Brands of Prednisolone  in Kenya

Cotipred ,Bottu S.A Laboratories

Dawasolone , Dawa Limited

Deslone , Radiance Pharmaceuticals Ltd

Pedsol , Laboratory & Allied Ltd

Plone,Zawadi Healthcare Ltd

Prednifil ,Fourrts (India) Laboratories Pvt. Limited

Predilone , Regal Pharmaceuticals Limited

Prednisolone ,Biodeal Laboratories Ltd

Prednisolone, Cosmos Limited

Prednisolone , Elys Chemical Industries Ltd

Pred-paed Solution ,Yash Pharma Laboratories Pvt. Ltd

Predsol forte | Predsol ,Borg pharmaceutical ltd

P Solon , Pharma Life Science Limited

Solone, Advanced Chemical Industries Limited 1PPB Drugs Retention Register

Prednisolone in Kenya
Prednisolone Chemical Structure


Prednisone decreases inflammation via suppression of the migration of polymorphonuclear leukocytes and reversing increased capillary permeability. It also suppresses the immune system by reducing the activity and the volume of the immune system.2Frey, Brigitte M., and Felix J. Frey. “Clinical pharmacokinetics of prednisone and prednisolone.” Clinical pharmacokinetics 19.2 (1990): 126-146.


Prednisolone is indicated in the management of all conditions deemed likely to benefit from short or long term glucocorticoid therapy. These include:

Allergic states

Severe, incapacitating allergies unresponsive to conventional treatment; asthma serum sickness; drug hypersensitivity reactions.

Collagen disorders

Eg systemic lupus erythematosus, polymyositis, polymyalgia rheumatica and temporal (giant cell) arteritis, mixed connective tissue disease syndrome, acute rheumatic carditis.

Rheumatic disorders

Usually given as an adjunctive therapy for short term administration during an acute episode or exacerbation of rheumatoid arthritis, psoriatic arthritis.

Skin conditions

Life-threatening or incapacitating skin conditions such as pemphigus and exfoliative dermatitis.

Neoplastic disease

Leukaemias and lymphomas in adults, acute leukaemia of childhood.

Gastro-Intestinal disease

During acute exacerbation in ulcerative colitis and regional ileitis (Crohn’s Disease).

Respiratory disease

Sarcoidosis (especially with hypercalcaemia), fulminating or disseminated pulmonary tuberculosis when used concurrently with appropriate antituberculosis chemotherapy.

Haematological disorders

Various blood dyscrasias eg selected cases of haemolytic anaemia, thrombocytopenic purpura.


Nephrotic syndrome.


20-40mg daily (acute conditions up to 80mg daily) reducing gradually to maintenance level when symptoms have subsided. Maintenance dosage is usually 5-20mg daily reached in about two weeks by reduction of the daily dosage by 5mg or 2.5mg, two or three times a week.

Paediatric population

Although appropriate fractions of the actual dose may be used, dosage will usually be determined by clinical response as in adults . Alternate day dosage is preferable where possible.

Corticosteroids cause growth retardation in infancy, childhood and adolescence which may be irreversible. Treatment should be limited to the minimum dosage for the shortest possible time. In order to minimise suppression of the hypothalamo-pituitary adrenal axis and growth retardation, treatment should be administered where possible as a single dose on alternate days.


Treatment of elderly patients, especially if long-term, should be planned bearing in mind the more serious consequences of the common side-effects of corticosteroids in old age, particularly diabetes, hypertension, hypokalaemia, osteoporosis, susceptibility to infection and thinning of the skin. Close clinical supervision is required to avoid life-threatening reactions.

The daily dose should be taken in the morning after breakfast. For further information with reference to dosage see warnings and precautions section.

The following therapeutic guidelines should be kept in mind for all therapy with corticosteroids:

Corticosteroids are palliative symptomatic treatment by virtue of their anti-inflammatory effects; they are never curative.

The appropriate individual dose must be determined by trial and error and must be re-evaluated regularly according to activity of the disease.

As corticosteroid therapy becomes prolonged and as the dose is increased, the incidence of disabling side-effects increases.

In general, initial dosage shall be maintained or adjusted until the anticipated response is observed. The dose should be gradually reduced until the lowest dose which will maintain an adequate clinical response is reached. Use of the lowest effective dose may also minimise side-effects (see ‘Special warnings and special precautions for use’).

In patients who have received more than physiological dose for systemic corticosteroids (approximately 7.5mg prednisolone 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 hypothalamic-pituitary-adrenal (HPA) suppression, the dose of corticosteroid may be reduced rapidly to physiological doses. Once a daily dose equivalent to 7.5mg of prednisolone 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 40mg daily of prednisolone, 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 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 40mg daily of prednisolone (or equivalent).

• patients repeatedly taking doses in the evening.

During prolonged therapy, dosage may need to be temporarily increased during periods of stress or during exacerbations of the disease . If there is lack of a satisfactory clinical response to Prednisolone , the drug should be gradually discontinued and the patient transferred to alternative therapy.

Intermittent dosage regimen A single dose of Prednisolone in the morning on alternate days or at longer intervals is acceptable therapy for some patients. When this regimen is practical, the degree of pituitary-adrenal suppression can be minimised.

Specific dosage guidelines The following recommendations for some corticosteroid-responsive disorders are for guidance only. Acute or severe disease may require initial high dose therapy with reduction to the lowest effective maintenance dose as soon as possible. Dosage reductions should not exceed 5-7.5mg daily during chronic treatment.

Allergic and skin disorders Initial doses of 5-15mg daily are commonly adequate.

Collagenosis Initial doses of 20-30mg daily are frequently effective. Those with more severe symptoms may require higher doses.

Rheumatoid arthritis The usual initial dose is 10-15mg daily. The lowest daily maintenance dose compatible with tolerable symptomatic relief is recommended.

Blood disorders and lymphoma An initial daily dose of 15-60mg is often necessary with reduction after an adequate clinical or haematological response. Higher doses may be necessary to induce remission in acute leukaemia.3Rose, James Q., Anthony M. Yurchak, and William J. Jusko. “Dose dependent pharmacokinetics of prednisone and prednisolone in man.” Journal of pharmacokinetics and biopharmaceutics 9.4 (1981): 389-417.


Hypersensitivity to the active substance or to any of the excipients .

Systemic infections unless specific anti-infective therapy is employed.

Patients with ocular herpes simplex due to the possibility of perforation.


Co-treatment with CYP3A inhibitors, including cobicistat-containing products, is expected to increase the risk of systemic side-effects. The combination should be avoided unless the benefit outweighs the increased risk of systemic corticosteroid side-effects, in which case patients should be monitored for systemic corticosteroid side-effects.

Hepatic microsomal enzyme inducers: Drugs that induce hepatic enzyme cytochrome P-450 (CYP) isoenzyme 3A4 such as phenobarbital, phenytoin, rifampicin, rifabutin, carbamazepine, primidone and aminoglutethimide may reduce the therapeutic efficacy of corticosteroids by increasing the rate of metabolism. Lack of expected response may be observed and dosage of Prednisolone Tablets may need to be increased.

Hepatic microsomal enzyme inhibitors: Drugs that inhibit hepatic enzyme cytochrome P-450 (CYP) isoenzyme 3A4 (e.g. ketoconazole, troleandomycin) may decrease glucocorticoid clearance. Dosages of glucocorticoids given in combination with such drugs may need to be decreased to avoid potential adverse effects.

Antidiabetic agents: Glucocorticoids may increase blood glucose levels. Patients with diabetes mellitus receiving concurrent insulin and/or oral hypoglycemic agents may require dosage adjustments of such therapy.

Non-steroidal anti-inflammatory drugs: Concomitant administration of ulcerogenic drugs such as indomethacin during corticosteroid therapy may increase the risk of GI ulceration. Aspirin should be used cautiously in conjunction with glucocorticoids in patients with hypoprothrombinaemia. Although concomitant therapy with salicylate and corticosteroids does not appear to increase the incidence or severity of GI ulceration, the possibility of this effect should be considered. Serum salicylate concentrations may decrease when corticosteroids are administered concomitantly. The renal clearance of salicylates is increased by corticosteroids and steroid withdrawal may result in salicylate intoxication. Salicylates and corticosteroids should be used concurrently with caution. Patients receiving both drugs should be observed closely for adverse effects of either drug.

Antibacterials: Rifamycins accelerate metabolism of corticosteroids and thus may reduce their effect. Erythromycin inhibits metabolism of methylprednisolone and possibly other corticosteroids.

Anticoagulants: Response to anticoagulants may be reduced or less often, enhanced by corticosteroids. Close monitoring of the INR or prothrombin time is required to avoid spontaneous bleeding.

Antiepileptics: Carbamazepine, phenobarbital, phenytoin and primidone accelerate metabolism of corticosteroids and may reduce their effect.

Antifungals: Risk of hypokalaemia may be increased with amphotericin, therefore concomitant use with corticosteroids should be avoided unless corticosteroids are required to control reactions; ketoconazole inhibits metabolism of methylprednisolone and possibly other corticosteroids.

Antivirals: Ritonavir possibly increases plasma concentrations of prednisolone and other corticosteroids.

Cardiac Glycosides: Increased toxicity if hypokalaemia occurs with corticosteroids.

Ciclosporin: Concomitant administration of prednisolone and ciclosporin may result in decreased plasma clearance of prednisolone (i.e. increased plasma concentration of prednisolone). The need for appropriate dosage adjustment should be considered when these drugs are administered concomitantly.

Cytotoxics: Increased risk of haematological toxicity with methotrexate.

Mifepristone: Effect of corticosteroids may be reduced for 3-4 days after mifepristone.

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

Oestrogens: Oestrogens may potentiate the effects of glucocorticoids and dosage adjustments may be required if oestrogens are added to or withdrawn from a stable dosage regimen.

Somatropin: Growth promoting effect may be inhibited.

Sympathomimetics: Increased risk of hypokalaemia if high doses of corticosteroids given with high doses of bambuterol, fenoteral, formoteral, ritodrine, salbutamol, salmeterol and terbutaline.

Antacids can reduce the absorbtion of prednisolone if given in high doses. Indigestion remedies should not be taken at the same time of day as Prednisolone.

Corticosteroids should not be used concurrently with retinoids and tetracyclines due to increased intracranial pressure.

Other: The desired effects of hypoglycaemic agents (including insulin), antihypertensives and diuretics are antagonised by corticosteroids; and the hypokalaemic effect of acetazolamide, loop diuretics, thiazide diuretics, carbenoxolone and theophylline are enhanced.4Jusko, William J., and James Q. Rose. “Monitoring prednisone and prednisolone.” Therapeutic drug monitoring 2.2 (1980): 169-176.


Fluid and Electrolyte Disturbances
Sodium retention. Fluid retention. Congestive heart failure in susceptible patients. Potassium loss. Hypokalemic alkalosis. Hypertension.

Muscle weakness. Steroid myopathy. Loss of muscle mass. Osteoporosis. Vertebral compression fractures. Aseptic necrosis of femoral and humeral heads. Pathologic fracture of long bones.

Peptic ulcer with possible perforation and hemorrhage. Pancreatitis. Abdominal distention. Ulcerative esophagitis.

Impaired wound healing. Thin fragile skin. Petechiae and ecchymoses. Facial erythema. Increased sweating. May suppress reactions to skin tests.

Convulsions. Increased intracranial pressure with papilledema (pseudotumor cerebri) usually after treatment. Vertigo. Headache.

Menstrual irregularities. Development of Cushingoid state. Suppression of growth in children. Secondary adrenocortical and pituitary unresponsiveness, particularly in times of stress, as in trauma, surgery, or illness. Decreased carbohydrate tolerance. Manifestations of latent diabetes mellitus. Increased requirements for insulin or oral hypoglycemic agents in diabetics.

Posterior subcapsular cataracts. Increased intraocular pressure. Glaucoma. Exophthalmos.

Negative nitrogen balance due to protein catabolism

Reporting of suspected adverse reactions:

The PPB Department of Pharmacovigilance was set up with a vision to develop, implement and continuously upgrade an appropriate system for detecting, reporting, and monitoring adverse drug reactions (ADRs) and other relevant problems with medicines in Kenya. The department strives to ensure the safety and efficacy of pharmaceutical products in Kenya.
Reporting suspected adverse reactions after authorization of the medicinal product are important. It allows continued monitoring of the benefit/risk balance of the medicinal product. Healthcare professionals/ Patients are encouraged to report any suspected adverse reactions via Pharmacovigilance Yellow Form, or clicking below button:

Prednisolone in Kenya
Prednisolone in Kenya
Prednisolone in Kenya
Prednisolone in Kenya
Prednisolone in Kenya
Prednisolone in Kenya
Prednisolone in Kenya
Prednisolone in Kenya
Prednisolone in Kenya

Clinical | Pharmacokinetic data

Pregnancy Category: A
Routes of Administration: By mouth, intravenous
Bioavailability: Not Available
Protein Binding: Not Available
Metabolosim: Not Available
Onset of Action: N/A
Elimination Half life: 2–3 hours
Excretion: urine

Legal Status | Dosage forms & Strengths

Prescription Category:
Prescription only Medicine (POM) , ℞-only
Narcotic Drugs and Psychotropic Substances (Control ) Act Schedule:
This drug is not a controlled substance under Narcotic Drugs and Psychotropic Substances (Control ) Act
Dosage Forms | Strengths:

Drug Indentifiers:

CAS Number
PubChem CID
CompTox Dashboard (EPA)
ECHA InfoCard

Drug Images

References/ Citation:

  1. PPB Drugs Retention Register
  2. Frey, Brigitte M., and Felix J. Frey. “Clinical pharmacokinetics of prednisone and prednisolone.” Clinical pharmacokinetics 19.2 (1990): 126-146.
  3. Rose, James Q., Anthony M. Yurchak, and William J. Jusko. “Dose dependent pharmacokinetics of prednisone and prednisolone in man.” Journal of pharmacokinetics and biopharmaceutics 9.4 (1981): 389-417.
  4. Jusko, William J., and James Q. Rose. “Monitoring prednisone and prednisolone.” Therapeutic drug monitoring 2.2 (1980): 169-176.

What was the patient being treated for
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