Methylprednisolone Tablets Instructions

Hanyu Pinyin:Jiaponilong Pian

[Ingredients

The main ingredient of this product is: methylprednisolone, whose chemical name is: 11b,17,21-trihydroxy-6a -methyl-pregna-1,4-diene-3,20-dione.

The structural formula is:

Molecular Formula:C₂₂ H₃₀O₅

Molecular weight: 374.48

Excipients:4 mg Tablets: lactose monohydrate, corn starch, dried corn starch, sucrose, calcium stearate.
16 mg Tablets: lactose monohydrate, sucrose, liquid paraffin, calcium stearate, corn starch.

[Properties]This product is a white tablet.

[Indications]

Glucocorticoids should only be used as symptomatic treatment. Only in certain cases of endocrine disorders should they be used as alternative medicines.

Methylprednisolone Tablets can be used for the following conditions:< span style="font-family:Times New Roman">

Non-Endocrine Disorders< span style="font-family:Times New Roman">

1. span>Rheumatic diseases

For short-term use as adjunctive therapy(to help patients through the acute or critical phase), for:

Psoriatic arthritis =”font-family:Times New Roman”>

Rheumatoid arthritis (Some patients may require low-dose maintenance therapy. = “font-family:Times New Roman”>)

Ankylosing spondylitis “font-family:Times New Roman”>

Acute or subacute bursitis

Acute nonspecific head-spinning bursitis

Acute Gouty Arthritis

Post-traumatic osteoarthritis =”font-family:Times New Roman”>

Osteoarthritis-induced synovitis

Synovitis of the upper ankle

2. style=”font-family:Arial”>Collagen disease

For use in critical illness or as maintenance therapy for:

Systemic lupus erythematosus =”font-family:Times New Roman”>

Systemic DermatomyositisSystemic Dermatomyositis(Polymyositis)

Rheumatic Polymyalgia “font-family:Times New Roman”>

Giant cell arthritis “font-family:Times New Roman”>

Acute rheumatic myocarditis

3. style=”font-family:Arial”>Dermal Diseases

Pemphigus

Herpetiform dermatitisHerpetiform dermatitisHerpetiform dermatitis =”font-family:Times New Roman”>

Severe erythema of all kinds (Steven-Johnson syndrome)

Exfoliative dermatitis

Temporal fungal disease

Severe psoriasis “font-family:Times New Roman”>

Severe seborrheic dermatitis

4. style=”font-family:Arial”>Allergic diseases

For the control of severe or impaired Allergic diseases that are functionally compromised:

Seasonal or year-round allergic rhinitis

Serum sickness

Bronchial asthma

Allergic reaction to medications “font-family:Times New Roman”>

Contact dermatitis

Atopic dermatitis

5. style=”font-family:Arial”>Eye disease

Severe acute and chronic allergic and inflammatory reactions of the eye and its adnexa, such as: /span>

Allergic corneal rim ulcers

Ocular Herpes ZosterOcular Herpes Zoster

Anterior retinitis

Diffuse posterior chamber uveitis and chorioretinitis span style=”font-family:Times New Roman”>

Sympathetic uveitis

Allergic conjunctivitis “font-family:Times New Roman”>

Keratitis

ChorioretinitisChorioretinitis =”font-family:Times New Roman”>

Optic neuritis

Iriditis, iridocyclitis

6. style=”font-family:Arial”>Respiratory disease

Symptomatic pulmonary sarcoidosis

Lüffler’s syndrome that cannot be controlled by other methods span style=”font-family:Times New Roman”>(Loeffler’s Syndrome)

Beryllium poisoning

Combined with appropriate antituberculosis chemotherapy for fulminant or disseminated tuberculosis

Combined with appropriate antituberculosis chemotherapy for fulminant or disseminated tuberculosis

Aspiration pneumonia

7. style=”font-family:Arial”>Hematological disorders

Adult Idiopathic Thrombocytopenic PurpuraAdult Idiopathic Thrombocytopenic Purpura span style=”font-family:Times New Roman”>

Adult secondary thrombocytopenia

Acquired (autoimmune) hemolytic anemiaAcquired (autoimmune) hemolytic anemia span style=”font-family:Times New Roman”>

Erythroblastopenia (RBCanemia)

Congenital (erythrocyte) hypoproliferative anemia span style=”font-family:Times New Roman”>

8.Tumors

For the palliative treatment of the following diseases;

Adult leukemia and lymphoma

Childhood acute leukemia =”font-family:Times New Roman”>

9. style=”font-family:Arial”>Oedema

For diuresis in spontaneous or lupus nephrotic syndrome without uremia and Relieve proteinuria

10.Gastrointestinal disorders

Helping patients through the critical phase of the following diseases:< span style="font-family:Times New Roman">

Ulcerative colitis “font-family:Times New Roman”>

Limited ileitisLimited ileitisLimited ileitisLimited ileitisLimited ileitis “font-family:Times New Roman”>

11. style=”font-family:Arial”>Nervous system

Acute deterioration of all types of sclerosis

Oedema due to brain tumors

12. style=”font-family:Arial”>Other

Combined with appropriate anti-tuberculosis chemotherapy for tuberculous meningitis with subarachnoid obstruction or tending to obstruct

Trichomoniasis involving nerves or myocardium

13. style=”font-family:Arial”>Organ transplantation

Endocrine Disorders

Primary or secondary adrenocortical insufficiency ( Hydrocortisone and cortisone are the drugs of choice, and synthetic glucocorticoids may be combined with salt corticosteroids if needed; in infancy, salt corticosteroid supply is particularly important)

Congenital adrenal hyperplasia

Nonsuppurative thyroiditis

Cancer-induced hypercalcemia

[Specifications]（1)4mg (2)16mg

[dosage]

According to the treatment needs of different diseases, the initial dose of methylprednisolone tablets may be as high as 0.5 mg/kg. The initial dose of methylprednisolone tablets may range from4 mg per dayto48mg is adjusted between. A lower dose is usually sufficient for milder symptoms; some patients may require a higher initial dose. Clinical conditions requiring higher doses include multiple sclerosis(200 mg/day) style=”font-family:Times New Roman”>), cerebral edema(200- 1000mg/day)and organ transplants(up to7mg/kg/day). If no satisfactory clinical outcome is seen after a period of adequate treatment, methylprednisolone tablets should be discontinued in favor of other appropriate treatment. In case of discontinuation of the drug after a long period of treatment, it is recommended to reduce the dosage step by step rather than withdrawing it suddenly. When clinical improvement occurs, the initial dose should be reduced over an appropriate period of time until the lowest dose that maintains the clinical effect is achieved, which is the optimal maintenance dose. The physician should also monitor the dose continuously and may need to adjust the dose when:

Changes in clinical presentation due to decreasing or increasing disease;< span style="font-family:Times New Roman">

Individual differences in patient response to drugs

Patients experiencing stressful conditions unrelated to the disease being treated

In the last case, depending on the patient’s condition, it may be necessary to a period of time to increase the dose of methylprednisolone tablets. It is important to emphasize here that dosing requirements are not set in stone and must be adjusted individually depending on the disease being treated and the patient’s response.

Other Day Therapy(ADT)

Everyday therapy is a method of taking corticosteroids method, which means giving a total of two days’ worth of corticosteroids at once on alternate mornings. This treatment is designed to provide the therapeutic effects of corticosteroids for patients who require long-term medication while reducing certain adverse effects such as suppression of the pituitary-adrenocortical axis, Cushing’s-like syndrome, corticosteroid withdrawal symptoms, and growth inhibition in children.

[Adverse Reactions]

Systemic adverse reactions may be observed. Although they occur rarely in very short-term treatment, they should still be followed carefully. This is part of the follow-up of steroid therapy and is not limited to a particular drug. Possible adverse reactions to glucocorticoids (e.g., methylprednisolone) are:

Infection and Infection.

Masking of infection (of symptoms), episodes of underlying infection, opportunistic infections, peritonitis^†.

† Peritonitis may be a major sign or symptom of gastrointestinal system disease such as perforation, obstruction, or pancreatitis (see [Cautions]).

Immune system abnormalities.

Anaphylactic drug reactions (including anaphylactic and allergic-like reactions), suppression of skin test reactions.

Endocrine system abnormalities.

A Cushing-like state, hypopituitarism, steroid withdrawal syndrome, interference with pituitary-adrenal axis function. Altered growth in children, especially when under stress.

Metabolic and nutritional disorders.

Metabolic acidosis, sodium retention, fluid retention, hypokalemic alkalosis, decreased glucose tolerance, increased need for insulin or oral hypoglycemic agents in patients with diabetes, dyslipidemia, increased appetite (which can lead to weight gain). Synthetic derivatives (e.g., methylprednisolone) are less likely to have saline corticosteroid effects than cortisone or hydrocortisone. A sodium-restricted, potassium-supplemented diet may be necessary. Epidural lipodystrophy, lipodystrophy.

Abnormalities of the blood and lymphatic system.

Leukocytosis.

Psychiatric abnormalities.

Emotional disorders (including mood instability, depressed mood, euphoria, psychological dependence, suicidal ideation), psychotic abnormalities (including mania, delusions, hallucinations, schizophrenia [exacerbated] ), blurred states of consciousness, psychotic disorders, anxiety, personality changes, mood swings, abnormal behavior, insomnia, irritability. .

Nervous system abnormalities.

Increased intracranial pressure (with optic papilloedema [benign intracranial hypertension]), convulsions, amnesia, cognitive impairment, dizziness, headache.

Ocular abnormalities.

Eye proptosis, posterior subcapsular cataract, chorioretinopathy, blurred vision (see [Precautions]). Long-term application of glucocorticoids can cause glaucoma (which may involve the optic nerve) and increase the chance of secondary fungal or viral infection of the eye. To prevent corneal perforation, glucocorticosteroids should be used with caution in patients with ocular herpes simplex.

Cardiac abnormalities.

Congestive heart failure, myocardial rupture after myocardial infarction, arrhythmias, and high-dose induced tachycardia in a susceptible population.

Vascular abnormalities.

Hypertension, hypotension, thrombotic events.

Respiratory, thoracic, and mediastinal abnormalities.

Pulmonary embolism, eruption.

Ear and vagal abnormalities.

Vertigo

Gastrointestinal system abnormalities.

Gastric bleeding, intestinal perforation, peptic ulcer (possible peptic ulcer perforation and peptic ulcer bleeding), pancreatitis, ulcerative esophagitis, esophagitis, abdominal pain, bloating, diarrhea, indigestion, nausea, vomiting.

Hepatobiliary abnormalities.

Elevated liver enzymes (elevated alanine aminotransferase, elevated aspartate aminotransferase).

Dermal and subcutaneous tissue abnormalities.

Angioedema, Hirsutism, Ecchymosis, Petechiae, Petechiae skin atrophy, striated skin, hypopigmented skin, hirsutism, rash, erythema, pruritus, urticaria, acne, hyperhidrosis.

Musculoskeletal and connective tissue abnormalities:

Osteonecrosis, pathological fractures, developmental delay, muscle atrophy, myopathy, osteoporosis, neurological arthropathy, arthralgia, muscle pain, muscle weakness< span style="color:black">, steroid myopathy, and aseptic necrosis.

Reproductive system and breast abnormalities.

Menstrual disorders.

Systemic abnormalities.

Decreased healing ability, peripheral edema, fatigue, malaise, inhibition of growth in children.

Check for abnormalities.

Elevated blood alkaline phosphatase, elevated intraocular pressure, decreased glucose tolerance, decreased blood potassium, increased urinary calcium, elevated blood urea, suppressed skin response, and negative nitrogen balance due to protein catabolism.

Injuries, toxicities and surgical complications.

Tendon ruptures (especially Achilles tendon), spinal compression fractures, pathological fractures.

[Contraindicated]

Systemic fungal infections span style=”font-family:Times New Roman”>

Known to be sensitive to methylprednisolone tablets, methylprednisolone or any of the excipients (see [ Ingredients]) in patients with a history of hypersensitivity.

Prohibited in patients receiving immunosuppressive doses of corticosteroids Use of live or live attenuated vaccines.

Relative contraindications

Special Risk Groups: Patients who belong to the following special risk groups should be Close medical supervision and the shortest possible duration of treatment (see also [Precautions] and [Adverse Reactions]): children; patients with diabetes mellitus; patients with hypertension; patients with a history of psychiatric disorders; certain infectious diseases with significant symptoms, such as tuberculosis; or certain viral diseases with significant symptoms, such as herpes and zoster affecting the eyes. herpes and shingles in the eye.

[Note]

Special Risk Groups : Patients in the following special risk groups should be under close medical supervision and have the shortest possible course of treatment.

– Children: long-term, daily divided Administration of glucocorticoids inhibits growth in children, and this treatment should only be used for very severe conditions. Growth should be closely monitored in infants and children receiving long-term corticosteroid therapy. This side effect can usually be avoided or reduced with alternate day therapy. Infants and children on long-term corticosteroid therapy are at special risk for increased intracranial pressure. High doses of corticosteroids may lead to pancreatitis in children.

– Older adults: Because of the increased osteoporosis potential increased risk of osteoporosis and increased risk of water retention and thus possible hypertension, the use of corticosteroids for long-term treatment in the elderly is recommended with caution.

– Diabetic patients: triggers potential diabetes or increase the need for insulin and oral hypoglycemic agents in diabetic patients.

– Patients with hypertension: worsens arterial hypertension worse.

– Patients with a history of psychosis: pre-existing mood swings and psychotic tendencies may be exacerbated by the use of corticosteroids.

Immunosuppressive effects/increased susceptibility to infection

Corticosteroids may increase susceptibility to infection. may mask some symptoms of infection, and new infections may develop during corticosteroid use. The use of corticosteroids may weaken resistance without limiting the infection. Infections caused by any of the pathogens, including viral, bacterial, fungal, protozoan, or helminthic organisms, that occur anywhere in the body may be associated with the use of corticosteroids alone or in combination with other immunosuppressive agents that affect cellular or humoral immunity, or neutrophil function. These infections may be mild, but they can also be severe and sometimes fatal. The incidence of infectious complications increases with increasing doses of corticosteroids. The possibility of appropriate antibiotic therapy must be considered.

People who are taking drugs that suppress the immune system are more likely than healthy individuals to develop infections . Chickenpox and measles, for example, can be more severe and even fatal in unimmunized children or adults who are on corticosteroids. Patients taking corticosteroids should not receive cowpox or other immunization measures, especially in high doses, because of the potential for neurological complications and a weakened antibody response.

Likewise, patients with known or suspected parasitic infections, such as roundworm (pinworm) infections, which may result in high levels of roundworm infection and dissemination with extensive larval migration, often with severe small bowel colitis and potentially fatal gram-negative bacterial sepsis, should be Corticosteroids should be used with great caution.

The use of corticosteroids is contraindicated in patients receiving immunosuppressive doses of Live or live attenuated vaccines. Inactivated vaccines may be used in patients being treated with corticosteroid immunosuppressive doses; however, the response to such vaccines may be attenuated or even ineffective. This suggests that patients being treated with a non-corticosteroid immunosuppressive dose may receive the applicable immunization schedule.

The use of corticosteroids in active TB should be limited to fulminant or disseminated TB. Corticosteroids are used in combination with appropriate antituberculosis therapy to control the disease.

If corticosteroids are used in patients with latent TB or tuberculin-positive reactions, they must be closely monitored for relapse. These patients should receive chemoprophylaxis while on long-term corticosteroids.

Kapozy’s sarcoma has been reported in patients being treated with corticosteroids. Corticosteroid withdrawal may bring about clinical remission. .

Immune system effects

Allergic reactions (e.g., angioedema) may occur. Because skin reactions and severe anaphylactic reactions (e.g., bronchospasm)/allergic-like reactions have occurred rarely in patients being treated with corticosteroids, appropriate precautions should be taken prior to administration, especially in patients with a history of any drug allergy.

Endocrine System Effects

Patients treated with corticosteroids undergo unusual When unusual stress is experienced, increased doses of rapid-acting corticosteroids are required before, during, and after the onset of the stressful situation.

Prolonged administration of pharmacological doses of corticosteroids may lead to hypothalamic –pituitary–adrenal (HPA) inhibition :Arial”>suppression (secondary adrenocortical insufficiency). The degree and duration of induced adrenocortical insufficiency varies from patient to patient, depending on the dose, frequency, and duration of administration, as well as the duration of glucocorticoid therapy. Evening day treatment may reduce this effect (see [DOSAGE AND ADMINISTRATION]– other day therapy).

In addition, if glucocorticoids are suddenly discontinued < span style="color:black">fatal outcomes resulting from acute adrenocortical insufficiency may occur. Therefore, gradual tapering of the dose may reduce the adrenocortical insufficiency that results from the use of the drug. This relative insufficiency may persist for several months after treatment has been discontinued, so medication should be resumed in the event of an emergency during this period. Salt and/or salt corticosteroids should be given concurrently because salt corticosteroid secretion may be impaired.

Steroids “discontinuation syndrome“ appears to be unrelated to adrenocortical insufficiency and may also occur after sudden discontinuation of glucocorticoids. This syndrome includes symptoms such as: anorexia, nausea, vomiting, drowsiness, headache, fever, joint pain, flaking, myalgia, weight loss, and/or hypotension. These effects are thought to be caused by sudden changes in glucocorticoid concentrations rather than by low levels of corticosteroids.

Because glucocorticoids can trigger or exacerbate Cushing’s syndrome, they should be avoided Use glucocorticoids in patients with Cushing’s disease.

Corticosteroids have been shown to be effective in patients with hypothyroidism. The effect of corticosteroids in patients with hypothyroidism has an enhanced effect. Over the course of treatment, it is recommended to gradually reduce the dose to find the lowest maintenance dose.

Metabolism and Nutrition

Corticosteroids, including methylprednisolone can raise blood glucose, exacerbate pre-existing diabetes, and predispose those on long-term corticosteroid therapy to develop diabetes.

Mental effects

When taking corticosteroids, psychosis may occur, manifesting as euphoria, insomnia, mood instability, personality changes, and major depression up to overt psychotic manifestations. In addition, corticosteroids may exacerbate pre-existing mood swings or psychotic tendencies.

Potentially serious psychiatric reactions may occur with systemic steroid therapy. Adverse reactions (see [Adverse Reactions]). Typical symptoms occur within days or weeks of treatment initiation. Although targeted treatment may be required, most reactions recover after dose reduction or discontinuation. Psychological effects have been reported after corticosteroid discontinuation, but the frequency is not known. Patients/caregivers should be encouraged to seek immediate medical attention if they develop psychological symptoms, especially if depressive mood or suicidal ideation is suspected. Patients/caregivers should be alert to the possibility of systemic steroid dose decreases in/caregivers should be alert to the possibility of systemic steroid dose decreases in/disorders that occur during or immediately after discontinuation.

Neurological effects

For patients with epilepsy and severe myasthenia gravis Corticosteroids should be used with caution.

While controlled clinical trials have demonstrated the role of corticosteroids in accelerating remission in the acute phase of multiple sclerosis accelerated remission during acute exacerbations, corticosteroids have not been shown to affect the final outcome or natural history of the disease. Studies do demonstrate that relatively high doses of corticosteroids are necessary to show significant effects. (See [Dosage]).

Corticosteroid use has been reported in patients with Epidural adiposity has been reported in patients on corticosteroids, typically occurring at high doses of long-term medication.

Eye Disease

Because of the potential for corneal perforation Corticosteroids should be used with caution in patients with ocular herpes simplex.

Long-term use of corticosteroids can cause posterior subcapsular cataract and nuclear cataract (especially in children), proptosis, or increased intraocular pressure, which may lead to glaucoma that may damage the optic nerve. It may also increase secondary fungal and viral infections in the eye in patients being treated with glucocorticoids.

Corticosteroid therapy is also associated with central placental chorioretinopathy, which may lead to retinal detachment.

Systemic use and topical corticosteroids may be reported with topical corticosteroids. visual disturbances may be reported with systemic use and topical corticosteroids. If a patient presents with blurred vision or other symptoms of visual disturbance, consideration should be given to referring the patient to an ophthalmologist for evaluation of possible causes, which may include cataracts, glaucoma, or rare diseases such as chorioretinopathy (CSCR< span style="font-family:Arial">), which have been reported after systemic use and topical topical corticosteroids.

Heart Dirty Impact<

Glucocorticoids have cardiovascular adverse effects, such as dyslipidemia and hypertension, and may predispose patients with pre-existing cardiovascular risk factors to cardiovascular adverse effects if used at high doses and for long periods of time. Therefore, corticosteroids should be used with caution in these patients. If needed, risk modification as well as increased cardiac monitoring should be noted. Low-dose and alternate-day therapy may reduce the incidence of complications from corticosteroid therapy.

Systemic corticosteroids should be used with caution in congestive heart failure.

Vascular effects

Steroids should be used with caution in patients with hypertension.

Corticosteroid use has been reported to Thrombosis, including venous thromboembolism, has been reported with corticosteroids. Therefore, corticosteroids should be used with caution in patients who have or may have thromboembolic disease.

Gastrointestinal System Effects

High doses of corticosteroids may trigger acute pancreatitis.

for< span style="font-family:Arial">there is no general consensus on whether corticosteroids per se are associated with peptic ulcers that develop during treatment, but it is the glucocorticoids treatment may mask the symptoms of peptic ulcers to the point where perforation or bleeding occurs without significant pain. Glucocorticoid therapy may mask peritonitis or other signs or symptoms associated with gastrointestinal system disease, such as perforation, obstruction, or pancreatitis. The risk of gastrointestinal ulcers is elevated when combined withNSAIDs.

Patients with nonspecific ulcerative colitis who have impending perforation, abscess, or other purulent infection, diverticulitis, a new intestinal anastomosis, or the possibility of an active or underlying peptic ulcer, corticosteroids should be used with caution.

Hepatobiliary system effects

In patients with cirrhosis, the effects of corticosteroids are increased. A transient increase in serum glutathione aminotransferase/and moderate increase in serum glutathione aminotransferase and alkaline phosphatase may occur, but does not lead to clinical disease. Reports have shown that in most cases, hepatobiliary abnormalities are reversible after cessation of therapy. Therefore, close monitoring is mandatory.

Musculoskeletal system effects

High-dose corticosteroid use has been reported to cause acute myopathy, most often in patients with neuromuscular transmission disorders (eg, myasthenia gravis) or in patients being treated with concomitant anticholinergic drugs such as neuromuscular blocking agents (eg, pancuronium bromide). Acute myopathy is systemic and may involve the muscles of the eye and respiratory system and may lead to tetraplegia. Elevation of creatine kinase may occur. Clinical improvement or recovery after corticosteroid withdrawal may take weeks to years.

Osteoporosis is a common but not often recognized side effect associated with long-term high-dose glucocorticoid use. Use glucocorticoids with caution in osteoporosis.

Renal and urinary tract abnormalities

Corticosteroids should be used with caution in patients with renal insufficiency.

Check

Hydrocortisone or Cortisoneat average and high doses can cause elevated blood pressure, salt and water retention, and increased potassium excretion. These effects are less likely to occur with synthetic derivatives unless used in high doses. Restriction of salt intake and potassium supplementation may be necessary. All corticosteroids increase calcium excretion.

Injury, poisoning and surgical complications

The results of a multicenter study suggest that methylprednisolone nylon sodium succinate should not be used in the routine treatment of traumatic brain injury. The results of the study showed that patients given methylprednisolone sodium succinate were more likely to have a higher rate of traumatic brain injury compared to placebo 2weeks orafter trauma. style=”font-family:Times New Roman”>6months for increased mortality. A causal relationship with methylprednisolone sodium succinate treatment has not been established.

Other    

Because the complications of glucocorticoid therapy are related to the dose and duration of drug administration a risk/benefit decision must be made in each case regarding dose and duration of therapy and whether to use daily or intermittent therapy.

Corticosteroids should be used at as low a dose as possible to manage the treatment situation, and when dose reduction is possible, it should be done gradually. The duration of therapy should usually be kept as short as possible. Long-term therapy is recommended under medical supervision (see [Dosage]). Discontinuation of the drug after long-term treatment should also be done under medical supervision (tapered dose by dose, assessment of adrenal cortical function). The most important symptoms of adrenocortical insufficiency are weakness, postural hypotension, and depression.

Convulsions have been reported with concomitant administration of methylprednisolone and cyclosporine. Because the two drugs inhibit each other’s metabolism, the convulsions and other side effects caused by taking either drug are more likely to occur when both drugs are taken together.

Pheochromocytoma crisis has been reported after the application of systemic corticosteroids, and this crisis can be be fatal. Corticosteroids should be applied to patients with suspected or confirmed pheochromocytoma only after an appropriate risk/benefit assessment has been performed.

Corticosteroid therapy should only be considered with reference to human biopsy reports and parameters (e.g. (e.g., subcutaneous tests, thyroid hormone levels) should only be considered.

Aspirin and non-steroidal anti-inflammatory drugs should be used with caution in combination with corticosteroids.

with CYP3A inhibitors (including those containing cobicistat () Cobicistat) drugs) may increase the risk of systemic side effects with combination therapy. This combination should be avoided unless the benefit outweighs the increased risk of systemic corticosteroid side effects, in which case the patient should be monitored for systemic corticosteroid side effects (see [Drug Interactions]).

There is no evidence that corticosteroids are carcinogenic or mutagenic.

Corticosteroid use may reduce or completely eliminate the skin test response .

Use with caution in athletes.

Important information about certain ingredients

This drug contains lactose. This product is contraindicated in patients with rare genetic disorders such as galactose intolerance, primary lactase deficiency or glucose–galactose absorption disorder .

This drug contains sucrose. If you suffer from fructose intolerance, glucose–galactose absorption disorder or sucrase–Rare genetic disorders such as isomaltase deficiency should be contraindicated in patients with this drug.

Impact on ability to drive and use machines

The effects of corticosteroids on the ability to drive or use machines have not been systematically evaluated. Adverse effects, such as dizziness, vertigo, visual disturbances, and fatigue, may occur after treatment with corticosteroids. Patients should not drive or operate machines if they are affected. .

[For Pregnant and Lactating Women]

Pregnancy

Animal studies have shown that high doses of corticosteroids during pregnancy may lead to fetal malformations. Because of the lack of adequate studies on the effects of methylprednisolone sodium succinate on human reproduction, it should be used during pregnancy only after careful evaluation of the benefit-to-risk ratio for the mother and fetus.

If long-term corticosteroid therapy needs to be discontinued during pregnancy (as with other long-term therapy As with other long-term therapy), the drug should be discontinued gradually (see [dosage]). In some cases (e.g., replacement therapy for adrenocortical insufficiency), therapy should be continued or even increased if necessary.

Corticosteroids are prone to cross the placenta. A retrospective study found an increased incidence of low birth weight in infants born to mothers being treated with corticosteroids. In humans, the risk of low birth weight appears to be dose-dependent, and this risk can be reduced by lowering the dose of corticosteroids. Although neonatal adrenocortical insufficiency appears to be rare in infants exposed to corticosteroids in utero, those whose mothers received high doses of corticosteroids during pregnancy should be carefully monitored and evaluated for signs of adrenocortical insufficiency. The effects of corticosteroids on labor and delivery are not known.

Mothers who have received long-term corticosteroid treatment during pregnancy have been found to The babies born had cataracts at birth.

Breastfeeding

Corticosteroids are secreted with breast milk. Corticosteroids distributed into breast milk may inhibit growth and interfere with endogenous glucocorticoid production in nursing infants. Because adequate studies of glucocorticoid use in humans are not available, only after careful evaluation of the benefit to mother and infant– risk ratio before using the drug during breastfeeding.

Only after carefully weighing the benefits of corticosteroids against It should only be used in pregnant or nursing women or women who may become pregnant after carefully weighing its potential risks to the mother, embryo, or fetus, and only under medical supervision if necessary.

Fertility<

Animal studies have shown that corticosteroids can impair fertility. (See [Pharmacological Toxicology])

[Children’s medication]

See [Dosage], [Adverse Reactions], [Contraindications] and [ Caution].

[medication for the elderly]

See [Dosage] and [Precautions] for more information.

[Drug Interactions]

Methylprednisolone is a cytochrome >P450enzyme () CYP), the substrate of which is mainly mediated byCYP3A4enzyme metabolism. CYP3A4is the most abundant in the adult liverCYPsubfamily of dominant enzymes. It catalyzes the 6β-hydroxylation of steroids, which is the basic first stage of metabolism of endogenous and synthetic corticosteroids. Many other compounds are also substrates of CYP3A4 through family:Times New Roman”>induction (upregulation) or inhibition of CYP3A4 enzymes, some of which (as well as other drugs) have been shown to alter glucocorticoid metabolism.

CYP3A4. span style=”font-family:Arial”>Inhibitors,—Inhibitors,inhibitors ofCYP3A4activity, which typically reduce hepatic clearance and increase >plasma concentrations of CYP3A4substrate drugs, such as methylprednisolone. Due to the presence of CYP3A4inhibitors, the dose of methylprednisolone may need to be adjusted to avoid steroid toxicity.

CYP3A4< span style="font-family:Arial">Inducer—inducingCYP3A4activity of the drug usually increases hepatic clearance, leading to< span style="font-family:Times New Roman">decreased plasma concentrations of CYP3A4substrate drugs. Concurrent administration may require an increased dose of methylprednisolone to achieve the desired effect.

CYP3A4< span style="font-family:Arial">Substrate—hepatic clearance of methylprednisolone may be impaired due to the presence of anotherCYP3A4substrate , requiring appropriate dose adjustment. Adverse reactions caused by the use of either drug may be more likely to occur when both drugs are used together.

Non-CYP3A4mediated effects —Other interactions and effects that occur with methylprednisolone are described in the table below.

The following table provides a list of the most common and

interactions or effects with methylprednisolone. common and/or clinically important drugs and descriptions.

Interaction with methylprednisolone/Effects of important drugs or substances

Harmful interactions

— drugs that are inducers of hepatic enzymes (e.g., phenobarbital, phenytoin sodium, and rifampin) may increase the clearance of methylprednisolone. An increased dose of methylprednisolone may be required to obtain the desired response.

— CYP3A4inhibitors (e.g., macrolides, triazole antifungals, and some calcium channel blockers) may inhibit the metabolism of methylprednisolone, thereby reducing the clearance of the drug. To avoid the toxic effects of steroids, the dose of methylprednisolone should be titrated.

[Drug overdose]

No acute overdose of corticosteroids was found to cause clinical syndrome. In acute overdose cases, cardiac arrhythmias and/ or cardiovascular deficits may occur. Long-term overdose can lead to the classic Cushing-like syndrome. Acute toxicity and/ or death due to corticosteroid overdose have been reported rarely. If an overdose occurs, there is no specific antidote and treatment is supportive and symptomatic. The product can be excreted via dialysis.

[Pharmacology and Toxicology]

Pharmacological effects

Methylprednisolone is a synthetic glucocorticoid. Glucocorticoids diffuse through the cell membrane, bind to specific receptors in the cytoplasm, and subsequently enter the nucleus to bind to DNA, initiate mRNA transcription, and synthesize a variety of enzymatic proteins. Glucocorticoids ultimately exert their pharmacological effects through these enzymes after systemic administration. Glucocorticoids affect inflammatory and immune processes, as well as carbohydrate, protein and lipid metabolism, and act on the cardiovascular system, bone marrow and muscular system, and central nervous system. The glucocorticoid-like effect (anti-inflammatory effect) of methylprednisolone 4mg is the same as that of hydrocortisone 20mg. Methylprednisolone has a lower salt corticosteroid-like effect.

Toxicological studies

Genotoxicity: The genotoxicity of methylprednisolone has not been evaluated. One structural analogue of methylprednisolone, methylprednisolone sulfonate, was negative in the Ames test and in the Chinese hamster ovary cell gene mutation test. Another structural analogue of methylprednisolone, farnesylate, was negative in an in-program DNA synthesis assay.

Reproductive toxicity: The effect of methylprednisolone on animal fertility has not been evaluated. Corticosteroids have been shown to be teratogenic, resulting in reversible fertility impairment, reduced prostate and seminal vesicle weights, and histopathological changes in male rats, as well as reduced embryo placement and live births in pregnant female rats.

Pregnant mice and rats given methylprednisolone at doses equivalent to clinical oral doses resulted in increased incidence of cleft palate in mouse fetuses and reduced cardiovascular defects and body weight in rat fetuses. Administration of methylprednisolone at doses lower than the clinical oral dose resulted in increased intrauterine mortality and fetal skeletal and central nervous system malformations in pregnant rabbits. The safe range of teratogenicity of methylprednisolone and the clinical significance of these findings are not known.

Carcinogenicity: Rodent carcinogenicity tests with methylprednisolone have not been performed. Studies have shown an increased incidence of hepatocellular adenomas and hepatocellular carcinomas in male rats following oral administration of glucocorticoids such as budesonide, prednisolone, and trenbolone at doses below clinical doses (based on body surface area). The clinical significance of the above findings is unclear.

[Pharmacokinetics]

Pharmacokinetics of methylprednisolone Linear, independent of route of administration.

Absorption

Methylprednisolone is rapidly absorbed, and normal healthy In adults, after each dose is administered orally for about 1.5to1.5. family:Times New Roman”>2.3hours to reach maximum plasma concentration. After oral administration, the absolute bioavailability of methylprednisolone is generally high in normal healthy adults (82%~< (span style="font-family:Times New Roman">89%).

Distribution

Methylprednisolone is widely distributed into tissues and It crosses the blood-brain barrier and can be secreted via breast milk. Its apparent volume of distribution is approximately 1.4L/kg. The human plasma protein binding rate of methylprednisolone is approximately 77%.

Biotransformation

Methylprednisolone is metabolized by the human liver to inactive metabolites, of which the main ones are20α-hydroxymethylprednisolone and20β-hydroxymethylprednisolone. Metabolized in the liver primarily by CYP3A4enzyme. (See [Drug Interactions] for a list of drug interactions based on CYP3A4mediated metabolism. (List of drug interactions.)

with manyCYP3A4substrates, methylprednisolone may also be an adenosine triphosphate-binding cassette (ABC) transporter proteinP-. family:Arial”>substrates for glycoproteins that affect tissue distribution and interaction with other drugs.

Clearance

The mean elimination half-life of total methylprednisolone is < /span>1.8~5.2hour range, with a total clearance rate of about 55~6 mL/min/kg.

[Storage] airtight,15℃～25 >C for storage.

[Packaging]

4mg: 30tablets >/box, 30 tablets/bottle >

16mg:20tablets/box,50 tablets/bottle style=”font-family:Times New Roman”>

[Expiration date]60months.

[Executive Standard]Imported Drug Registration Standard JX20100157and in accordance with the Chinese Pharmacopoeia2015year edition requirements.

[approval number]

Imported drug registration certificate number: >

(1)4mg< span style="font-family:Arial">Specification:H20150245

(2)16mg< span style="font-family:Arial">Specification:H20150244

[Manufacturer]

Corporate Name:Pfizer Italia Srl

Manufacturing Address:Localita’ Marino del Tronto, 63100 Ascoli Piceno (AP), Italy

Domestic Contact:

Chaoyangmen North Street, Dongcheng District, Beijing3-7Minmetals PlazaBBlock8-13Floor

Postal Code: 100010

Tel: 010-85167000

Product Inquiry Hotline:400 623 6717