Information about the drug Methylprednisolone – “Medrol”.

By | February 6, 2019

Buy Generic Medrol – Methylprednisolone

Medrol – official instructions for useGeneric medrol

Tradename: Medrol®

International non-proprietary name: Methylprednisolone.

One pill contains: active ingredient methylprednisolone 4 mg, 16 mg or 32 mg;
Excipients: lactose, sucrose, liquid paraffin (in pills with dosages of 16 mg and 32 mg), calcium stearate, corn starch, dried corn starch (in pills with dosage of 4 mg).

Dosage Form: Pills

4 mg pills: white elliptical, 2 risks crosswise applied on one side of the pill, UPJOHN extruded on the other side.
16 mg pills: white elliptical, on the one side of the pill 2 risks are applied crosswise, on the other side UPJOHN 73 is extruded.
32 mg pills: white elliptical, on one side of the pill 2 risks are applied crosswise, on the other side UPJOHN 176 is extruded.

Pharmacotherapeutic group: glucocorticosteroid agent.

ATH code: Н02АВ04.


Glucocorticosteroids (GCS), penetrating through cell membranes, form complexes with specific cytoplasmic receptors. Then these complexes penetrate into the cell nucleus, bind to DNA (chromatin) and stimulate the transcription of mRNA and the subsequent synthesis of various enzymes, which explains the effect of GCS during systemic use. GCS not only have a significant effect on the inflammatory process and immune response, but also affect carbohydrate, protein and fat metabolism. They also affect the cardiovascular system, skeletal muscle and the central nervous system.

Influence on the inflammatory process and the immune response. Most of the indications for the use of corticosteroids due to their anti-inflammatory, immunosuppressive and anti-allergic properties. Thanks to these properties, the following therapeutic effects are achieved:

  • decrease in the number of immunoactive cells near the focus of inflammation;
  • reduction of vasodilation;
  • stabilization of lysosomal membranes;
  • inhibition of phagocytosis;
  • reduced production of prostaglandins and their related compounds.

A dose of 4 mg of methylprednisolone has the same anti-inflammatory effect as 20 mg of hydrocortisone.

Methylprednisolone has only a slight mineralocorticoid activity (200 mg of methylprednisolone is equivalent to 1 mg of deoxycorticosterone).

Effect on carbohydrate and protein metabolism:
GCS have a catabolic effect on proteins. The released amino acids are converted in the process of gluconeogenesis in the liver into glucose and glycogen. The consumption of glucose in peripheral tissues is reduced, which can lead to hyperglycemia and glycosuria, especially coal, with the risk of developing diabetes.

Effect on fat metabolism:
GCS have a lipolytic effect, which is primarily manifested in the limbs. GCS also have a lipogenetic effect, which is most pronounced in the chest, neck and head. All this leads to a redistribution of body fat.

Endocrine diseases

  • Primary and secondary adrenal insufficiency (drugs of choice are hydrocortisone or cortisone;
  • If necessary, synthetic analogues can be used in combination with mineralocorticoid;
  • Mineralocorticoid addition is of particular importance in pediatric practice);
  • Congenital adrenal hyperplasia;
  • Chronic and Subacute Thyroiditis;
  • Hypercalcemia in malignant neoplasms;

Not endocrine diseases

1. Diseases of the musculoskeletal system (including rheumatic) (as an adjunctive therapy for a short time to remove from an acute condition or during exacerbation)

  • Psoriatic arthritis
  • Rheumatoid arthritis, including juvenile rheumatoid arthritis (in some cases, low-dose maintenance therapy may be required)
  • Ankylosing Spondylitis
  • Acute and Subacute Bursitis
  • Acute non-specific tendosynovit
  • Acute gouty arthritis
  • Postgravical osteoarthritis
  • Synovitis in osteoarthritis
  • Epicondylitis

2. Systemic diseases of the connective tissue (in the period of exacerbation or in some cases as maintenance therapy)

  • Acute rheumatic heart disease
  • Systemic lupus erythematosus
  • Systemic dermatomyositis (polymyositis)
  • Rheumatic polymyalgia
  • Giant cell arteritis

3. Skin diseases

  • Pemphigus
  • Dermatitis herpetiformis
  • Severe erythema multiforme (Stevens-Johnson syndrome)
  • Exfoliative dermatitis
  • Mushroom mycosis
  • Severe seborrheic dermatitis

4. Allergic reactions (severe non-recoverable conditions in which conventional therapy is ineffective)

Seasonal or perennial allergic rhinitisSerum sickness
Bronchial asthma
Drug Hypersensitivity Reactions
Contact dermatitis
Atopic dermatitis

5. Eye diseases (severe acute and chronic allergic and inflammatory processes with eye damage)

Allergic Corneal Ulcers
Eye herpes zoster
Inflammation of the anterior segment of the eye
Diffuse posterior uveitis and choroiditis
Sympathetic ophthalmia
Allergic Conjunctivitis
Optic neuritis
Irit and iridocyclitis

6. Respiratory Diseases

Symptomatic sarcoidosis
Leffler syndrome, which is not amenable to therapy by other means
Fulminant or disseminated pulmonary tuberculosis in combination with appropriate anti-tuberculosis chemotherapy
Aspiration pneumonitis

7. Hematological diseases

Idiopathic thrombocytopenic purpura in adults
Secondary thrombocytopenia in adults
Acquired (autoimmune) hemolytic anemia
Erythroblastopenia (erythrocyte anemia)
Congenital (erythroid) hypoplastic anemia

8. Oncological diseases (as palliative therapy)

Leukemia and Lymphomas in Adults
Acute leukemia in children

9. Edema syndrome

To stimulate diuresis and achieve remission of proteinuria in patients with nephrotic syndrome without uremia, or nephritic syndrome of idiopathic type, or caused by systemic lupus erythematosus.

10. Diseases of the gastrointestinal tract (for removing a patient from a critical condition)

Ulcerative colitis
Regional enteritis

11. Nervous system

Exacerbations of multiple sclerosis
Swelling of the brain due to a tumor

12. Other indications for use.

Tuberculous meningitis with subarachnoid block or with a threat of block (in combination with appropriate anti-tuberculosis chemotherapy)
Trichinosis with damage to the nervous system or myocardium

13. Organ Transplantation

Mepresone product


Hypersensitivity to any component of the drug in history. Systemic fungal infections

With a CAUTION, the drug should be used in the following cases: gastric ulcer and duodenal ulcer, esophagitis, gastritis, acute or latent peptic ulcer, intestinal anastomosis (in the immediate history), ulcerative colitis with the threat of perforation or abscess, diverticulitis; sugar dibet and predisposition to it; hyperlipidemia; myasthenia gravis, osteoporosis, hypothyroidism, hyperthyroidism, acute psychosis, acute and subacute myocardial infarction, congestive heart failure, arterial hypertension, severe impaired liver function (especially accompanied by hypoalbuminemia) or kidney, open-angle glaucoma, herpes simplex (eye pattern), eye pattern measles, strongyloidosis, AIDS, HIV infection; active and latent tuberculosis, severe bacterial or viral infectious diseases (increases the risk of developing superinfection, masks the symptoms of the disease), it is permissible to use the drug only on the background of specific therapy.


Inside. The initial dose of the drug can be from 4 mg to 48 mg of methylprednisolone per day, depending on the nature of the disease. For less serious diseases, it is usually sufficient to use lower doses, although individual patients may require higher doses. High doses may be required for such diseases and conditions as multiple sclerosis (200 mg / day), brain edema (200-1000 mg / day) and organ transplantation (up to 7 mg / kg / day). If after a sufficient period of time a satisfactory clinical effect is not obtained, the drug should be discontinued and a different type of therapy prescribed to the patient.

For children, the doctor determines the dose based on the weight or surface of the body. With adrenal insufficiency – inside 0.18 mg / kg or 3.33 mg / sq. M per day in 3 divided doses, for other indications – 0.42-1.67 mg / kg or 12.5-50 mg / sq. . m per day in 3 doses.

It should be emphasized that the required dose may vary and must be chosen individually, depending on the nature of the disease and the patient’s response to therapy. The abolition of the drug after long-term therapy is recommended gradually. If a good effect is obtained during treatment, an individual maintenance dose should be selected to the patient by gradually reducing the initial dose at certain intervals until the lowest dose is found, which allows to maintain the achieved clinical effect. It should be remembered that the constant monitoring of the dosing regimen of the drug.

There may be situations in which a dose adjustment is required, for example, changes in the clinical condition due to the onset of remission or exacerbation of the disease, the patient’s individual response to the drug, and the effect on the patient of stressful situations not directly related to the main disease to which the therapy is directed; in the latter case, it may be necessary to increase the dose of the drug for a certain period of time, depending on the patient’s condition.


Alternating therapy is a dosing regimen in which a double daily dose of GCS is administered every other day in the morning. The goal of such therapy is to achieve a maximum clinical effect in a patient taking the drug for a long time, while minimizing some undesirable effects, such as suppression of the pituitary-adrenal system, Cushing’s syndrome, GCS and growth retardation in children.


Disorders of water and electrolyte balance: sodium retention, chronic heart failure in patients with a corresponding predisposition, increased blood pressure, fluid retention in the body, loss of potassium and hypopotassemia alkalosis.

Musculoskeletal: steroid myopathy, muscle weakness, osteoporosis, pathological fractures, vertebral compression fractures, aseptic necrosis of the tubular bones, tendon ruptures, especially the Achilles tendon.

Gastrointestinal: peptic ulcer with possible perforation and bleeding, gastric bleeding, pancreatitis, esophagitis, bowel perforation.

After treatment with GCS, an increase in the level of alanine transaminase (ALT), aspartate transaminase (ACT) and serum alkaline phosphatase was observed. Usually these changes are minor, not associated with any clinical syndromes and are reversible after cessation of treatment.

Dermatological: slow wound healing, petechiae and ecchymosis, thinning and reducing the strength of the skin.

Metabolic: negative nitrogen balance due to protein catabolism.

Neurological: increased intracranial pressure, pseudotumor of the brain, mental disorders, convulsions.

Endocrine: menstrual disorders, hirsutism, the development of Cushing’s syndrome, suppression of the pituitary-adrenal system, reduced tolerance to carbohydrates, the emergence of latent diabetes, increased insulin or oral glucose-lowering agents in diabetic patients, growth retardation in children.

Ophthalmic: posterior subcapsular cataract, increased intraocular pressure with risk of damage to the optic nerve, exophthalmos

Immunological: erased clinical picture in infectious diseases, activation of latent infections, the occurrence of infections caused by opportunistic pathogens, hypersensitivity reactions, including allergic systemic reactions, possible suppression of reactions during skin tests. Others: GCS withdrawal syndrome.

Clinical syndrome of acute overdose is not described. Cases of acute toxicity in overdose of corticosteroids are extremely rare. There is no specific antidote. Frequent re-admission (daily or several times a week) for a long time can lead to the development of Cushing’s syndrome and other complications characteristic of long-term therapy of GCS. Symptomatic treatment. Methylprednisolone is derived from dialysis.

The following examples of drug interactions may be of significant clinical importance. The combined use of methylprednisolone and cyclosporine causes mutual inhibition of metabolism, so it is likely that side effects associated with the use of each of these drugs as monotherapy, when used together, may occur more often (with the joint use of these drugs, there were cases of seizures).

The therapeutic effect of methylprednisolone is reduced under the influence of inducers of microsomal liver enzymes (ephedrine, theophylline, phenobarbital, phenytoin, rifampicin), which may require an increase in the dose of the drug to obtain the desired effect.

Oleandomycin, ketoconazole. Oral estrogen-containing contraceptives can suppress GCS metabolism and reduce their clearance, increase the half-life, therapeutic and toxic effects of methylprednisolone. In this case, to avoid the effects of overdose, reduce the dose of methylprednisolone.

Methylprednisolone can increase the clearance of acetylsalicylic acid, taken in high doses for a long period, which may lead to a decrease in the level of salicylates in the serum or increase the risk of toxicity of salicylates with the abolition of methylprednisolone. When combined with salicylates, the risk of gastropathy increases. In patients with hypoprothrombinemia, acetylsalicylic acid should be prescribed in combination with GCS with extreme caution.

Methylprednisolone affects the effects of oral anticoagulants. It is reported about strengthening or reducing the effect of anticoagulants taken simultaneously with methylprednisolone. To maintain the desired effect of the anticoagulant, a constant determination of coagulation parameters is necessary.

Due to the resulting hypokalemia increases the toxicity of cardiac glycosides (development of arrhythmias).

Thiazide diuretics, carbonic anhydrase inhibitors, other corticosteroids and amphotericin B increase the risk of hypokalemia, sodium-containing drugs – edema and increase blood pressure.

Alcohol and NSAIDs increase the risk of gastrointestinal ulceration and bleeding. In combination with NSAIDs for the treatment of arthritis, a reduction in the dose of methylprednisolone is possible due to the addition of a therapeutic effect.

In combination with paracetamol, the risk of hepatotoxicity increases (induction of hepatic enzymes and the formation of a toxic metabolite of paracetamol).

Methylprednisolone reduces the effect of hypoglycemic agents.

The simultaneous appointment of antacids reduces the absorption of methylprednisolone.

High doses of methylprednisolone reduce the effectiveness of somatotropin.

Androgens in combination with methylprednisolone increase the risk of edema. Methylprednisolone reduces the effectiveness of vaccines (live vaccines against methylprednisolone can cause illness).

Mitotan and other inhibitors of the function of the adrenal cortex may necessitate an increase in the dose.

Antithyroid drugs and thyroid hormones: clearance of methylprednisolone decreases with hypothyroidism and increases with hyperthyroidism, therefore, the dose of methylprednisolone should be selected based on the results of functional tests.

Methylprednisolone accelerates the metabolism of isoniazid, meksiletin, which leads to a decrease in plasma concentrations of drugs, especially in “fast” acetylators.


Since the complications of GCS therapy depend on the size of the dose and the duration of treatment, in each particular case, based on an analysis of the risk / benefit ratio, they decide on the need for such treatment, and also determine the duration of treatment and the frequency of treatment.
You should apply the lowest dose of the drug, providing a sufficient therapeutic effect, if necessary, the dose should be reduced gradually.
On the background of GCS therapy, the development of various mental disorders is possible: from euphoria, insomnia, mood instability, personality changes and severe depression to acute psychotic manifestations. In addition, existing emotional instabilities or inclinations to psychotic reactions may increase.
Patients who may be exposed to stress during GCS therapy are shown to increase the dose before, during and after a stressful situation.
Administration of live or live attenuated vaccines is contraindicated in patients receiving GCS in doses that have an immunosuppressive effect, but killed or inactivated vaccines can be administered, but the response to the introduction of such vaccines may be reduced. Patients receiving treatment of corticosteroids in doses that do not have immunosuppressive effects, according to appropriate indications can be immunized.
On the background of the GCS therapy, some infections may occur in a worn form, in addition, new infections may develop. When using GCS, a decrease in resistance to infections is possible, as well as the body’s ability to localize the infection process. The development of infections caused by various pathogenic organisms, such as viruses, bacteria, fungi, protozoa or helminths, which are localized in various systems of the human body, may be associated with the use of GCS, both as monotherapy and in combination with other immunosuppressants that affect cellular immunity, humoral immunity or neutrophil function. These infections can occur easily, however, in some cases it may be severe and even fatal. Moreover, the higher doses of GCS are used, the higher the likelihood of developing infectious complications.
The use of Medrol in active tuberculosis should be limited to cases of fulminant and disseminated tuberculosis, when GCS is used to treat the disease in combination with appropriate anti-tuberculosis chemotherapy. If the drug is prescribed to patients with latent tuberculosis or with positive tuberculin tests, the treatment should be carried out under strict medical supervision, since reactivation of the process is possible. During prolonged treatment of GCS, such patients should receive appropriate prophylactic treatment.
The drug should be used with caution in case of damage to the eyes caused by the herpes simplex virus, as this may result in perforation of the cornea.
Prolonged use of corticosteroids can lead to the appearance of a posterior subcapsular cataract, glaucoma with possible damage to the optic nerve and provoke the addition of a secondary eye fungal or viral infection. Allergic reactions may develop (for example, angioedema).
Medium and large doses of hydrocortisone or cortisone can cause high blood pressure, retention of sodium and water ions, and increased excretion of potassium. These effects are less likely when using synthetic corticosteroids (including methylprednisolone), unless they are used in high doses. It is necessary to limit the consumption of table salt with food and the prescription of potassium preparations. All GKS increase calcium excretion.
Osteoporosis is a frequent and, at the same time, a rarely diagnosed side effect that develops with the long-term use of high doses of GCS.
In children receiving the drug for a long time every day several times a day, growth retardation may occur, so this dosing regimen should be used only in absolute testimony. The use of alternating therapy usually avoids or minimizes this side effect.
Manifestations of secondary insufficiency of the adrenal cortex, developing on the background of GCS therapy, can be minimized by gradually reducing the dose. This type of relative deficiency can be observed within a few months after the end of treatment, therefore, in any stressful situations during this period, GCS should be reappointed. At the same time, mineralocorticoid secretion may be impaired, and therefore the concomitant use of electrolytes and / or mineralocorticoids is necessary.
There is a more pronounced effect of GCS in patients with hypothyroidism and cirrhosis of the liver.
There is no consensus about the likelihood of developing peptic ulcers during the treatment of corticosteroids. GCS therapy can mask the symptoms of peptic ulcers, and therefore the occurrence of perforation or bleeding without marked pain syndrome is possible.
GCS should be prescribed with caution in ulcerative colitis, if there is a threat of perforation of the gastrointestinal wall, development of an abscess or other purulent infection, as well as diverticulitis, in the presence of fresh intestinal anastomoses, with active or latent peptic ulcer, renal failure, arterial hypertension, osteoporosis, myasthenia gravis.
Cases of the development of Kalosha’s sarcoma in patients who received GCS therapy have been noted (if they are canceled, clinical remission may occur).
The carcinogenic and mutagenic effects of the drug, as well as its adverse effects on reproductive functions, have not been established.

Pregnancy and breastfeeding
A number of animal studies have shown that the administration of high doses of corticosteroids to females can lead to fetal deformities. Since the relevant studies of the effect of GCS on the reproductive function of humans have not yet been carried out, the use of these drugs during pregnancy, in nursing mothers or women of childbearing age requires an assessment of the likely positive effect of the drug compared to the potential risk to the mother, the embryo or the fetus. GCS should be prescribed during pregnancy only in absolute indications.

GCS easily penetrate the placenta. Children born to mothers who received significant doses of corticosteroids during pregnancy should be carefully examined to identify possible symptoms of adrenal hypofunction. The effect of GCS on the course and outcome of labor is unknown.

GCS is excreted in breast milk, so if necessary, the appointment of the drug Medrol during breastfeeding should stop breastfeeding.


4 mg pills:

1,3 or 10 blisters made of PVC / A1-foil 10 pills each with instructions for use in a carton box
1 bottle of dark glass on 30 pills with the application instruction in a cardboard pack.

16 mg pills:

1 blister made of PVC / A1-foil, 14 pills each, or 5 blisters, 10 pills each, with instructions for use in a carton box.
1 bottle of dark glass on 50 pills with the application instruction in a cardboard pack

32 mg pills

1 bottle of dark glass on 20 or 50 pills with the application instruction in a cardboard pack
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