of overdose
Hydrocortisone when administered intramuscularly, intravenously and intraarticularly can provoke the appearance of edema, the development of heart failure, arrhythmia, osteoporosis and bone fractures, medicinal ulcers of the digestive tract, increased blood and intracranial pressure, muscle cramps, a decrease in the body's defenses, Itsenko-Cushing syndrome.
Skin ointment most often causes the following undesirable reactions: local redness, irritation, dryness, itching, burning, swelling and atrophy.
Use of the ophthalmic form of Hydrocortisone can lead to mixed injection, eyelid eczema, exophthalmos, cataracts, hormonal glaucoma, and corneal perforation.
An overdose of the drug is manifested by increased side effects, the appearance of dyspeptic syndrome and a violation of the general condition of the body.
In such a situation, it is important to gradually discontinue hydrocortisone and carry out competent symptomatic therapy.
Hydrocortisone
Interacts with specific cytoplasmic receptors (receptors for glucocorticosteroids (GCS) are found 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).
Protein metabolism: reduces the amount of globulins in plasma, increases albumin synthesis in the liver and kidneys (with an increase in the albumin/globulin ratio), reduces synthesis and increases protein catabolism 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 developed 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 carboxylase and the synthesis of aminotransferases (activation of gluconeogenesis); promotes the development of hyperglycemia. Water-electrolyte metabolism: retains Na+ and water in the body, stimulates the excretion of K+ (mineralocorticoid activity), reduces the absorption of Ca2+ from the gastrointestinal tract, causes “leaching” of calcium from the bones and increases its renal excretion, reduces bone mineralization.
The anti-inflammatory effect is associated with inhibition of the release of inflammatory mediators by zosinophils 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 on all stages of the inflammatory process: inhibits the synthesis of prostaglandins (Pg) at the level of arachidonic acid (lipocortin inhibits phospholipase A2, suppresses the liberation of arachidonic acid and inhibits the biosynthesis of endoperoxides, leukotrienes, which contribute to the processes of inflammation, allergies, etc.), the synthesis of “pro-inflammatory cytokines" (interleukin 1, tumor necrosis factor alpha, etc.); increases the resistance of the cell membrane to the action of various damaging factors.
The immunosuppressive effect is caused by the involution of lymphoid tissue, 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; interferon gamma) from lymphocytes and macrophages and decreased antibody formation.
The antiallergic effect develops as a result of a decrease in the synthesis and secretion of allergic 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, T- and B-lymphocytes, mast cells, suppression of the development of lymphoid and connective tissue, decreased sensitivity of effector cells to mediators, allergies, inhibition of antibody formation, changes in the body's immune response.
In obstructive diseases of the respiratory tract, the effect is mainly due to inhibition of inflammatory processes, prevention or reduction of the severity of swelling of the mucous membranes, reduction of eosinophilic infiltration of the submucosal layer of the bronchial epithelium and deposition of circulating immune complexes in the bronchial mucosa, as well as inhibition of erosion and desquamation of the mucosa. Increases the sensitivity of beta-adrenergic receptors of small and medium-sized bronchi 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 corticosteroids. Inhibits connective tissue reactions during the inflammatory process and reduces the possibility of scar tissue formation.
Instructions for use of Hydrocortisone
Skin ointment is applied to the affected areas in a thin layer 2 to 3 times a day. The course of treatment is no more than 3 weeks, otherwise the likelihood of side effects increases.
Hydrocortisone-POS (ophthalmic form) is placed in a strip into the lower conjunctival sac up to 3 times a day. The duration of treatment is no more than 14 days. When using eye drops simultaneously, apply the ointment after them 10 minutes later.
A single dose of Hydrocortisone for systemic therapy is from 50 to 300 mg, and a daily dose is from 1000 to 1500 mg. The required amount of the drug is determined by the attending physician, based on the severity of the underlying disease and the presence of concomitant diseases. The frequency of administration and duration of therapy are also selected individually.
Drug interactions
The effectiveness of Hydrocortisone when used systemically can be reduced by drugs of the following pharmacological groups:
- Antihistamines.
- Diuretics.
- Anticonvulsants.
Taking this drug together with non-steroidal anti-inflammatory drugs significantly increases the risk of drug ulcers.
Hydrocortisone reduces the effectiveness of glucose-lowering medications, and its simultaneous use with amphotericin B provokes the development of cardiovascular failure.
HYDROCORTISONE-RICHTER susp. d/injection 125 mg vial. 5 ml
Interaction
Hydrocortisone increases the toxicity of cardiac glycosides (due to the resulting hypokalemia, the risk of developing arrhythmias increases).
Accelerates the elimination of acetylsalicylic acid, reduces the content of its metabolites in the blood (with its abolition, the concentration of salicylates in the blood increases and the risk of side effects increases). When used simultaneously with live (attenuated) vaccines and against the background of other types of immunizations, it increases the risk of viral activation and the development of infections. Increases the metabolism of isoniazid, mexiletine (especially in “fast acetylators”), which leads to a decrease in their plasma concentrations. Increases the risk of developing the hepatotoxic effect of paracetamol (induction of “liver” enzymes and the formation of a toxic metabolite of paracetamol).
Hypokalemia caused by hydrocortisone may increase the severity and duration of muscle blockade due to muscle relaxants.
In high doses, it reduces the effect of somatropin.
Hydrocortisone reduces the effect of oral hypoglycemic drugs.
Strengthens the anticoagulant effect of coumarin derivatives.
Weakens the effect of vitamin D on calcium absorption in the intestinal lumen. Ketoconazole (reduces clearance) increases the toxicity of hydrocortisone.
Thiazide diuretics, carbonic anhydrase inhibitors, other glucocorticoids and amphotericin B increase the risk of hypokalemia, sodium-containing drugs - edema and increased blood pressure. Nonsteroidal anti-inflammatory drugs and ethanol increase the risk of ulceration of the gastrointestinal tract (GIT) mucosa and bleeding. In combination with non-steroidal anti-inflammatory drugs for the treatment of arthritis, it is possible to reduce the dose of hydrocortisone due to the additive therapeutic effect.
Indomethacin, displacing hydrocortisone from its connection with albumin, increases the risk of developing its side effects.
Amphotericin B and carbonic anhydrase inhibitors increase the risk of osteoporosis.
The therapeutic effect of hydrocortisone is reduced under the influence of phenytoin, barbiturates, ephedrine, theophylline, rifampicin and other inducers of “liver” microsomal enzymes (increased metabolic rate). Mitotane and other steroid synthesis inhibitors may necessitate an increase in the dose of hydrocortisone.
The clearance of hydrocortisone increases against the background of thyroid hormone preparations.
Immunosuppressants increase the risk of developing infections and lymphoma or other lymphoproliferative disorders associated with Epstein-Barr virus.
Estrogens (including oral estrogen-containing contraceptives) reduce the clearance of hydrocortisone, prolong T1/2 and their therapeutic and toxic effects. The appearance of hirsutism and acne is facilitated by the simultaneous use of hydrocortisone and steroid hormonal drugs - androgens, estrogens, anabolic steroids, oral contraceptives. Tricyclic antidepressants may increase the severity of depression caused by taking hydrocortisone (not indicated for the treatment of these side effects).
The risk of developing cataracts increases when used in conjunction with other glucocorticoids, antipsychotic drugs (neuroleptics), carbutamide and azathioprine.
Simultaneous administration with nitrates, m-anticholinergics (including antihistamines, tricyclic antidepressants) increases intraocular pressure.
