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PREDNISOLONE SODIUM PHOSPHATE
What is Millipred?
Millipred Oral Solution (10 mg Prednisolone per 5 mL) is a dye free, pale to light yellow solution. Each 5 mL (teaspoonful) of Millipred Oral Solution contains 13.4 mg prednisolone sodium phosphate (10 mg prednisolone base) in a palatable, aqueous vehicle. Inactive Ingredients: Millipred Oral Solution (10 mg Prednisolone per 5 mL) contains the following inactive ingredients: anti-bitter mask, corn syrup, edetate disodium, glycerin, grape flavor, hydroxyethylcellulose, methylparaben, potassium phosphate dibasic, potassium phosphate monobasic, purified water, and sodium saccharin.
Prednisolone sodium phosphate occurs as white or slightly yellow, friable granules or powder. It is freely soluble in water; soluble in methanol; slightly soluble in alcohol and in chloroform; and very slightly soluble in acetone and in dioxane. The chemical name of prednisolone sodium phosphate is pregna-1,4-diene-3,20-dione,11,17- dihydroxy-21- (phosphonooxy)- disodium salt, (11β)-. The empirical formula is C21H27Na2O8P; the molecular weight is 484.39. Its chemical structure is:
Pharmacological Category: Glucocorticoid
What does Millipred look like?
What are the available doses of Millipred?
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What should I talk to my health care provider before I take Millipred?
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How should I use Millipred?
Millipred Oral Solution (10 mg Prednisolone per 5 mL) is indicated in the following conditions:
The initial dosage of Millipred Oral Solution (10 mg Prednisolone per 5 mL) may vary from 2.5 mL to 30 mL (5 to 60 mg prednisolone base) per day depending on the specific disease entity being treated. In situations of less severity, lower doses will generally suffice while in selected patients higher initial doses may be required. The initial dosage should be maintained or adjusted until a satisfactory response is noted. If after a reasonable period of time, there is a lack of satisfactory clinical response, Millipred Oral Solution (10 mg Prednisolone per 5 mL) should be discontinued and the patient placed on other appropriate therapy. 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 which will maintain an adequate clinical response is reached. It should be kept in mind that constant monitoring is needed in regard to drug dosage. Included in the 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 Millipred Oral Solution (10 mg Prednisolone per 5 mL) 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 200 mg of prednisolone for a week followed by 80 mg every other day or 4 to 8 mg dexamethasone every other day for one month have been shown to be effective.
In pediatric patients, the initial dose of Millipred Oral Solution (10 mg Prednisolone per 5 mL) may vary depending on the specific disease entity being treated. The range of initial doses is 0.14 to 2 mg/kg/day in three or four divided doses (4 to 60 mg/mbsa/day).
The standard regimen used to treat nephrotic syndrome in pediatric patients is 60 mg/m/day given in three divided doses for 4 weeks, followed by 4 weeks of single dose alternate-day therapy at 40 mg/m/day.
The National Heart, Lung, and Blood Institute (NHLBI) recommended dosing for systemic in children whose asthma is uncontrolled by inhaled corticosteroids and long-acting bronchodilators is 1-2 mg/kg/day in single or divided doses. It is further recommended that short course, or "burst" therapy, be continued until a child achieves a peak expiratory flow rate of 80% of his or her personal best or symptoms resolve. This usually requires 3 to 10 days of treatment, although it can take longer. There is no evidence that tapering the dose after improvement will prevent a relapse.
For the purpose of comparison, 5 mL of Millipred Oral Solution (13.4 mg Prednisolone sodium phosphate) is equivalent to the following milligram dosage of the various glucocorticoids:
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.
What interacts with Millipred?
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What are the warnings of Millipred?
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What are the precautions of Millipred?
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What are the side effects of Millipred?
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What should I look out for while using Millipred?
Systemic fungal infections. Hypersensitivity to the drug or any of its components.
What might happen if I take too much Millipred?
The effects of accidental ingestion of large quantities of prednisolone over a very short period of time have not been reported, but prolonged use of the drug can produce mental symptoms, moon face, abnormal fat deposits, fluid retention, excessive appetite, weight gain, hypertrichosis, acne, striae, ecchymosis, increased sweating, pigmentation, dry scaly skin, thinning scalp hair, increased blood pressure, tachycardia, thrombophlebitis, decreased resistance to infection, negative nitrogen balance with delayed bone and wound healing, headache, weakness, menstrual disorders, accentuated menopausal symptoms, neuropathy, fractures, osteoporosis, peptic ulcer, decreased glucose tolerance, hypokalemia, and adrenal insufficiency. Hepatomegaly and abdominal distention have been observed in children.
Treatment of acute overdosage is by immediate gastric lavage or emesis followed by supportive and symptomatic therapy. For chronic overdosage in the face of severe disease requiring continuous steroid therapy, the dosage of prednisolone may be reduced only temporarily, or alternate day treatment may be introduced.
How should I store and handle Millipred?
Store at 20° - 25° C (68° - 77° F) [See USP Controlled Room Temperature].Each 5 mL (teaspoonful) of Millipred Oral Solution contains 13.4 mg Prednisolone sodium phosphate (10 mg Prednisolone base) in a grape flavored solution.NDC 23594-510-08 8 fl oz (237 mL) bottle Dispense in tight, light-resistant glass or PET plastic containers as defined in the USP.Each 5 mL (teaspoonful) of Millipred Oral Solution contains 13.4 mg Prednisolone sodium phosphate (10 mg Prednisolone base) in a grape flavored solution.NDC 23594-510-08 8 fl oz (237 mL) bottle Dispense in tight, light-resistant glass or PET plastic containers as defined in the USP.
Chemical StructureNo Image found
Naturally occurring glucocorticoids (hydrocortisone), which also have salt-retaining properties, are used as replacement therapy in adrenocortical deficiency states. Their synthetic analogs are primarily used for their potent anti-inflammatory effects in disorders of many organ systems.
Prednisolone is a synthetic adrenocortical steroid drug with predominantly glucocorticoid properties. Some of these properties reproduce the physiologi- cal actions of endogenous glucocorticosteroids, but others do not necessarily reflect any of the adrenal hormones" normal functions; they are seen only after administration of large therapeutic doses of the drug. The pharmacological effects of prednisolone which are due to its glucocorticoid properties include: promotion of gluconeogenesis; increased deposition of glycogen in the liver; inhibition of the utilization of glucose; anti-insulin activity; increased catabolism of protein; increased lipolysis; stimulation of fat synthesis and storage; increased glomerular filtration rate and resulting increase in urinary excretion of urate (creatinine excretion remains unchanged); and increased calcium excretion.
Depressed production of eosinophils and lymphocytes occurs, but erythropoiesis and production of polymorphonuclear leukocytes are stimulated. Inflammatory processes (edema, fibrin deposition, capillary dilatation, migration of leukocytes and phagocytosis) and the later stages of wound healing (capillary proliferation, deposition of collagen, cicatrization) are inhibited. Prednisolone can stimulate secretion of various components of gastric juice. Suppression of the production of corticotropin may lead to suppression of endogenous corticosteroids. Prednisolone has slight mineralocorticoid activity, whereby entry of sodium into cells and loss of intracellular potassium is stimulated. This is particularly evident in the kidney, where rapid ion exchange leads to sodium retention and hypertension.
Prednisolone is rapidly and well absorbed from the gastrointestinal tract following oral administration. Millipred Oral Solution (10 mg Prednisolone per 5 mL) produces a 14% higher peak plasma level of prednisolone which occurs 20% faster than that seen with tablets. Prednisolone is 70-90% protein bound in the plasma, and it is eliminated from the plasma with a half-life of 2 to 4 hours. It is metabolized mainly in the liver and excreted in the urine as sulfate and glucuronide conjugates.
The systemic availability, metabolism and elimination of prednisolone after administration of single weight-based doses (0.8 mg/ kg) of intravenous (IV) prednisolone and oral prednisone were reported in a small study of 19 young (23 to 34 years) and 12 elderly (65 to 89 years) subjects. Results showed that the systemic availability of total and unbound prednisolone, as well as interconversion between prednisolone and prednisone were independent of age. The mean unbound fraction of prednisolone was higher, and steady- state volume of distribution (Vss) of unbound prednisolone was reduced in elderly patients. Plasma prednisolone concentrations were higher in elderly subjects, and the higher AUCs of total and unbound prednisolone were most likely reflective of an impaired metabolic clearance, evidenced by reduced fractional urinary clearance of 6β-hydroxyprednisolone. Despite these findings of higher total and unbound prednisolone concentra- tions, elderly subjects had higher AUCs of cortisol, suggesting that the elderly population is less sensitive to suppression of endogenous cortisol or their capacity for hepatic inactivation of cortisol is diminished.
Non-Clinical ToxicologySystemic fungal infections. Hypersensitivity to the drug or any of its components.
Drugs such as barbiturates, phenytoin, ephedrine, and rifampin, which induce hepatic microsomal drug metabolizing enzyme activity may enhance metabolism of prednisolone and require that the dosage of Millipred Oral Solution (10 mg Prednisolone per 5 mL) be increased.
Increased activity of both cyclosporin and corticosteroids may occur when the two are used concurrently. Convulsions have been reported with this concurrent use.
Estrogens may decrease the hepatic metabolism of certain corticosteroids thereby increasing their effect.
Ketoconazole has been reported to decrease the metabolism of certain corticosteroids by up to 60% leading to an increased risk of corticosteroid side effects.
Coadministration 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.
Concomitant use of aspirin (or other nonsteroidal anti-inflammatory agents) and corticosteroids increases the risk of gastrointestinal side effects. Aspirin should be used cautiously in conjunction with corticosteroids in hypoprothrombinemia. The clearance of salicylates may be increased with concurrent use of corticosteroids.
When corticosteroids are administered concomitantly with potassium-depleting agents (i.e., diuretics, amphotericin-B), patients should be observed closely for development of hypokalemia. Patients on digitalis glycosides may be at increased risk of arrhythmias due to hypokalemia.
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.
Due to inhibition of antibody response, patients on prolonged corticosteroid therapy may exhibit a diminished response to toxoids and live or inactivated vaccines. Corticosteroids may also potentiate the replication of some organisms contained in live attenuated vaccines. If possible, routine administration of vaccines or toxoids should be deferred until corticosteroid therapy is discontinued. Because corticosteroids may increase blood glucose concentrations, dosage adjustments of antidiabetic agents may be required. Corticosteroids may suppress reactions to skin tests.
The lowest possible dose of corticosteroid should be used to control the condition under treatment, and when reduction in dosage is possible, the reduction should be gradual.
Since complications of treatment with glucocorticoids are dependent on the size of the dose and the duration of treatment, a risk/benefit decision must be made in each individual case as to dose and duration of treatment and as to whether daily or intermittent therapy should be used.
There is an enhanced effect of corticosteroids in patients with hypothyroidism and in those with cirrhosis.
Kaposi's sarcoma has been reported to occur in patients receiving corticosteroid therapy, most often for chronic conditions. Discontinuation of corticosteroids may result in clinical improvement.
Fluid and Electrolyte Disturbances:
This information is obtained from the National Institute of Health's Standard Packaging Label drug database.
While we update our database periodically, we cannot guarantee it is always updated to the latest version.
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