- Prednisolone Sodium Phosphate
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- Prednisolone sodium phosphate oral solution usp monograph
Prednisolone sodium phosphate oral solution usp monograph
Prednisolone Sodium Phosphate. Pregna-1,4-diene-3,dione, 11,dihydroxy phosphonooxy - disodium salt, 11. Change to read:. B: The residue from the ignition of about 20 mg of it meets the requirements of the tests for Sodium and for Phosphate Test solution: 10 mg per mL, in a mixture of pH 7. Water, Method I : not more than 6. This solution contains the equivalent of 0. Add 1 mL each of Phosphate reagent A and Phosphate reagent Bdilute with water to 25 mL, mix, and allow to stand at room temperature for 30 minutes.
Similarly and concomitantly, prepare a standard solution, using 5. Concomitantly determine the absorbances of both solutions in 1-cm cells at nm, with a suitable spectrophotometer, using water as the blank.
The absorbance of the test solution is not more than that of the standard solution. The limit is 1. Selenium : 0. Delete the following:. Add the following:. Dilute quantitatively, and stepwise if necessary, with Mobile phase to obtain a solution having a known concentration of about 0.
Dilute quantitatively, and stepwise if necessary, with Mobile phase to obtain a solution having a known concentration of about 1 mg per mL. The run time is about four times the retention time of prednisolone sodium phosphate.
Table 1. After 10 minutes, add g of water and dissolve the contents while stirring. Adjust with phosphoric acid to a pH of 6. Add g of acetonitrile, mix by stirring, and then sonicate for not more than 2 minutes. The column temperature is maintained at 35and the injector temperature is maintained at 6. The flow rate is about 1. Chromatograph the System suitability solution, and record the peak responses as directed for Procedure: the relative retention times are about 0.
Change to read: » Prednisolone Sodium Phosphate contains not less than Pipet 5 ml of the solution into a glass-stoppered, ml tube, add Determine the absorbance of the methylene chloride solution in a 1-cm cell at nm, with a suitable spectrophotometer, using methylene chloride as the blank.
Calculate the quantity, in mg, of free prednisolone in the portion of Prednisolone Sodium Phosphate weighed by comparison with the absorbance of the untreated methylene chloride solution of USP Prednisolone RS obtained as directed in the Assay: not more than 0.
The percentage limit of each individual impurity is given in Table 1. Table 1 Component. Daniel K. Bempong, Ph. Senior Scientist
❾-50%}Prednisolone sodium phosphate oral solution usp monograph
OverdoseAn overdose of Benzac AC 2. In such species, contact your doctor immediately. InteractionsAll resolves interact differently for overall to person. You should only all the possible interactions with your skin before starting any loss.
Return Home Inxight Drugs. Search Substances. US Approved Rx Source:. First approved in Source:. Structure Search. Elks and C. Ganellin, p. Glucocorticoid, Antiinflammatory agent, Glucocorticoid receptor agonist. CNS Activity. CNS Penetrant. Nobile, A. Approval Year. Glucocorticoid receptor. Allergic States Control of severe or incapacitating allergic conditions intractable to adequate trials of conventional treatment in adult and pediatric populations with: seasonal or perennial allergic rhinitis; asthma; contact dermatitis; atopic dermatitis; serum sickness; drug hypersensitivity reactions.
Dermatologic Diseases Pemphigus; bullous dermatitis herpetiformis; severe erythema multiforme Stevens-Johnson syndrome ; exfoliative erythroderma; mycosis fungoides. Edematous States To induce diuresis or remission of proteinuria in nephrotic syndrome in adults with lupus erythematosus and in adults and pediatric populations, with idiopathic nephrotic syndrome, without uremia.
Endocrine Disorders Primary or secondary adrenocortical insufficiency hydrocortisone or cortisone is the first choice; synthetic analogs may be used in conjunction with mineralocorticoids where applicable; in infancy mineralocorticoid supplementation is of particular importance ; congenital adrenal hyperplasia; hypercalcemia associated with cancer; nonsuppurative thyroiditis.
Gastrointestinal Diseases To tide the patient over a critical period of the disease in: ulcerative colitis; regional enteritis. Hematologic Disorders Idiopathic thrombocytopenic purpura in adults; selected cases of secondary thrombocytopenia; acquired autoimmune hemolytic anemia; pure red cell aplasia; Diamond-Blackfan anemia. Neoplastic Diseases For the treatment of acute leukemia and aggressive lymphomas in adults and children.
Nervous System Acute exacerbations of multiple sclerosis. Ophthalmic Diseases Uveitis and ocular inflammatory conditions unresponsive to topical corticosteroids; temporal arteritis; sympathetic ophthalmia.
Studies support the efficacy of systemic corticosteroids for the treatment of these conditions: allergic bronchopulmonary aspergillosis, idiopathic bronchiolitis obliterans with organizing pneumonia.
Rheumatic Disorders As adjunctive therapy for short term administration to tide the patient over an acute episode or exacerbation in: psoriatic arthritis; rheumatoid arthritis, including juvenile rheumatoid arthritis selected cases may require low dose maintenance therapy ; ankylosing spondylitis; acute and subacute bursitis; acute nonspecific tenosynovitis; acute gouty arthritis; epicondylitis.
For the treatment of systemic lupus erythematosus, dermatomyositis polymyositispolymyalgia rheumatica, Sjogren's syndrome, relapsing polychondritis, and certain cases of vasculitis. Miscellaneous Tuberculous meningitis with subarachnoid block or impending block, tuberculosis with enlarged mediastinal lymph nodes causing respiratory difficulty, and tuberculosis with pleural or pericardial effusion appropriate antituberculous chemotherapy must be used concurrently when treating any tuberculosis complications ; trichinosis with neurologic or myocardial involvement; acute or chronic solid organ rejection with or without other agents.
Mycosis fungoides. Primary or secondary adrenocortical insufficiency. Hematologic disorders. Acute leukemia. Multiple sclerosis. Symptomatic sarcoidosis. Rheumatic diseases. Inflammation and pain. Approved Use Antiinflammatory agent. Allergic conjunctivitis. Approved Use Steroid responsive inflammatory conditions of the palpebral and bulbar conjunctiva, cornea, and anterior segment of the globe such as allergic conjunctivitis, acne rosacea, superficial punctate keratitis, herpes zoster keratitis, iritis, cyclitis, selected infective conjunctivitides, when the inherent hazard of steroid use is accepted to obtain an advisable diminution in edema and inflammation; corneal injury from chemical, radiation, or thermal burns, or penetration of foreign bodies.
Acne rosacea. Superficial punctate keratitis. Herpes zoster keratitis. Approved Use Prednisolut is indicated in shock and emergency medicine: Shock due to a severe allergic reaction anaphylactic shockafter previous treatment with epinephrine, progressive forms of allergic reactions in insect bites and snake bites.
Brain edema. Approved Use Brain swelling brain edematriggered by brain tumor, neurosurgery, brain abscess, bacterial meningitis meningitis. Acute asthma attack. Approved Use Prednisolut is indicated to treat acute asthma attack, pulmonary edema by inhalation of toxic substances such as chlorga's, isocyanates, hydrogen sulphide, phosgene, nitrose gas, ozone, also nitrogen oxide, by gastric juice aspiration, and by drown.
Pulmonary edema. Rheumatoid arthritis. Selleck Chemicals. Prednisolone Hydroretrocortine. Title Date PubMed Intravenous hydrocortisone hemisuccinate and prednisolone hemisuccinate. Sample Use Guides. Two drops topically in the eye s four times daily. Route of Administration: Other. PMNLs spontaneously released thromboxane B2 TXB2 during 60 min incubation, and the rate of formation was significantly reduced in the presence of 20 microM or microM prednisolone.
Agonist Approved Launch Date Sixtysix Approved Use Antiinflammatory agent. OMNIPRED Approved Use Steroid responsive inflammatory conditions of the palpebral and bulbar conjunctiva, cornea, and anterior segment of the globe such as allergic conjunctivitis, acne rosacea, superficial punctate keratitis, herpes zoster keratitis, iritis, cyclitis, selected infective conjunctivitides, when the inherent hazard of steroid use is accepted to obtain an advisable diminution in edema and inflammation; corneal injury from chemical, radiation, or thermal burns, or penetration of foreign bodies.
Launch Date 1. Prednisolut Approved Use Prednisolut is indicated in shock and emergency medicine: Shock due to a severe allergic reaction anaphylactic shockafter previous treatment with epinephrine, progressive forms of allergic reactions in insect bites and snake bites.
Prednisolut Approved Use Brain swelling brain edematriggered by brain tumor, neurosurgery, brain abscess, bacterial meningitis meningitis. Prednisolut Approved Use Prednisolut is indicated to treat acute asthma attack, pulmonary edema by inhalation of toxic substances such as chlorga's, isocyanates, hydrogen sulphide, phosgene, nitrose gas, ozone, also nitrogen oxide, by gastric juice aspiration, and by drown. In vivo effects of orally administered prednisolone on prostaglandin and leucotriene production in ulcerative colitis.
Role of platelet-activating factor in ulcerative colitis. Enhanced production during active disease and inhibition by sulfasalazine and prednisolone. Comparative study of availability of prednisolone after intestinal infusion of prednisolone metasulfobenzoate and prednisone.
Prednisone is more effective than prednisolone metasulfobenzoate in the treatment of bullous pemphigoid. Inhibition of calcineurin activity and protection against cyclosporine A induced cytotoxicity by prednisolone sodium succinate in human peripheral mononuclear cells.
Comparison of suppressive potency between prednisolone and prednisolone sodium succinate against mitogen-induced blastogenesis of human peripheral blood mononuclear cells in-vitro. Effects of octreotide acetate and amniotic membrane on wound healing in experimental glaucoma surgery. Prednisolone oral solution plus inhaled procaterol for acute asthma in children: a double-blind randomized controlled trial.
Effects of prednisolone on the systemic release of mediators of cell-mediated cytotoxicity during human endotoxemia. Clinical trial: oral prednisolone metasulfobenzoate Predocol vs. Protective effect of selected calcium channel blockers and prednisolone, a phospholipase-A2 inhibitor, against gentamicin and carbon tetrachloride-induced nephrotoxicity.
The steroids for corneal ulcers trial SCUT : secondary month clinical outcomes of a randomized controlled trial. Preparation, characterization and evaluation of novel elastic nano-sized niosomes ethoniosomes for ocular delivery of prednisolone. Locators: MI Sources:. EPA CompTox. Description: A white to light yellow, crystalline powder or granules. Category: Corticosteroid. Storage: Prednisolone sodium phosphate should be kept in a tightly closed container, protected from light. Labelling: The designation Prednisolone sodium phosphate for sterile noninjectable use indicates that the substance complieswith the additional requirement and may be used for sterile applications.
Expiry date. Additional information: Prednisolone sodium phosphate is hygroscopic. Requirements: Prednisolone sodium phosphate contains not less than
Prednisolone Oral Solution contains not less than percent and not more M solution of citric acid in water, adjust with 1 N sodium hydroxide to a pH. Prednisolone Sodium Phosphate Oral Solution is a dye free, pale yellow solution. Each 5 mL (teaspoonful) of prednisolone sodium phosphate oral solution. Prednisolone Sodium Phosphate Oral Solution (10 mg Prednisolone per 5 mL) is indicated in the following conditions: 1. Allergic States Control of severe or. Prednisolone Sodium Phosphate Oral Solution is a dye free, pale yellow solution. Each 5 mL (teaspoonful) of prednisolone sodium phosphate oral solution. Standard solution— Accurately weigh a known quantity of USP Prednisolone Sodium Phosphate RS into an appropriate volumetric flask. If chickenpox develops, treatment with antiviral agents should be considered. Corticosteroids may suppress reactions to skin tests. Determine the absorbance of the methylene chloride solution in a 1-cm cell at nm, with a suitable spectrophotometer, using methylene chloride as the blank.If you are a consumer or patient please visit this version. Prednisolone Sodium Phosphate Oral Solution is a dye free, pale yellow solution. Each 5 mL teaspoonful of prednisolone sodium phosphate oral solution contains Inactive Ingredients: Prednisolone Sodium Phosphate Oral Solution equivalent to 15 mg prednisolone per 5 mL contains the following inactive ingredients: alcohol 1.
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. Its chemical structure is:. 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 physiological 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.
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. 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 the steady-state volume of distribution Vss of unbound prednisolone was reduced in elderly patients.
Despite these findings of higher total and unbound prednisolone concentrations, 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.
Prednisolone sodium phosphate oral solution is indicated in the following conditions:. In patients on corticosteroid therapy subjected to unusual stress, increased dosage of rapidly acting corticosteroids before, during and after the stressful situation is indicated. Average and large doses of hydrocortisone or cortisone can cause elevation of blood pressure, salt 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.
Corticosteroids can produce reversible hypothalamic-pituitary adrenal HPA axis suppression with the potential for glucocorticosteroid insufficiency after withdrawal of treatment.
Metabolic clearance of corticosteroids is decreased in hypothyroid patients and increased in hyperthyroid patients. Changes in thyroid status of the patient may necessitate adjustment in dosage.
Persons who are on drugs which suppress the immune system are more susceptible to infections than healthy individuals. There may be decreased resistance and inability to localize infection when corticosteroids are used. Infection with any pathogen including viral, bacterial, fungal, protozoan or helminthic infection, in any location of the body, may be associated with the use of corticosteroids alone or in combination with other immunosuppressive agents that affect humoral or cellular immunity, or neutrophil function.
These infections may be mild to severe, and, with increasing doses of corticosteroids, the rate of occurrence of infectious complications increases. Corticosteroids may also mask some signs of infection after it has already started. Chickenpox and measles, for example, can have a more serious or even fatal course in non-immune children or adults on corticosteroids.
In such children or adults who have not had these diseases, particular care should be taken to avoid exposure. How the dose, route and duration of corticosteroid administration affect the risk of developing a disseminated infection is not known. If exposed to chickenpox, prophylaxis with varicella zoster immune globulin VZIG may be indicated.
If exposed to measles, prophylaxis with immunoglobulin IG may be indicated. If chickenpox develops, treatment with antiviral agents should be considered. Use of corticosteroids may produce posterior subcapsular cataracts, glaucoma with possible damage to the optic nerves, and may enhance the establishment of secondary ocular infections due to bacteria, fungi or viruses.
The use of oral corticosteroids is not recommended in the treatment of optic neuritis and may lead to an increase in the risk of new episodes.
Corticosteroids should not be used in active ocular herpes simplex. Latent disease may be activated or there may be an exacerbation of intercurrent infections due to pathogens, including those caused by Candida, Mycobacterium, Ameba, Toxoplasma, Pneumocystis, Cryptococcus, Nocardia, etc. Corticosteroids may activate latent amebiasis. Therefore, it is recommended that latent or active amebiasis be ruled out before initiating corticosteroid therapy in any patient who has spent time in the tropics or in any patient with unexplained diarrhea.
Similarly, corticosteroids should be used with great care in patients with known or suspected Strongyloides threadworm infestation. In such patients, corticosteroid-induced immunosuppression may lead to Strongyloides hyperinfection and dissemination with widespread larval migration, often accompanied by severe enterocolitis and potentially fatal gram-negative septicemia.
The use of prednisolone in active tuberculosis should be restricted to those cases of fulminating or disseminated tuberculosis in which the corticosteroid is used for the management of the disease in conjunction with an appropriate antituberculous regimen. If corticosteroids are indicated in patients with latent tuberculosis or tuberculin reactivity, close observation is necessary as reactivation of the disease may occur.
During prolonged corticosteroid therapy these patients should receive chemoprophylaxis. Administration of live or live, attenuated vaccines is contraindicated in patients receiving immunosuppressive doses of corticosteroids. Killed or inactivated vaccines may be administered, however, the response to such vaccines can not be predicted. Immunization procedures may be undertaken in patients who are receiving corticosteroids as replacement therapy, e. 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.
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. As sodium retention with resultant edema and potassium loss may occur in patients receiving corticosteroids, these agents should be used with caution in patients with hypertension, congestive heart failure, or renal insufficiency.
Drug-induced secondary adrenocortical insufficiency 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.
Steroids should be used with caution in nonspecific ulcerative colitis, if there is a probability of impending perforation, abscess or other pyogenic infection; diverticulitis; fresh intestinal anastomoses; active or latent peptic ulcer.
Signs of peritoneal irritation following gastrointestinal perforation in patients receiving corticosteroids may be minimal or absent. Corticosteroids decrease bone formation and increase bone resorption both through their effect on calcium regulation i. This, together with a decrease in the protein matrix of the bone secondary to an increase in protein catabolism, and reduced sex hormone production, may lead to inhibition of bone growth in children and adolescents and the development of osteoporosis at any age.
Special consideration should be given to patients at increased risk of osteoporosis i. Although controlled clinical trials have shown corticosteroids to be effective in speeding the resolution of acute exacerbations of multiple sclerosis, they do not show that they affect the ultimate outcome or natural history of the disease. The studies do show that relatively high doses of corticosteroids are necessary to demonstrate a significant effect.
An acute myopathy has been observed with the use of high doses of corticosteroids, most often occurring in patients with disorders of neuromuscular transmission e. This acute myopathy is generalized, may involve ocular and respiratory muscles, and may result in quadriparesis.
Elevation of creatinine kinase may occur. Clinical improvement or recovery after stopping corticosteroids may require weeks to years.
Psychic derangements may appear when corticosteroids are used, ranging from euphoria, insomnia, mood swings, personality changes, and severe depression, to frank psychotic manifestations.
Also, existing emotional instability or psychotic tendencies may be aggravated by corticosteroids. Intraocular pressure may become elevated in some individuals. If steroid therapy is continued for more than 6 weeks, intraocular pressure should be monitored.
Patients should be warned not to discontinue the use of prednisolone sodium phosphate oral solution abruptly or without medical supervision, to advise any medical attendants that they are taking it, and to seek medical advice at once should they develop fever or other signs of infection. Persons who are on immunosuppressant doses of corticosteroids should be warned to avoid exposure to chickenpox or measles. Patients should also be advised that if they are exposed, medical advice should be sought without delay.
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 prednisolone sodium phosphate oral solution 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. 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 non-steroidal 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. 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.
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