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  药店国别: 新加坡药房
产地国家: 印度
所属类别: 抗过敏药物->消炎药物
处方药:处方药
包装规格: 1mg x 100 tablets
计价单位:
   
生产厂家英文名:
Lupin
该药品相关信息网址1:
http://www.Shire.com
原产地英文商品名:
Generic Calcort 1mg x 100 tablets
原产地英文药品名:
deflazacort
原产地英文化合物名称:
(11β,16β)-21-(Acetyloxy)-11-hydroxy-2'-methyl-5'H-pregna-1,4-dieno[17,16-d]oxazole-3,20-dione
中文参考商品译名:
地夫可特
中文参考化合物名称:
(11β,16β)-21-(Acetyloxy)-11-hydroxy-2'-methyl-5'H-pregna-1,4-dieno[17,16-d]oxazole-3,20-dione
原产地国家批准上市年份:
0000/00/00
英文适应病症1:
reduce inflammation
英文适应病症2:
suppress allergic reactions and immune system activity
临床试验期:

中文适应病症参考翻译1:
消炎
中文适应病症参考翻译2:
抗过敏
中文适应病症参考翻译3:
免疫抑制
药品信息:

 

Shire Pharmaceuticals Limited


Hampshire International Business Park
Chineham
Basingstoke
Hampshire
RG24 8EP


Telephone:  +44 (0)1256 894 000
WWW:  http://www.shire.com
Medical Information direct line:  0800 055 6614
Customer Care direct line:  +44 (0)1256 894 107
Medical Information e-mail:  medinfoglobal@shire.com
Document last updated on the eMC: Tue 20 September 2005
Calcort 1mg, 6mg and 30 mg
Table of Contents

1. NAME OF THE MEDICINAL PRODUCT

2. QUALITATIVE AND QUANTITATIVE COMPOSITION

3. PHARMACEUTICAL FORM

4. CLINICAL PARTICULARS

4.1 Therapeutic indications

4.2 Posology and method of administration

4.3 Contraindications

4.4 Special warnings and precautions for use

4.5 Interaction with other medicinal products and other forms of interaction

4.6 Pregnancy and lactation

4.7 Effects on ability to drive and use machines

4.8 Undesirable effects

4.9 Overdose

5. PHARMACOLOGICAL PROPERTIES

5.1 Pharmacodynamic properties

5.2 Pharmacokinetic properties

5.3 Preclinical safety data

6. PHARMACEUTICAL PARTICULARS

6.1 List of excipients

6.2 Incompatibilities

6.3 Shelf life

6.4 Special precautions for storage

6.5 Nature and contents of container

6.6 Special precautions for disposal and other handling

7. MARKETING AUTHORISATION HOLDER

8. MARKETING AUTHORISATION NUMBER(S)

9. DATE OF FIRST AUTHORISATION/RENEWAL OF THE AUTHORISATION

10. DATE OF REVISION OF THE TEXT

LEGAL CATEGORY


   

1. NAME OF THE MEDICINAL PRODUCT To the top of the page
 

 

Calcort® 1mg, Calcort 6mg, Calcort 30mg.

 

 

2. QUALITATIVE AND QUANTITATIVE COMPOSITION To the top of the page
 

 

Active ingredient:

 

1mg tablet: deflazacort 1mg

 

6mg tablet: deflazacort 6mg

 

30mg tablet: deflazacort 30mg

 

 

3. PHARMACEUTICAL FORM To the top of the page
 

 

1mg tablets: Round, white, uncoated tablets, plain on one face with a 1 on the other face.

 

6mg tablets: Round, white, uncoated tablets, marked with a cross on one face and a 6 on the other face.

 

30mg tablets: Round, white, uncoated tablets, marked with a cross on one face and 30 on the other face.

 

 

4. CLINICAL PARTICULARS To the top of the page
   


4.1 Therapeutic indications To the top of the page
 

 

A wide range of conditions may sometimes need treatment with glucocorticoids. The indications include:

 

• Anaphylaxis, asthma, severe hypersensitivity reactions.

 

• Rheumatoid arthritis, juvenile chronic arthritis, polymyalgia rheumatica.

 

• Systemic lupus erythematosus, dermatomyositis, mixed connective tissue disease (other than systemic sclerosis), polyarteritis nodosa, sarcoidosis.

 

• Pemphigus, bullous pemphigoid, pyoderma gangrenosum.

 

• Minimal change nephrotic syndrome, acute interstitial nephritis.

 

• Rheumatic carditis.

 

• Ulcerative colitis, Crohn's disease.

 

• Uveitis, optic neuritis.

 

• Autoimmune haemolytic anaemia, idiopathic thrombocytopenic purpura.

 

• Acute and lymphatic leukaemia, malignant lymphoma, multiple myeloma.

 

• Immune suppression in transplantation.

 

 


4.2 Posology and method of administration To the top of the page
 

 

Deflazacort is a glucocorticoid derived from prednisolone and 6mg of deflazacort and has approximately the same anti-inflammatory potency as 5mg prednisolone or prednisone.

 

Doses vary widely in different diseases and different patients. In more serious and life-threatening conditions, high doses of deflazacort may need to be given. When deflazacort is used long term in relatively benign chronic diseases, the maintenance dose should be kept as low as possible. Dosage may need to be increased during periods of stress or in exacerbation of illness.

 

The dosage should be individually titrated according to diagnosis, severity of disease and patient response and tolerance. The lowest dose that will produce an acceptable response should be used (see Warnings and Precautions).

 

Adults

 

For acute disorders, up to 120 mg/day deflazacort may need to be given initially. Maintenance doses in most conditions are within the range 3 - 18 mg/day. The following regimens are for guidance only.

 

Rheumatoid arthritis: The maintenance dose is usually within the range 3 NON-BREAKING HYPHEN (8209) 18 mg/day. The smallest effective dose should be used and increased if necessary.

 

Bronchial asthma: In the treatment of an acute attack, high doses of 48 NON-BREAKING HYPHEN (8209) 72 mg/day may be needed depending on severity and gradually reduced once the attack has been controlled. For maintenance in chronic asthma, doses should be titrated to the lowest dose that controls symptoms.

 

Other conditions: The dose of deflazacort depends on clinical need titrated to the lowest effective dose for maintenance. Starting doses may be estimated on the basis of ratio of 5mg prednisone or prednisolone to 6mg deflazacort.

 

Hepatic Impairment

 

In patients with hepatic impairment, blood levels of deflazacort may be increased. Therefore the dose of deflazacort should be carefully monitored and adjusted to the minimum effective dose.

 

Renal Impairment

 

In renally impaired patients, no special precautions other than those usually adopted in patients receiving glucocorticoid therapy are necessary.

 

Elderly

 

In elderly patients, no special precautions other than those usually adopted in patients receiving glucocorticoid therapy are necessary. The common adverse effects of systemic corticosteroids may be associated with more serious consequences in old age (see Warnings and Precautions).

 

Children

 

There has been limited exposure of children to deflazacort in clinical trials.

 

In children, the indications for glucocorticoids are the same as for adults, but it is important that the lowest effective dosage is used. Alternate day administration may be appropriate (see Warnings and Precautions).

 

Doses of deflazacort usually lie in the range 0.25 - 1.5 mg/kg/day. The following ranges provide general guidance:

 

Juvenile chronic arthritis: The usual maintenance dose is between 0.25 NON-BREAKING HYPHEN (8209) 1.0 mg/kg/day.

 

Nephrotic syndrome: Initial dose of usually 1.5 mg/kg/day followed by down titration according to clinical need.

 

Bronchial asthma: On the basis of the potency ratio, the initial dose should be between 0.25 - 1.0 mg/kg deflazacort on alternate days.

 

Deflazacort withdrawal

 

In patients who have received more than physiological doses of systemic corticosteroids (approximately 9mg per day or equivalent) for greater than 3 weeks, withdrawal should not be abrupt. How dose reduction should be carried out depends largely on whether the disease is likely to relapse as the dose of systemic corticosteroids is reduced. Clinical assessment of disease activity may be needed during withdrawal. If the disease is unlikely to relapse on withdrawal of systemic corticosteroids but there is uncertainty about HPA suppression, the dose of systemic corticosteroids may be reduced rapidly to physiological doses. Once a daily dose equivalent to 9mg deflazacort is reached, dose reduction should be slower to allow the HPA-axis to recover.

 

Abrupt withdrawal of systemic corticosteroid treatment, which has continued up to 3 weeks, is appropriate if it is considered that the disease is unlikely to relapse. Abrupt withdrawal of doses up to 48 mg daily of deflazacort, or equivalent for 3 weeks is unlikely to lead to clinically relevant HPA-axis suppression, in the majority of patients. In the following patient groups, gradual withdrawal of systemic corticosteroid therapy should be considered even after courses lasting 3 weeks or less:

 

• Patients who have had repeated courses of systemic corticosteroids, particularly if taken for greater than 3 weeks.

 

• When a short course has been prescribed within one year of cessation of longNON-BREAKING HYPHEN (8209)term therapy (months or years).

 

• Patients who may have reasons for adrenocortical insufficiency other than exogenous corticosteroid therapy.

 

• Patients receiving doses of systemic corticosteroid greater than 48 mg daily of deflazacort (or equivalent),

 

• Patients repeatedly taking doses in the evening.

 

 


4.3 Contraindications To the top of the page
 

 

Systemic infection unless specific anti-infective therapy is employed. Hypersensitivity to deflazacort or any of the ingredients. Patients receiving live virus immunisation.

 

 


4.4 Special warnings and precautions for use To the top of the page
 

 

A patient information leaflet should be supplied with this product.

 

Patients with rare hereditary problems of galactose intolerance, the Lapp lactose deficiency or glucose-galactose malabsorption should not take this medicine.

 

Undesirable effects may be minimised by using the lowest effective dose for the minimum period, and by administering the daily requirement as a single morning dose or whenever possible as a single morning dose on alternate days. Frequent patient review is required to appropriately titrate the dose against disease activity (see Dosage section).

 

Adrenal suppression

 

Adrenal cortical atrophy develops during prolonged therapy and may persist for years after stopping treatment. Withdrawal of corticosteroids after prolonged therapy must therefore always be gradual to avoid acute adrenal insufficiency, being tapered off over weeks or months according to the dose and duration of treatment. During prolonged therapy, any intercurrent illness, trauma or surgical procedure will require a temporary increase in dosage; if corticosteroids have been stopped following prolonged therapy, they may need to be temporarily re-introduced.

 

Patients should carry 'Steroid treatment' cards, which give clear guidance on the precautions to be taken to minimise risk and which provide details of prescriber, drug, dosage and the duration of treatment.

 

Anti-inflammatory/immunosuppressive effects and infection

 

Suppression of the inflammatory response and immune function increases the susceptibility to infections and their severity. The clinical presentation may often be atypical and serious infections such as septicaemia and tuberculosis may be masked and may reach an advanced stage before being recognised.

 

Chickenpox is of particular concern since this normally minor illness may be fatal in immunosuppressed patients. Patients (or parents of children) without a definite history of chicken pox should be advised to avoid close personal contact with chickenpox or herpes zoster and, if exposed, they should seek urgent medical attention. Passive immunisation with varicella zoster immunoglobulin (VZIG) is needed by exposed non-immune patients who are receiving systemic corticosteroids or who have used them within the previous 3 months; this should be given within 10 days of exposure to chickenpox. If a diagnosis of chickenpox is confirmed, the illness warrants specialist care and urgent treatment. Corticosteroids should not be stopped and the dose may need to be increased.

 

Patients should be advised to take particular care to avoid exposure to measles and to seek immediate medical advice if exposure occurs. Prophylaxis with intramuscular normal immunoglobulin may be needed.

 

Live vaccines should not be given to individuals with impaired responsiveness. The antibody response to other vaccines may be diminished.

 

Prolonged use of glucocorticoids may produce posterior subcapsular cataracts, glaucoma with possible damage to the optic nerves and may enhance the establishment of secondary ocular infections due to fungi or viruses.

 

Use in active tuberculosis should be restricted to those cases of fulminating and disseminated tuberculosis in which deflazacort is used for management with appropriate antituberculosis regimen. If glucocorticoids are indicated in patients with latent tuberculosis or tuberculin reactivity, close observation is necessary as reactivation of the disease may occur. During prolonged glucocorticoid therapy, these patients should receive chemoprophylaxis.

 

Special precautions

 

The following clinical conditions require special caution and frequent patient monitoring is necessary: -

 

• Cardiac disease or congestive heart failure (except in the presence of active rheumatic carditis), hypertension, thromboembolic disorders. Glucocorticoids can cause salt and water retention and increased excretion of potassium. Dietary salt restriction and potassium supplementation may be necessary.

 

• Gastritis or oesophagitis, diverticulitis, ulcerative colitis if there is probability of impending perforation, abscess or pyogenic infections, fresh intestinal anastomosis, active or latent peptic ulcer.

 

• Diabetes mellitus or a family history, osteoporosis, myasthenia gravis, renal insufficiency.

 

• Emotional instability or psychotic tendency, epilepsy.

 

• Previous corticosteroid-induced myopathy.

 

• Liver failure.

 

• Hypothyroidism and cirrhosis, which may increase glucocorticoid effect.

 

• Ocular herpes simplex because of possible corneal perforation.

Use in Children

 

Corticosteroids cause dose-related growth retardation in infancy, childhood and adolescence, which may be irreversible.

 

Use in Elderly

 

The common adverse effects of systemic corticosteroids may be associated with more serious consequences in old age, especially osteoporosis, hypertension, hypokalaemia, diabetes, susceptibility to infection and thinning of the skin. Close clinical supervision is required to avoid life-threatening reactions.

 

Since complications of glucocorticoid therapy are dependent on dose and duration of therapy, the lowest possible dose must be given and a risk/benefit decision must be made as to whether intermittent therapy should be used.

 

 


4.5 Interaction with other medicinal products and other forms of interaction To the top of the page
 

 

The same precautions should be exercised as for other glucocorticoids. Deflazacort is metabolised in the liver. It is recommended to increase the maintenance dose of deflazacort if drugs, which are liver enzyme inducers, are co-administered, e.g. rifampicin, rifabutin, carbamazepine, phenobarbitone, phenytoin, primidone and aminoglutethimide. For drugs, which inhibit liver enzymes, e.g. ketoconazole it may be possible to reduce the maintenance dose of deflazacort.

 

In patients taking estrogens, corticosteroid requirements may be reduced.

 

The desired effects of hypoglycaemic agents (including insulin), antiNON-BREAKING HYPHEN (8209)hypertensives and diuretics are antagonised by corticosteroids and the hypokalaemic effects of acetazolamide, loop diuretics, thiazide diuretics and carbenoxolone are enhanced.

 

The efficacy of coumarin anticoagulants may be enhanced by concurrent corticosteroid therapy and close monitoring of the INR or prothrombin time is required to avoid spontaneous bleeding.

 

In patients treated with systemic corticosteroids, use of non-depolarising muscle relaxants can result in prolonged relaxation and acute myopathy. Risk factors for this include prolonged and high dose corticosteroid treatment, and prolonged duration of muscle paralysis. This interaction is more likely following prolonged ventilation (such as in the ITU setting).

 

The renal clearance of salicylates is increased by corticosteroids and steroid withdrawal may result in salicylate intoxication.

 

As glucocorticoids can suppress the normal responses of the body to attack by microorganisms, it is important to ensure that any anti-infective therapy is effective and it is recommended to monitor patients closely. Concurrent use of glucocorticoids and oral contraceptives should be closely monitored as plasma levels of glucocorticoids may be increased. This effect may be due to a change in metabolism or binding to serum proteins. Antacids may reduce bioavailability; leave at least 2 hours between administration of deflazacort and antacids.

 

 


4.6 Pregnancy and lactation To the top of the page
 

Pregnancy

 

The ability of corticosteroids to cross the placenta varies between individual drugs, however, deflazacort does cross the placenta.

 

Administration of corticosteroids to pregnant animals can cause abnormalities of foetal development including cleft palate, intra-uterine growth retardation and effects on brain growth and development. There is no evidence that corticosteroids result in an increased incidence of congenital abnormalities, such as cleft palate/lip in man. However, when administered for prolonged periods or repeatedly during pregnancy, corticosteroids may increase the risk of intra-uterine growth retardation. Hypoadrenalism may, in theory, occur in the neonate following prenatal exposure to corticosteroids but usually resolves spontaneously following birth and is rarely clinically important. As with all drugs, corticosteroids should only be prescribed when the benefits to the mother and child outweigh the risks. When corticosteroids are essential however, patients with normal pregnancies may be treated as though they were in the non-gravid state.

 

Lactation

 

Corticosteroids are excreted in breast milk, although no data are available for deflazacort. Doses of up to 50 mg daily of deflazacort are unlikely to cause systemic effects in the infant. Infants of mothers taking higher doses than this may have a degree of adrenal suppression but the benefits of breast-feeding are likely to outweigh any theoretical risk.

 

 


4.7 Effects on ability to drive and use machines To the top of the page
 

 

On the basis of the pharmacodynamic profile and reported adverse events, it is unlikely that deflazacort will produce an effect on the ability to drive and use machines.

 

 


4.8 Undesirable effects To the top of the page
 

 

The incidence of predictable undesirable effects, including hypothalamicNON-BREAKING HYPHEN (8209)pituitary-adrenal suppression correlates with the relative potency of the drug, dosage, timing of administration and the duration of treatment (see Warnings and Precautions).

 

Endocrine/metabolic

 

Suppression of the hypothalamic-pituitary-adrenal axis, growth suppression in infancy, childhood and adolescence, menstrual irregularity and amenorrhoea. Cushingoid facies, hirsutism, weight gain, impaired carbohydrate tolerance with increased requirement for anti-diabetic therapy. Negative protein and calcium balance. Increased appetite.

 

Anti-inflammatory and immunosuppressive effects

 

Increased susceptibility and severity of infections with suppression of clinical symptoms and signs, opportunistic infections, recurrence of dormant tuberculosis (see Warnings and Precautions).

 

Musculoskeletal

 

Osteoporosis, vertebral and long bone fractures, avascular osteonecrosis, tendon rupture. Muscle wasting or myopathy (acute myopathy may be precipitated by non-depolarising muscle relaxants – see section 4.5), negative nitrogen balance.

 

Fluid and electrolyte disturbance

 

Sodium and water retention with hypertension, oedema and heart failure, potassium loss, hypokalaemic alkalosis.

 

Neuropsychiatric

 

Headache, vertigo, euphoria, psychological dependence, hypomania or depression, insomnia, restlessness and aggravation of schizophrenia. Increased intra-cranial pressure with papilloedema in children (pseudotumour cerebri), usually after treatment withdrawal. Aggravation of epilepsy.

 

Ophthalmic

 

Increased intra-ocular pressure, glaucoma, papilloedema, posterior subcapsular cataracts especially in children, corneal or scleral thinning, exacerbation of ophthalmic viral or fungal diseases.

 

Gastrointestinal

 

Dyspepsia, peptic ulceration with perforation and haemorrhage, acute pancreatitis (especially in children), candidiasis. Nausea.

 

Dermatological

 

Impaired healing, skin atrophy, bruising, telangiectasia, striae, acne.

 

General

 

Hypersensitivity including anaphylaxis has been reported. Leucocytosis. Thromboembolism. Rare incidence of benign intracranial hypertension.

 

Withdrawal symptoms and signs

 

Too rapid a reduction of corticosteroid dosage following prolonged treatment can lead to acute adrenal insufficiency, hypotension and death (see Warnings and Precautions).

 

A 'withdrawal syndrome' may also occur including fever, myalgia, arthralgia, rhinitis, conjunctivitis, painful itchy skin nodules and loss of weight. This may occur in patients even without evidence of adrenal insufficiency.

 

 


4.9 Overdose To the top of the page
 

 

It is unlikely that treatment is needed in cases of acute overdosage. The LD50 for the oral dose is greater than 4000 mg/kg in laboratory animals.

 

 

5. PHARMACOLOGICAL PROPERTIES To the top of the page
   


5.1 Pharmacodynamic properties To the top of the page
 

 

Deflazacort is a glucocorticoid. Its anti-inflammatory and immunosuppressive effects are used in treating a variety of diseases and are comparable to other antiNON-BREAKING HYPHEN (8209)inflammatory steroids. Clinical studies have indicated that the average potency ratio of deflazacort to prednisolone is 0.69-0.89.

 

 


5.2 Pharmacokinetic properties To the top of the page
 

 

Orally administered deflazacort appears to be well absorbed and is immediately converted by plasma esterases to the pharmacologically active metabolite (D 21NON-BREAKING HYPHEN (8209)OH), which achieves peak plasma concentrations in 1.5 to 2 hours. It is 40% protein-bound and has no affinity for corticosteroid binding globulin (transcortin). Its elimination plasma half-life is 1.1 to 1.9 hours. Elimination takes place primarily through the kidneys; 70% of the administered dose is excreted in the urine. The remaining 30% is eliminated in the faeces. Metabolism of D 21-OH is extensive; only 18% of urinary excretion represents D 21-OH. The metabolite of D 21-OH, deflazacort 6-beta-OH, represents one third of the urinary elimination.

 

 


5.3 Preclinical safety data To the top of the page
 

 

Safety studies have been carried out in the rat, dog, mouse and monkey. The findings are consistent with other glucocorticoids at comparable doses. Teratogenic effects demonstrated in rodents and rabbits are typical of those caused by other glucocorticoids. Deflazacort was not found to be carcinogenic in the mouse, but studies in the rat produced carcinogenic findings consistent with the findings with other glucocorticoids.

 

 

6. PHARMACEUTICAL PARTICULARS To the top of the page
   


6.1 List of excipients To the top of the page
 

 

1mg and 30mg tablets: Microcrystalline cellulose, lactose, maize starch and magnesium stearate.

 

6mg tablets: Microcrystalline cellulose, lactose, sucrose, maize starch and magnesium stearate.

 

 


6.2 Incompatibilities To the top of the page
 

 

None reported.

 

 


6.3 Shelf life To the top of the page
 

 

1mg tablets: 3 years

 

6mg and 30mg tablets: 5 years.

 

 


6.4 Special precautions for storage To the top of the page
 

 

Store in the original package. Do not store above 25ºC.

 

 


6.5 Nature and contents of container To the top of the page
 

 

Deflazacort is packed in blister packs of polyvinylchloride and aluminium foil presented in cardboard cartons.

 

1mg tablets: 100 tablets per pack.

 

6mg tablets: 60 tablets per pack

 

30mg tablets: 30 tablets per pack

 

 


6.6 Special precautions for disposal and other handling To the top of the page
 

 

No special instructions for use or handling are required.

 

 

7. MARKETING AUTHORISATION HOLDER To the top of the page
 

 

Shire Pharmaceuticals Limited

 

Hampshire International Business Park

 

Chineham

 

Basingstoke

 

Hampshire RG24 8EP

 

United Kingdom

 

 

8. MARKETING AUTHORISATION NUMBER(S) To the top of the page
 

 

1mg tablets: 08557/0036

 

6mg tablets: 08557/0037

 

30mg tablets: 08557/0038

 

 

9. DATE OF FIRST AUTHORISATION/RENEWAL OF THE AUTHORISATION To the top of the page
 

 

1mg and 6mg tablets: 14 December 1997

 

30mg tablets: 31 October 1997

 

 

10. DATE OF REVISION OF THE TEXT To the top of the page
 

 

January 2005

 

 


LEGAL CATEGORY To the top of the page
 

 

POM
 

 

2010年1月26日更新
更新日期:  
附件:
200812108372110.doc    

 
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