for a week followed by 80 mg every other day.1-2 mg/kg/day P.O. USP DI: drug information for the health care provider. • Instruct patient to take oral form of drug with food or milk. with only half the potency of hydrocortisone but is a more potent glucocorticoid, having four times the potency of equal weight

May repeat longitudinal measurements as often as every 6 months to detect possible bone loss. bacterial infections. dizziness, and fainting. May cause hypokalemia, increase risk of toxicity in patients receiving these drugs.Reduces metabolism of prednisolone via increased level of transcortin; half-life of corticosteroid prolonged because of increased • Watch for depression or psychotic episodes, especially during high-dose therapy. Select one or more newsletters to continue. duration of action. (See Advanced Pulmonary and Extrapulmonary Tuberculosis under Uses.

of the hypothalamic-pituitary-adrenal axis, cushingoid appearance, muscle weakness, and osteoporosis. until a child achieves a peak expiratory flow rate of 80% of his or her personal best or symptoms resolve. • Instruct patient to avoid exposure to infections and call if exposure occurs. We comply with the HONcode standard for trustworthy health information - of action, and may be given P.O., I.M., or I.V. • May increase glucose and cholesterol levels. • Diabetic patient may need increased insulin. Glucocorticoids are responsible for a wide range of physiological effects – including anti-inflammatory, immunosuppressive, anti-proliferative and vasoconstrictive effects. Methods for monitoring bone mineralization (e.g., dual-energy x-ray absorptiometry [DEXA]) in children and adolescents are similar to those in adults.Ensure children and adolescents consistently ingest adequate calcium and vitamin D, either through diet or supplementation.With prolonged therapy, muscle wasting, muscle pain or weakness, delayed wound healing, and atrophy of the protein matrix of the bone resulting in osteoporosis, vertebral compression fractures, aseptic necrosis of femoral or humeral heads, or pathologic fractures of long bones may occur.Before initiating glucocorticoid therapy in postmenopausal women, consider that such women are especially prone to osteoporosis.Patients with cirrhosis show an exaggerated response to glucocorticoids.Associated with long-term therapy: Bone loss, cataracts, indigestion, muscle weakness, back pain, bruising, oral candidiasis.Inhibitors of CYP3A4: Potential pharmacokinetic interaction (decreased prednisolone metabolism).Inducers of CYP3A4: Potential pharmacokinetic interaction (enhanced metabolism of prednisolone).May enhance the potassium-wasting effect of glucocorticoidsConflicting reports of diminished as well as enhanced response to anticoagulantsMonitor coagulation indices to maintain desired anticoagulant effectSevere weakness with concomitant use of anticholinesterase agents and corticosteroids in patients with myasthenia gravisIf possible, withdraw antichlolinesterase therapy ≥24 hours before initiating corticosteroid therapyGlucocorticoids may increase blood glucose concentrationMay require dosage adjustment of concurrent insulin and/or oral hypoglycemic agentsWith concurrent use, increased risk for arrhythmias as a result of potential hypokalemia.Decreased plasma clearance of prednisolone; increased activity of both cyclosporine and corticosteroidConsider possibility of exacerbated toxicity (seizures), as well as need for dosage adjustment with concomitant useEnhance the potassium-wasting effects of glucocorticoidsDosage adjustment of corticosteroids may be required if estrogens are added to or withdrawn from a stable dosage regimenMay need to decrease dosage of concomitant glucocorticoids to avoid potential adverse effectsIncreases the risk of adverse GI effects (ulceration)With indomethacin and prednisolone administration, plasma concentrations of free prednisolone were increased; total plasma prednisolone concentrations were unchanged.Observe patients receiving both drugs closely for adverse effects of either salicylates or corticosteroidMay be necessary to increase salicylate dosage when corticosteroids are administered concurrently or decrease salicylate dosage when corticosteroids are discontinuedUse aspirin and corticosteroids with caution in hypoprothrombinemiaMay produce false-negative results in the nitroblue tetrazolium test for systemic bacterial infectionMay decrease iodine 131 uptake and protein-bound iodine concentrations, making it difficult to monitor the therapeutic response of patients receiving the drugs for thyroiditisDepresses skin reactivity to antigen-antibody interactionsMay need to decrease dosage of concomitant corticosteroids to avoid potential adverse effectsMay cause a diminished response to toxoids and live or inactivated vaccinesMay potentiate replication of some organisms contained in live, attenuated vaccinesCan aggravate neurologic reactions to some vaccines (supraphysiologic dosages) Following oral administration in patients with asthma, effects may not be evident for several hours.The duration of anti-inflammatory activity of prednisolone approximately equals the duration of HPA-axis suppression, about 1.25–1.5 days for a single 50-mg oral dose.Most corticosteroids removed rapidly from blood and distributed to muscles, liver, skin, intestines, and kidneys.Has a high affinity for transcortin and competes with cortisol for binding to this binding protein.Corticosteroids metabolized in most tissues, but primarily in liver, to inactive compounds.In patients with hypothyroidism, metabolic clearance of corticosteroids decreased.In patients with hyperthyroidism, metabolic clearance of corticosteroids increased.Changes in thyroid status may necessitate adjustment of glucocorticoid dosage.Principally an anti-inflammatory or immunosuppressant agent.Has approximately half the mineralocorticoid activity of hydrocortisone and cortisone.Decreases inflammation by stabilizing leukocyte lysosomal membranes, preventing release of destructive acid hydrolases from leukocytes, or reducing leukocyte adhesion to capillary endothelium.Inhibits macrophage accumulation in inflamed areas.Reduces capillary wall permeability and edema formation.Antagonizes histamine activity and release of kinin from substrates.Reduces fibroblast proliferation, collagen deposition, and subsequent scar tissue formation.Stimulates erythroid cells of bone marrow, prolongs survival time of erythrocytes and platelets, and produces neutrophilia and eosinopenia.Promotes gluconeogenesis, redistribution of fat from peripheral to central areas of the body, and protein catabolism, which results in negative nitrogen balance.Reduces intestinal absorption and increase renal excretion of calcium.Suppresses the immune response by reducing activity and volume of the lymphatic system, producing lymphocytopenia.Decreases immunoglobulin and complement concentrations and passage of immune complexes through basement membranes.Depresses reactivity of tissue to antigen-antibody interactions.In patients receiving long-term therapy, importance of not discontinuing the drug abruptly.Importance of notifying a clinician of any infections, signs of infections (e.g., fever, sore throat, pain during urination, muscle aches), or injuries that develop during therapy or within 12 months after therapy is discontinued.Importance of carrying identification cards listing the diseases being treated, the glucocorticoid regimen, and the name and telephone number of the clinician.When surgery is required, importance of informing the attending physician, dentist, or anesthesiologist of recent (within 12 months) glucocorticoid therapy.Advise patients receiving orally inhaled glucocorticoid therapy who are currently being withdrawn or who have been withdrawn from systemic therapy to immediately resume full therapeutic dosages of systemic glucocorticoids and to contact their clinician for further instructions during stressful periods (e.g., severe infection, severe asthmatic attack).In immunosuppressed patients, importance of avoiding exposure to certain infections (e.g., chickenpox, measles) and of the importance of obtaining medical advice if such exposure occurs.Importance of informing clinicians of existing or contemplated concomitant therapy, including prescription and OTC drugs, as well as any concomitant illnesses.Importance of women informing clinicians if they are or plan to become pregnant or to breast-feed.Importance of informing patients of other important precautionary information.

n. Tam LS, Li EK, Leung CB et al. Methylprednisolone. They are used to treat a wide variety of disorders – including allergic, inflammatory and malignant disorders – and so remain a vital and relevant drug class in the clinical setting.

Mechanism of Action.

for less than 3 weeks, even at large dosage ranges. 200 mg/day P.O. Therapeutic issues in oral glucocorticoid use.

Prednisone and prednisolone are synthetic (man-made) corticosteroids (steroids) used for suppressing the immune system and inflammation.

• Warn patient on long-term therapy about cushingoid effects (moonface, buffalo hump) and the need to report sudden weight gain supplement. Prednisolone acetate and tebutate are suspensions that may be administered by intra-articular, intrasynovial, intrabursal, intralesional, or soft-tissue injection. Patient may need medication to prevent GI irritation. by intra-articular, intrasynovial, intrabursal, intralesional, or soft-tissue injection.

There are two classes of corticosteroid – glucocorticoid and mineralocorticoid.