Cortef, tablets 10 mg 100 pcs

Hydrocortisone, a synthetic analog of the natural glucocorticosteroid (GCS), has anti-inflammatory effects and is used for diseases of various organs and systems. It also has moderate mineralocorticoid properties and can be used for replacement therapy for adrenal cortex hormone deficiency conditions. Like other GCSs, hydrocortisone has a pronounced effect on various metabolic processes. In addition, hydrocortisone suppresses the body’s immune response.

Pharmacokinetics

Hydrocortisone is well absorbed from the gastrointestinal ‑tract (GIT) and reaches maximum concentration in blood approximately 1 hour after taking the drug. The plasma elimination half-life of hydrocortisone is about 100 min. More than 90% of hydrocortisone is bound to plasma proteins.

Hydrocortisone is metabolized in the liver and most body tissues to hydrogenated and degraded forms such as tetrahydrocortisone and tetrahydrocortisol, which are excreted by the kidneys, mainly as glucuronides; in addition, a very small portion of hydrocortisone is excreted unchanged by the kidneys.

Hydrocortisone readily passes through the placenta.

Indications

Active ingredient

Composition

How to take, the dosage

Interaction

Drugs such as troleandomycin and ketoconazole may inhibit GCS metabolism and decrease its clearance. In this case, the dose of GCS should be reduced to avoid overdose events.

The GCS may increase clearance of acetylsalicylic acid taken in high doses over a long period, which may decrease serum concentrations of salicylates or increase the risk of salicylate toxicity upon withdrawal of GCS. In patients with hypoprothrombinemia, acetylsalicylic acid in combination with GCS should be prescribed with caution.

There have been reports of both an increase and a decrease in the effect of oral anticoagulants taken concomitantly with GCS. Continuous determination of coagulation rates is necessary to maintain adequate anticoagulant effect.

In concomitant use with live antiviral vaccines and other forms of immunization, GCS increase the risk of viral activation and infection.

The GKS accelerate the metabolism of isoniazid, mexiletine, which leads to a decrease in their plasma concentrations.

Adds the risk of hepatotoxic effects of paracetamol due to the induction of “hepatic” enzymes and the formation of the toxic metabolite of paracetamol.

Long-term GCS therapy may require higher doses of folic acid.

Hypokalemia caused by GCS may increase the severity and duration of muscle block with myorelaxant therapy.

In high doses, GCS reduce the effect of somatropin.

Hydrocortisone reduces the effect of hypoglycemic drugs.

The sodium-containing drugs increase the risk of edema and high blood pressure.

Non-steroidal anti-inflammatory drugs (NSAIDs) and ethanol increase the risk of gastrointestinal mucosal ulceration and bleeding, but the therapeutic effect is increased when GCS is used in combination with NSAIDs to treat arthritis, so the dose of GCS may decrease.

When combined with mitotane and other adrenal cortex inhibitors, it may be necessary to increase the dose of GCS.

With GCS use, immunosuppressants increase the risk of infections and lymphoma or other lymphoproliferative disorders caused by Epstein-Barr virus.

The concomitant use of androgens or anabolic steroids may increase the risk of edema and acne.

The concomitant use with m-cholinoblockers may increase intraocular pressure.

The GCS increase toxicity of cardiac glycosides (resulting hypokalemia increases risk of arrhythmias), and decrease the ability of vitamin D to absorb calcium in the intestinal lumen.

Thiazide diuretics, carbohydrate inhibitors, other GCS, and amphotericin B increase the risk of hypokalemia.

Indomethacin, by displacing GCS from binding to albumin, increases the risk of their side effects.

Amphotericin B and carboanhydrase inhibitors increase the risk of osteoporosis.

The clearance of GCS is increased with the use of thyroid hormone medications.

Estrogens (including oral estrogen-containing contraceptives) decrease GCS clearance, prolong their half-life and their therapeutic and toxic effects.

Tricyclic antidepressants may increase the severity of depression caused by GCS (not indicated for therapy of these side effects).

The risk of cataracts is increased when used with other GCS, antipsychotic medications (neuroleptics), carbutamide and azathioprine.

Special Instructions

Patient information: Persons receiving GCS at immunosuppressive doses should avoid contact with patients with chickenpox or measles; patients should be informed that if contact occurs, they should seek immediate medical attention.

Contraindications

Side effects

Endocrine system disorders: adrenal function inhibition, secondary adrenal and pituitary reactivity of various genesis, development of Icenko-Cushing’s syndrome, menstrual disorders, decreased glucose tolerance, manifestation of latent diabetes, increased requirement for insulin or oral hypoglycemic agents in diabetic patients.

Digestive system disorders: peptic ulcer with possible perforation and bleeding, pancreatitis (nausea, vomiting), abdominal bloating, erosive/ulcerative esophagitis.

After GCS treatment, increases in serum alanine transaminase (ALT), aspartate transaminase (AST) and alkaline phosphatase have been observed.Usually these changes are mild, not associated with any clinical syndrome and are reversible after discontinuation of treatment.

Cardiovascular system disorders: chronic heart failure in patients with appropriate predisposition, increased arterial pressure, in patients with acute and subacute myocardial infarction – expansion of necrosis focus, delayed formation of scar tissue, which may lead to rupture of the heart muscle.

Nervous system disorders:increased intracranial pressure with optic disc edema (pseudotumor of the brain), especially after treatment, seizures, dizziness, headache, delirium, disorientation, euphoria, hallucinations, manic-depressive psychosis, depression, paranoia.

Sensory organs:posterior subcapsular cataract, increased intraocular pressure, glaucoma with possible optic nerve damage, exophthalmus, tendency to develop secondary bacterial, fungal or viral eye infections.

Metabolic side:negative nitrogen balance due to protein catabolism.

Induced by ISS activity:sodium and fluid retention in the body,hypokalemic alkalosis,muscle weakness,potassium loss.

Motor system disorders: “steroid” myopathy, decreased muscle mass, osteoporosis, tendon ruptures, especially Achilles tendon, vertebral compression fractures, aseptic necrosis of femoral and humerus epiphyses, pathological fractures of long bones, growth retardation in children.

The skin: slow wound healing, thinning and decreased skin strength, petechiae, ecchymosis, facial erythema, possible suppression of reaction in skin tests, hirsutism, increased sweating.

Allergic reactions:generalized (skin rash/ hives).

When using other GKS there have been reports of the following side effects: increased appetite, hiccups, arrhythmias, hypercoagulation, thrombosis, corneal trophic changes, increased calcium excretion, hypocalcemia, development or worsening of infections (the appearance of this side effect is contributed by co-administration of immunosuppressants and vaccination). When using Cortef® there are currently no reports of the above side effects.

Overdose

Pregnancy use

Similarities