INN monograph
Dexamethasone / Chlorpheniramine
Corticosteroid [EPC] · POM
Source-linked · Updated 03 Aug 2026 · Source: Local active-ingredient clinical extract; FDA drug label via OpenFDA/DailyMed; Component monographs (multi-source pipeline); Professional class pharmacology (Corticosteroid)
Kenya market
Wholesale / list prices where loaded
Risk first
Contraindications
- CONTRAINDICATIONS Contraindicated in systemic fungal infections (see WARNINGS : Infections: Fungal Infections ) and patients with known hypersensitivity to the product and its consituents.
Precautions
- WARNINGS General Rare instances of anaphylactoid reactions have occurred in patients receiving corticosteroid therapy (see ADVERSE REACTIONS ).
- Increased dosage of rapidly acting corticosteroids is indicated in patients on corticosteroid therapy subjected to any unusual stress before, during, and after the stressful situation.
- Cardio-Renal Average and large doses of corticosteroids can cause elevation of blood pressure, sodium and water retention, and increased excretion of potassium.
- These effects are less likely to occur with the synthetic derivatives except when used in large doses.
- Dietary salt restriction and potassium supplementation may be necessary.
- All corticosteroids increase calcium excretion.
- Literature reports suggest an apparent association between use of corticosteroids and left ventricular free wall rupture after a recent myocardial infarction
- therefore, therapy with corticosteroids should be used with great caution in these patients.
- Endocrine Corticosteroids can produce reversible hypothalamic-pituitary adrenal (HPA) axis suppression with the potential for corticosteroid insufficiency after withdrawal of treatment.
- Adrenocortical insufficiency may result from too rapid withdrawal of corticosteroids and may be minimized by gradual reduction of dosage.
- This type of relative insufficiency may persist for months after discontinuation of therapy
- therefore, in any situation of stress occurring during that period, hormone therapy should be reinstituted.
Point of care
Dosing
Adult
DOSAGE AND ADMINISTRATION For Oral Administration The initial dosage varies from 0.75 to 9 mg a day depending on the disease being treated. It Should Be Emphasized That Dosage Requirements Are Variable And Must Be Individualized On The Basis Of The Disease Under Treatment And The Response Of The Patient. After a favorable response is noted, the proper maintenance dosage should be determined by decreasing the initial drug dosage in small decrements at appropriate time intervals until the lowest dosage that maintains an adequate clinical response is reached. Situations which may make dosage adjustments necessary are changes in clinical status secondary to remissions or exacerbations in the disease process, the patient's individual drug responsiveness, and the effect of patient exposure to stressful situations not directly related to the disease entity under treatment. In this latter situation it may be necessary to increase the dosage of the corticosteroid for a period of time consistent with the patient's condition. If after long-term therapy the drug is to be stopped, it is recommended that it be withdrawn gradually rather than abruptly. In the treatment of acute exacerbations of multiple sclerosis, daily doses of 30 mg of dexamethasone for a week followed by 4 to 12 mg every other day for one month have been shown to be effective (see PRECAUTIONS : Neuro-Psychiatric ). In pediatric patients, the initial dose of dexamethasone may vary depending on the specific disease entity being treated. The range of initial doses is 0.02 to 0.3 mg/kg/day in three or four divided doses (0.6 to 9 mg/m2bsa/day). For the purpose of comparison, the fo ll owing is the equivalent mi lli gram dosage of the various corticosteroids: Dexamethasone, 1.5 Methylprednisolone, 8 Prednisone, 10 Triamcinolone, 8 Prednisolone, 10 Betamethasone, 1.5 Hydrocortisone, 40 Paramethasone, 4 Cortisone, 50 These dose relationships apply only to oral or intravenous administration of these compounds. When these substances or their derivatives are injected intramuscularly or into joint spaces, their relative properties may be greatly altered. In acute, self-limited allergic disorders or acute exacerbations of chronic allergic disorders, the following dosage schedule combining parenteral and oral therapy is suggested: Dexamethasone sodium phosphate injection, 4 mg per mL First Day 1 or 2 mL, intramuscularly Dexamethasone tablets, 0.75 mg Second Day 4 tablets in two divided doses Third Day 4 tablets in two divided doses Fourth Day 2 tablets in two divided doses Fifth Day 1 tablet Sixth Day 1 tablet Seventh Day No treatment Eighth Day Follow-up visit This schedule is designed to ensure adequate therapy during acute episodes, while minimizing the risk of overdosage in chronic cases. In cerebral edema , dexamethasone sodium phosphate injection is generally administered initially in a dosage of 10 mg intravenously followed by 4 mg every six hours intramuscularly until the symptoms of cerebral edema subside. Response is usually noted within 12 to 24 hours and dosage may be reduced after two to four days and gradually discontinued over a period of five to seven days. For pal l iative management of patients with recurrent or inoperable brain tumors, maintenance therapy with either dexamethasone sodium phosphate injection or dexamethasone tablets in a dosage of 2 mg two or three times daily may be effective. Dexamethasone Suppression Tests 1. Tests for Cushing’s syndrome Give 1.0 mg of dexamethasone orally at 11:00 p.m. Blood is drawn for plasma cortisol determination at 8:00 a.m. the following morning. For greater accuracy, give 0.5 mg of dexamethasone orally every 6 hours for 48 hours. Twenty-four hour urine co l ections are made for determination of 17-hydroxycorticosteroid excretion. 2. Test to distinguish Cushing’s syndrome due to pituitary ACTH excess from Cushing’s syndrome due to other causes. Give 2.0 mg of dexamethasone orally every 6 hours for 48 hours. Twenty-four hour urine co l ections are made for determination of 17-hydroxycorticosteroid excretion.
Paediatric
Pediatric Use The efficacy and safety of corticosteroids in the pediatric population are based on the we l -established course of effect of corticosteroids, which is similar in pediatric and adult populations. Published studies provide evidence of efficacy and safety in pediatric patients for the treatment of nephrotic syndrome (patients >2 years of age), and aggressive lymphomas and leukemias (patients >1 month of age). Other indications for pediatric use of corticosteroids, e.g., severe asthma and wheezing, are based on adequate and we l -controlled trials conducted in adults, on the premises that the course of the diseases and their pathophysiology are considered to be substantially similar in both populations. The adverse effects of corticosteroids in pediatric patients are similar to those in adults (see ADVERSE REACTIONS ). Like adults, pediatric patients should be carefully observed with frequent measurements of blood pressure, weight, height, intraocular pressure, and clinical evaluation for the presence of infection, psychosocial disturbances, thromboembolism, peptic ulcers, cataracts, and osteoporosis. Pediatric patients who are treated with corticosteroids by any route, including systemically administered corticosteroids, may experience a decrease in their growth velocity. This negative impact of corticosteroids on growth has been observed at low systemic doses and in the absence of laboratory evidence of hypothalamic-pituitary-adrenal (HPA) axis suppression (i.e., cosyntropin stimulation and basal cortisol plasma levels). Growth velocity may therefore be a more sensitive indicator of systemic corticosteroid exposure in pediatric patients than some commonly used tests of HPA axis function. The linear growth of pediatric patients treated with corticosteroids should be monitored, and the potential growth effects of prolonged treatment should be weighed against clinical benefits obtained and the availability of treatment alternatives. In order to minimize the potential growth effects of corticosteroids, pediatric patients should be titrated to the lowest effective dose.
Renal
Fluid retention/hypertension — care in renal disease.
- CrCl 0–120: Confirm renal dosing in product SmPC / primary label.
Hepatic
Prednisone needs hepatic activation to prednisolone.
Safety
Drug interactions
- Fixed-dose/multi-ingredient product.
- Clinical details partially inherited from component monographs: Dexamethasone, Chlorpheniramine.
- Confirm combination SmPC for exact dosing.
Safety
Adverse effects
- ADVERSE REACTIONS (listed alphabetica ll y, under each subsection) The following adverse reactions have been reported with dexamethasone or other corticosteroids: A ll ergic Reactions: Anaphylactoid reaction, anaphylaxis, angioedema.
- Cardiovascular: Bradycardia, cardiac arrest, cardiac arrhythmias, cardiac enlargement, circulatory co l apse, congestive heart failure, fat embolism, hypertension, hypertrophic cardiomyopathy in premature infants, myocardial rupture following recent myocardial infarction (see WARNINGS: Cardio-Renal ), edema, pulmonary edema, syncope, tachycardia, thromboembolism, thrombophlebitis, vasculitis.
- Dermatologic: Acne, allergic dermatitis, dry scaly skin, ecchymoses and petechiae, erythema, impaired wound healing, increased sweating, rash, striae, suppression of reactions to skin tests, thin fragile skin, thinning scalp hair, urticaria.
- Endocrine: Decreased carbohydrate and glucose tolerance, development of cushingoid state, hyperglycemia, glycosuria, hirsutism, hypertrichosis, increased requirements for insulin or oral hypoglycemic agents in diabetes, manifestations of latent diabetes mellitus, menstrual irregularities, secondary adrenocortical and pituitary unresponsiveness (particularly in times of stress, as in trauma, surgery, or ill ness), suppression of growth in pediatric patients.
- Fluid and Electrolyte Disturbances: Congestive heart failure in susceptible patients, fluid retention, hypokalemic alkalosis, potassium loss, sodium retention, tumor lysis syndrome.
- Gastrointestinal: Abdominal distention, elevation in serum liver enzyme levels (usually reversible upon discontinuation), hepatomegaly, increased appetite, nausea, pancreatitis, peptic ulcer with possible perforation and hemorrhage, perforation of the small and large intestine (particularly in patients with inflammatory bowel disease), ulcerative esophagitis.
- Metabolic: Negative nitrogen balance due to protein catabolism.
- Musculoskeletal: Aseptic necrosis of femoral and humeral heads, loss of muscle mass, muscle weakness, osteoporosis, pathologic fracture of long bones, steroid myopathy, tendon rupture, vertebral compression fractures.
- Neurological/Psychiatric: Convulsions, depression, emotional instability, euphoria, headache, increased intracranial pressure with papilledema (pseudotumor cerebri) usually following discontinuation of treatment, insomnia, mood swings, neuritis, neuropathy, paresthesia, personality changes, psychic disorders, vertigo.
- Ophthalmic: Exophthalmos, glaucoma, increased intraocular pressure, posterior subcapsular cataracts.
- Other: Abnormal fat deposits, decreased resistance to infection, hiccups, increased or decreased motility and number of spermatozoa, malaise, moon face, weight gain.
Use
Indications
- INDICATIONS AND USAGE A l l ergic States: Control of severe or incapacitating a llergic conditions intractable to adequate trials of conventional treatment in asthma, atopic dermatitis, contact dermatitis, drug hypersensitivity reactions, perennial or seasonal allergic rhinitis, and serum sickness.
- Dermatologic Diseases: Bul l ous dermatitis herpetiformis, exfoliative erythroderma, mycosis fungoides, pemphigus, and severe erythema multiforme (Stevens-Johnson syndrome).
- Endocrine Disorders: Primary or secondary adrenocortical insufficiency (hydrocortisone or cortisone is the drug of choice
- may be used in conjunction with synthetic mineralocorticoid analogs where applicable
- in infancy mineralocorticoid supplementation is of particular importance), congenital adrenal hyperplasia, hypercalcemia associated with cancer, and nonsuppurative thyroiditis.
- Gastrointestinal Diseases: To tide the patient over a critical period of the disease in regional enteritis and ulcerative colitis.
- Hematologic Disorders: Acquired (autoimmune) hemolytic anemia, congenital (erythroid) hypoplastic anemia (Diamond-Blackfan anemia), idiopathic thrombocytopenic purpura in adults, pure red cell aplasia, and selected cases of secondary thrombocytopenia.
- Misce l l aneous: Diagnostic testing of adrenocortical hyperfunction, trichinosis with neurologic or myocardial involvement, tuberculous meningitis with subarachnoid block or impending block when used with appropriate antituberculous chemotherapy.
- Neoplastic Diseases: For the palliative management of leukemias and lymphomas.
- Nervous System: Acute exacerbations of multiple sclerosis, cerebral edema associated with primary or metastatic brain tumor, craniotomy, or head injury.
- Ophthalmic Diseases: Sympathetic ophthalmia, temporal arteritis, uveitis, and ocular inflammatory conditions unresponsive to topical corticosteroids.
- Renal Diseases: To induce a diuresis or remission of proteinuria in idiopathic nephrotic syndrome or that due to lupus erythematosus.
Pharmacology
Mode of action
See under Dexamethasone and Chlorpheniramine respectively Corticosteroids bind intracellular glucocorticoid receptors, modulating gene transcription to suppress inflammatory cytokines, inhibit phospholipase A2 via lipocortins, reduce leukocyte migration and stabilise membranes — potent anti-inflammatory and immunosuppressive effects.
Full mechanism text
See under Dexamethasone and Chlorpheniramine respectively Corticosteroids bind intracellular glucocorticoid receptors, modulating gene transcription to suppress inflammatory cytokines, inhibit phospholipase A2 via lipocortins, reduce leukocyte migration and stabilise membranes — potent anti-inflammatory and immunosuppressive effects. Mineralocorticoid activity varies by agent.
ADME
Pharmacokinetics & PD
| Onset | Hours–days |
|---|---|
| Duration | Agent and route dependent |
| Route | ORAL / IV / IM / INHALED / TOPICAL / NASAL / OPHTHALMIC |
Full PK/PD text
CLINICAL PHARMACOLOGY Glucocorticoids, naturally occurring and synthetic, are adrenocortical steroids that are readily absorbed from the gastrointestinal tract. Glucocorticoids cause varied metabolic effects. In addition, they modify the body's immune responses to diverse stimuli. Naturally occurring glucocorticoids (hydrocortisone and cortisone), which also have sodium-retaining properties, are used as replacement therapy in adrenocortical deficiency states. Their synthetic analogs, including dexamethasone, are primarily used for their anti-inflammatory effects in disorders of many organ systems. At equipotent anti-inflammatory doses, dexamethasone almost completely lacks the sodium-retaining property of hydrocortisone and closely related derivatives of hydrocortisone.
Kenya
Brands & prices
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|---|---|---|---|
| No brands linked yet. | |||
Special populations
Pregnancy & lactation
Pregnancy
Pregnancy Teratogenic Effects: Pregnancy Category C. Corticosteroids have been shown to be teratogenic in many species when given in doses equivalent to the human dose. Animal studies in which corticosteroids have been given to pregnant mice, rats, and rabbits have yielded an increased incidence of cleft palate in the offspring. There are no adequate and well-controlled studies in pregnant women. Corticosteroids should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus. Infants born to mothers who have received substantial doses of corticosteroids during pregnancy should be carefully observed for signs of hypoadrenalism.
Lactation
Nursing Mothers Systemically administered corticosteroids appear in human milk and could suppress growth, interfere with endogenous corticosteroid production, or cause other untoward effects. Because of the potential for serious adverse reactions in nursing infants from corticosteroids, a decision should be made whether to discontinue nursing or to discontinue the drug, taking into account the importance of the drug to the mother.
Diet
Food & alcohol
- Drug & food interactions (label) Drug Interactio ns Aminoglutethimide: Aminoglutethimide may diminish adrenal suppression by corticosteroids. Amphotericin B injection and potassium-depleting agents: When corticosteroids are administered concomitantly with potassium-depleting agents (e.g., amphotericin B, diuretics), patients should be observed closely for development of hypokalemia. In addition, there have been cases reported in which concomitant use of amphotericin B and hydrocortisone was followed by cardiac enlargement and congestive heart failure. Antibiotics: Macrolide antibiotics have been reported to cause a significant decrease in corticosteroid clearance (see Drug Interactions: Hepatic Enzyme Inducers, Inhibitors and Substrates ). Anticholinesterases: Concomitant use of anticholinesterase agents and corticosteroids may produce severe weakness in patients with myasthenia gravis. If possible, anticholinesterase agents should be withdrawn at least 24 hours before initiating corticosteroid therapy. Anticoagulants, Oral: Co-administration of corticosteroids and warfarin usually results in inhibition of response to warfarin, although there have been some conflicting reports. Therefore, coagulation indices should be monitored frequently to maintain the desired anticoagulant effect. Antidiabetics: Because corticosteroids may increase blood glucose concentrations, dosage adjustments of antidiabetic agents may be required. Antitubercular Drugs: Serum concentrations of isoniazid may be decreased. Cholestyramine: Cholestyramine may increase the clearance of corticosteroids. Cyclosporine: Increased activity of both cyclosporine and corticosteroids may occur when the two are used concurrently. Convulsions have been reported with this concurrent use. Dexamethasone Suppression Test (DST): False-negative results in the dexamethasone suppression test (DST) in patients being treated with indomethacin have been reported. Thus, results of the DST should be interpreted with caution in these patients. Digitalis Glycosides: Patients on digitalis glycosides may be at increased risk of arrhythmias due to hypokalemia. Ephedrine: Ephedrine may enhance the metabolic clearance of corticosteroids, resulting in decreased blood levels and lessened physiologic activity, thus requiring an increase in corticosteroid dosage. Estrogens, including Oral Contraceptives: Estrogens may decrease the hepatic metabolism of certain corticosteroids, thereby increasing their effect. Hepatic Enzyme Inducers, Inhibitors and Substrates: Drugs which induce cytochrome P450 3A4 (CYP 3A4) enzyme activity (e.g., barbiturates, phenytoin, carbamazepine, rifampin) may enhance the metabolism of corticosteroids and require that the dosage of the corticosteroid be increased. Drugs which inhibit CYP 3A4 (e.g., ketoconazole, macrolide antibiotics such as erythromycin) have the potential to result in increased plasma concentrations of corticosteroids. Dexamethasone is a moderate inducer of CYP 3A4. Co-adminstration with other drugs th
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Sources & disclaimer
Source: Local active-ingredient clinical extract; FDA drug label via OpenFDA/DailyMed; Component monographs (multi-source pipeline); Professional class pharmacology (Corticosteroid)
Clinical review date not recorded.
Decision support only — not a substitute for clinical judgment, product SmPC, or Kenya STG/EML.