Dexamethasone, 8 mg/2 ml solution for injection

Drug form: Ampoules for injection

ATC category: Glucocorticoids

Trade name – Dexamethasone International non-property name– Dexamethasone COMPOSITION Each 1 ml Dexamethasone, solution for injection, contains: active ingredient: Dexamethasone sodium phosphate – 4.37 mg (equivalent to 4 mg dexamethasone phosphate). inactive ingredients: methylparaben, propylparaben, edetate disodium, sodium citrate, citric acid, water for injection. CHEMICAL NAME AND CAS NUMBER 9-Fluoro-11b,17-dihydroxy-16a-methyl-3,20-dioxopregna-1,4-dien-21-yl-disodium phosphate. 2392-39-4 PHARMACOLOGICAL GROUP AND ATC CODE Glucocorticoids. ATC code- H02AB02. PHARMACOLOGICAL ACTION Dexamethasone is a synthetic adrenocorticoid with approximately a 7 times higher anti-inflammatory potency than prednisolone and 30 times that of hydrocortisone. Adrenocorticoids act on the HPA at specific receptors on the plasma membrane. On other tissues the adrenocorticoids diffuse across cell membranes and complex with specific cytoplasmic receptors which enter the cell nucleus and stimulate protein synthesis.. Adrenocorticoids have anti-allergic, antitoxic, antishock, antipyretic and immunosuppressive properties. Dexamethasone has only minor mineralocorticoid activities and does therefore, not induce water and sodium retention. PHARMACOKINETICS After administration of Dexamethasone Injection, dexamethasone sodium phosphate is rapidly hydrolysed to dexamethasone. After an iv dose of 20mg dexamethasone plasma levels peak within 5 minutes. Dexamethasone is bound (up to 77%) by plasma proteins, mainly albumin. There is a high uptake of dexamethasone by the liver, kidney and adrenal glands. Metabolism in the liver is slow and excretion is mainly in the urine, largely as unconjugated steroids. The plasma half life is 3.5-4.5 hours but as the effects outlast the significant plasma concentrations of steroids the plasma half-life is of little relevance and the use of biological half life is more applicable. The biological half life of dexamethasone is 36-54 hours, therefore dexamethasone is especially suitable in conditions where continuous glucocorticoid action is desirable. USES Dexamethasone can be used for all forms of general and local glucocorticoid injection therapy and all acute conditions in which intravenous glucocorticoids may be life-saving. A. By intravenous or intramuscular injection when oral therapy is not feasible: 1. Endocrine disorders: Primary or secondary adrenocortical insufficiency (hydrocortisone or cortisone is the drug of choice; synthetic analogs may be used in conjunction with mineralocorticoids where applicable; in infancy, mineralocorticoid supplementation is of particular importance). Acute adrenocortical insufficiency (hydrocortisone or cortisone is the drug of choice; mineralocorticoid supplementation may be necessary, particularly when synthetic analogs are used). Preoperatively, and in the event of serious trauma or illness, in patients with known adrenal insufficiency or when adrenocortical reserve is doubtful. Shock unresponsive to conventional therapy if adrenocortical insufficiency exists or is suspected. 2. Rheumatic Disorders: As adjunctive therapy for short-term administration (to tide the patient over an acute episode or exacerbation) in: Post-traumatic osteoarthritis. Synovitis of osteoarthritis. Acute nonspecific tenosynovitis. Acute gouty arthritis. 3. Dermatologic Diseases: Toxic epidermal necrolysis 4. Allergic States: Bronchial asthma. Angioneurotic oedema and anaphylaxis 5. Gastrointestinal Diseases: To tide the patient over a critical period of the disease in: Ulcerative colitis (systemic therapy). Crohn’s disease 6. Respiratory Diseases: Fulminating or disseminated pulmonary tuberculosis when used concurrently with appropriate antituberculous chemotherapy. Aspiration pneumonitis. 7. Cerebral Edema associated with primary or metastatic brain tumor, craniotomy, or head injury. Use in cerebral edema is not a substitute for careful neurosurgical evaluation and definitive management such as neurosurgery or other specific therapy. Raised intracranial pressure secondary infantile spasm
  1. Shock
Adjunctive treatment where high pharmacological doses are needed. Treatment is an adjunct to and not a substitute for, specific and supportive measures the patient may require. Dexamethasone has been shown to be beneficial when used in the early treatment of shock, but it may not influence overall survival. B. By intra-articular or soft tissue injection: As adjunctive therapy for short-term administration (to tide the patient over an acute episode or exacerbation) in: Synovitis of osteoarthritis. Acute nonspecific tenosynovitis. Post-traumatic osteoarthritis. Acute gouty arthritis. POSOLOGY AND METHOD OF ADMINISTRATION Dexamethasone 8mg/ 2 ml solution for injection can be given without mixing or dilution, but if preferred, can be added without loss of potency to sodium chloride injection or dextrose injection and given by intravenous drip. The infusion mixture must be used within 24 hours and the usual aseptic techniques for injections should be observed. Solutions used for intravenous administration or further dilution of this product should be preservative-free when used in the neonate, especially the premature infant. All dosage recommendations are given in units of dexamethasone base. Intravenous and intramuscular injection General considerations Dosage must be individualised on the basis of the disease and the response of the patient. In order to minimise side effects, the lowest possible dosage adequate to control the disease process should be used Usually the parenteral dosage ranges are one-third to one-half of the oral dose, given every 12 hours. The usual initial dosage is 0.4 mg – 16.6 mg (0.12 ml – 5.0 ml) a day. In situations of less severity, lower doses will generally suffice. However, in certain overwhelming, acute, life-threatening situations, administration in dosages exceeding the usual dosage may be justified. In these circumstances, the slower rate of absorption by intramuscular administration should be recognised. Both the dose in the evening, which is useful in alleviating morning stiffness and the divided dosage regimen are associated with greater suppression of the hypothalamopituitary-adrenal axis. After a favourable response is noted, the proper maintenance dosage should be determined by decreasing the initial dosage by small amounts at appropriate intervals to the lowest dosage which will maintain an adequate clinical response. Chronic dosage should preferably not exceed 500 micrograms dexamethasone daily. Close monitoring of the drug dosage is needed. To avoid hypoadrenalism and/or a relapse of the underlying disease, it may be necessary to withdraw the drug gradually . Whenever possible, the intravenous route should be used for the initial dose and for as many subsequent doses as are given while the patient is in shock (because of the irregular rate of absorption of any medicament administered by any other route in such patients). When the blood pressure responds, use the intramuscular route until oral therapy can be substituted. For the comfort of the patient, not more than 2 ml should be injected intramuscularly at any one site. In emergencies, the usual dose of Dexamethasone 8 mg/ 2ml solution for injection by intravenous or intramuscular injection is 3.3 mg – 16.6 mg (1.0 ml – 5.0 ml) – in shock use only the i.v. route. This dose may be repeated until adequate response is noted. After initial improvement, single doses of 1.7 mg – 3.3 mg (0.5 ml – 1.0 ml), repeated as necessary, should be sufficient. The total daily dosage usually need not exceed 66.4 mg (20.0 ml), even in severe conditions. When constant maximal effect is desired, dosage must be repeated at three-hour or four-hour intervals or maintained by slow intravenous drip. Intravenous or intramuscular injections are advised in acute illness. When the acute stage has passed, oral steroid therapy should be substituted as soon as feasible. Shock (of haemorrhagic, traumatic, or surgical origin): Usually 1.7 mg – 5.0 mg/kg (0.5 ml – 1.5 ml/kg) bodyweight as a single intravenous injection. This may be repeated in two to six hours if shock persists. Alternatively, this may be followed immediately by the same dose in an intravenous infusion. Therapy with Dexamethasone 3.3 mg/ml solution for injection is an adjunct to and not a replacement for conventional therapy. Administration of these high doses should be continued only until the patient’s condition has stabilised and usually no longer than 48-72 hours. Cerebral oedema: Associated with primary or metastatic brain tumour, preoperative preparation of patients with increased intracranial pressure secondary to brain tumour: initially 8.3 mg (2.5ml) intravenously, followed by 3.3 mg (1.0 ml) intramuscularly every six hours until symptoms of cerebral oedema subside. Response is usually noted within 12-24 hours; dosage may be reduced after two to four days and gradually discontinued over five to seven days. High doses of Dexamethasone 8 mg/2ml solution for injection are recommended for initiating short-term intensive therapy for acute life-threatening cerebral oedema. Following the high-loading dose schedule of the first day therapy, the dose is scaled down over the seven- to ten- day period of intensive therapy and subsequently reduced to zero over the next seven to ten days. When maintenance therapy is required, substitute oral dexamethasone as soon as possible . Palliative management of recurrent or inoperable brain tumours: Maintenance therapy should be determined for each patient; 1.7 mg (0.5 ml) two or three times a day may be effective. The smallest dose necessary to control cerebral oedema should be used. Suggested high-dose schedule in cerebral oedema Adults: Initial dose 41.5 mg (12.5 ml) i.v. 1stday - 6.6 mg (2.0 ml) i.v. every 2 hours 2ndday - 6.6 mg (2.0 ml) i.v. every 2 hours 3rdday - 6.6 mg (2.0 ml) i.v. every 2 hours 4th day - 3.3 mg (1.0 ml) i.v. every 2 hours 5th-8th days - 3.3 mg (1.0 ml) i.v. every 4 hours Thereafter decrease by daily reduction of 3.3 mg (1.0 ml) Children (35 kg and over): Initial dose 20.8 mg (6.25 ml) i.v. 1st day - 3.3 mg (1.0 ml) i.v. every 2 hours 2ndday - 3.3 mg (1.0 ml) i.v. every 2 hours 3rdday - 3.3 mg (1.0 ml) i.v. every 2 hours 4thday - 3.3 mg (1.0 ml) i.v. every 4 hours 5th-8th days - 3.3 mg (1.0 ml) i.v. every 6 hours Thereafter decrease by daily reduction of 1.7 mg (0.5 ml) Children (below 35 kg): Initial dose 16.6 mg (5.0 ml) i.v. 1st day - 3.3 mg (1.0 ml) i.v. every 3 hours 2ndday - 3.3 mg (1.0 ml) i.v. every 3 hours 3rdday - 3.3 mg (1.0 ml) i.v. every 3 hours 4thday - 3.3 mg (1.0 ml) i.v. every 6 hours 5th-8th days - 1.7 mg (0.5 ml) i.v. every 6 hours Thereafter decrease by daily reduction of 0.83 mg (0.25 ml) Dual therapy: In acute self-limiting allergic disorders or acute exacerbations of chronic allergic disorders, the following schedule combining oral and parenteral therapy is suggested: First day: Dexamethasone 3.3 mg/ml solution for injection, 3.3 mg – 6.6 mg (1.0 ml – 2.0 ml) intramuscularly Second day: Two 500 microgram dexamethasone tablets twice a day Third day: Two 500 microgram dexamethasone tablets twice a day Fourth day: One 500 microgram dexamethasone tablet twice a day Fifth day: One 500 microgram dexamethasone tablet twice a day Sixth day: One 500 microgram dexamethasone tablet once daily Seventh day: One 500 microgram dexamethasone tablet once daily Eighth day: Reassessment day Intraarticular, intrabursal or intralesional injection In general, these injections are employed when only one or two joints or areas are Some of the usual single doses are:
Large joint (e.g. knee) 1.7 mg – 3.3 mg (0.5 ml – 1.0 ml)
Small joints (e.g. interphalangeal, temporomandibular) 0.66 mg – 0 .8 mg (0.2 ml – 0.25 ml)
Bursae 1.7 mg – 2 .5 mg (0.5 ml – 0.75 ml)
Tendon sheaths* 0.33 mg – 0.8 mg (0.1 ml – 0.25 ml)
Soft-tissue infiltration 1.7 mg – 5.0 mg (0.5 ml – 1.5 ml)
Ganglia 0.8 mg – 1.7 mg (0.25 ml – 0.5 ml)
*Injection should be made into the tendon sheath and not directly into the tendon. Frequency of injection: once every three to five days to once every two to three weeks, depending on response. Use in children: Dosage should be limited to a single dose on alternate days to lessen retardation of growth and minimise suppression of the hypothalamo-pituitary adrenal axis. Use in the elderly: Treatment of elderly patients, particularly if long term, should be planned bearing in mind the more serious consequences of the common side effects of corticosteroids in old age, especially osteoporosis, diabetes, hypertension, hypokalaemia, susceptibility to infection and thinning of the skin. Close clinical supervision is required to avoid life threatening reactions ADVERSE EFFECTS Side-effects Local adverse reactions include post-injection flare, and a painless destruction of the joint reminiscent of Charcots arthropathy especially with repeated intra-articular injection. The incidence of predictable undesirable effects, including hypothalamic-pituitary-adrenal suppression correlates with the relative potency of the drug, dosage, timing of administration and the duration of treatment. Cases of ruptured tendon have been reported . Local injection of glucocorticoid may produce systemic effects. Endocrine/metabolic Suppression of the hypothalamic-pituitary-adrenal axis, premature epiphyseal closure, growth suppression in infancy, childhood and adolescence, menstrual irregularity and amenorrhoea. Cushingoid faces, 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. Diminished lymphoid tissue and immune response. Opportunistic infections, recurrence of dormant tuberculosis and decreased responsiveness to vaccination and skin tests. Musculoskeletal Osteoporosis, vertebral and long bone fractures, avascular osteonecrosis, tendon rupture. Proximal myopathy. Fluid and electrolyte disturbance Sodium and water retention, hypertension, potassium loss, hypokalaemic alkalosis. Neuropsychiatric A wide range of psychiatric reactions including affective disorders (such as irritable, euphoric, depressed and labile mood, and suicidal thoughts), psychotic reactions (including mania, delusions, hallucinations, and aggravation of schizophrenia), behavioural disturbances, irritability, anxiety, sleep disturbances, and cognitive dysfunction including confusion and amnesia have been reported. Reactions are common and may occur in both adults and children. In adults, the frequency of severe reactions has been estimated to be 5-6%. Psychological effects have been reported on withdrawal of corticosteroids; the frequency is unknown Increased intra-cranial pressure with papilloedema in children (pseudotumour cerebri), usually after treatment withdrawal. Aggravation of epilepsy. Psychological dependence. Ophthalmic Increased intra-ocular pressure, glaucoma, papilloedema, posterior subcapsular cataracts, corneal or scleral thinning, exacerbation of opthalmic viral or fungal diseases. Gastrointestinal Dyspepsia, peptic ulceration with perforation and haemorrhage, acute pancreatitis, candidiasis. Dermatological Impaired healing, skin atrophy, bruising, telangiectasia, striae, increased sweating and acne. General Hypersensitivity including anaphylaxis, has been reported. Leucocytosis. Thromboembolism. A transient burning or tingling sensation mainly in the perineal area following intravenous injection of large doses of corticosteroid phosphates. Withdrawal symptoms and signs Too rapid a reduction of corticosteroid dosage following prolonged treatment can lead to acute adrenal insufficiency, hypotension and death. A 'withdrawal syndrome' may also occur including, fever, myalgia, arthralgia, rhinitis, conjunctivitis, painful itchy skin nodules and loss of weight. OVERDOSAGE It is difficult to define an excessive dose of a corticosteroid as the therapeutic dose will vary according to the indication and patient requirements. Massive i.v. corticosteroid doses given as a pulse in emergencies are relatively free from hazardous effects. Exaggeration of corticosteroid related adverse effects may occur. Treatment should be asymptomatic and supportive as necessary. Contraindications Systemic infection unless specific anti-infective therapy is employed. Hypersensitivity to any ingredient. Local injection of a glucocorticoid is contraindicated in bacteraemia and systemic fungal infections, unstable joints, infection at the injection site e.g. septic arthritis resulting from gonorrhoea or tuberculosis. PRECAUTIONS A patient information leaflet should be supplied with this product. Patients and/or carers should be warned that potentially severe psychiatric adverse reactions may occur with systemic steroids. Symptoms typically emerge within a few days or weeks of starting the treatment. Risks may be higher with high doses/systemic exposure pharmacokinetic interactions that can increase the risk of side effects), although dose levels do not allow prediction of the onset, type severity or duration of reactions. Most reactions recover after either dose reduction or withdrawal, although specific treatment may be necessary. Patients/carers should be encouraged to seek medical advice if worrying psychological symptoms develop, especially if depressed mood or suicidal ideation is suspected. Patients/carers should also be alert to possible psychiatric disturbances that may occur either during or immediately after dose tapering/withdrawal of systemic steroids, although such reactions have been reported infrequently. Particular care is required when considering the use of systemic corticosteroids in patients with existing or previous history of severe affective disorders in themselves or in their first degree relatives. These would include depressive or manic-depressive illness and previous steroid psychosis. 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 alternative days. Frequent patient review is required to appropriately titrate the dose against disease activity. After parenteral administration of glucocorticoids serious anaphylactoid reactions, such as glottis oedema, urticaria and bronchospasm, have occasionally occurred, particularly in patients with a history of allergy. If such an anaphylactoid reaction occurs, the following measures are recommended: immediate slow intravenous injection of 0.1 - 0.5 ml of adrenaline (solution of 1:1000: 0.1 - 0.5 mg adrenaline dependent on body weight), intravenous administration of aminophylline and artificial respiration if necessary. Corticosteroids should not be used for the management of head injury or stroke because it is unlikely to be of any benefit and may even be harmful. The results of a randomised, placebo-controlled study suggest an increase in mortality if methylprednisolone therapy starts more than two weeks after the onset of Acute Respiratory Distress Syndrome (ARDS). Therefore, treatment of ARDS with corticosteroids should be initiated within the first two weeks of onset of ARDS. Dexamethasone withdrawal 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. In patients who have received more than physiological doses of systemic corticosteroids (approximately 1 mg dexamethasone) 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 corticosteroid may be reduced rapidly to physiological doses. Once a daily dose of 1mg dexamethasone 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 of up to 6mg daily of dexamethasone 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 long-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 6mg daily of dexamethasone. • Patients repeatedly taking doses in the evening. 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. Appropriate antimicrobial therapy should accompany glucocorticoid therapy when necessary e.g. in tuberculosis and viral and fungal infections of the eye. 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 chickenpox 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.
  1. 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 immunoglobin may be needed.
Live vaccines should not be given to individuals with impaired immune responsiveness. The antibody response to other vaccines may be diminished. Special precautions Particular care is required when considering the use of systemic corticosteroids in patients with the following conditions and frequent patient monitoring is necessary. a. Osteoporosis (post-menopausal females are particularly at risk). b. Hypertension or congestive heart failure. c. Existing or previous history of severe affective disorders (especially previous steroid psychosis). d. Diabetes mellitus (or a family history of diabetes). e. History of tuberculosis, since glucocorticoids may induce reactivation. f. Glaucoma (or a family history of glaucoma). g. Previous corticosteroid-induced myopathy. h. Liver failure. i. Renal insufficiency. j. Epilepsy. k. Gastro-intestinal ulceration. l. Migraine m. Certain parasitic infestations in particular amoebiasis. n. Incomplete statural growth since glucocorticoids on prolonged administration may accelerate epiphyseal closure o. Patients with Cushing's syndrome In the treatment of conditions such as tendinitis or tenosynovitis care should be taken to inject into the space between the tendon sheath and the tendon as cases of ruptured tendon have been reported. Use in children Corticosteroids cause dose-related growth retardation in infancy, childhood and adolescence, which may be irreversible. Dexamethasone has been used 'off label' to treat and prevent chronic lung disease in preterm infants. Clinical trials have shown a short term benefit in reducing ventilator dependence but no long term benefit in reducing time to discharge, the incidence of chronic lung disease or mortality. Recent trials have suggested an association between the use of dexamethasone in preterm infants and the development of cerebral palsy. In view of this possible safety concern, an assessment of the risk:benefit should be made on an individual patient basis. Use in the 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. PREGNANCY AND BREAST FEEDING The ability of corticosteroids to cross the placenta varies between individual drugs, however, dexamethasone readily crosses the placenta. Administration of corticosteroids to pregnant animals can cause abnormalities of foetal development including cleft palate, intra-uterine growth retardation and affects 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 may pass into breast milk, although no data are available for dexamethasone. Infants of mothers taking high doses of systemic corticosteroids for prolonged periods may have a degree of adrenal suppression.
DRUG INTERACTIONS Rifampicin, rifabutin, ephedrine, carbamazepine, phenylbutazone, phenobarbital, phenytoin, primidone, and aminoglutethimide enhance the metabolism of corticosteroids and its therapeutic effects may be reduced. The effects of anticholinesterases are antagonised by corticosteroids in myasthenia gravis. The desired effects of hypoglycaemic agents (including insulin), anti-hypertensives, cardiac glycosides 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. The renal clearance of salicylates is increased by corticosteroids and steroid withdrawal may result in salicylate intoxication. There may be interaction with salicylates in patients with hypoprothrombinaemia.
Aspirin should be used cautiously in conjunction with corticosteroids in hypoprothrombinaemia. False-negative results in the dexamethasone suppression test in patients being treated with indometacin have been reported. The desired effects of hypoglycaemic agents (including insulin) are antagonised by corticosteroids. When corticosteroids are administered concomitantly with potassium-depleting diuretics, patients hould be observed closely for development of hypokalaemia. Corticosteroids may affect the nitroblue tetrazolium test for bacterial infection and produce false-negative results. PRESCRIPTION STATUS To be dispensed with prescription. IDENTIFICATION Clear colorless solution PRESENTATION 5 ampoules with 2 ml sterile solution in PVC- container. 2 containers with leaflet inserted in cardboard box. STORAGE conditions Store at a temperature (15-250C), in a dry place, out of the reach of children. Protect from light. EXPIRY DATE 3 years.