Prednisolone phosphate

440.423921

440.42

206-120-1

752SY38R6C

DTXSID7047481

C61904

141

0

P201, P202, P281, P308+P313, P405, P501

H360

|Danger|H360 (33.33%): May damage fertility or the unborn child [Danger Reproductive toxicity]|P201, P202, P260, P281, P308+P313, P314, P405, and P501|Aggregated GHS information provided by 3 companies from 3 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

Data regarding acute overdose is not readily available. However, patients experiencing chronic overdose may present with mental symptoms, moon face, abnormal fat deposits, and fluid retention. Acute oral overdose may be treated with immediate gastric lavage or emesis followed by symptomatic and supportive treatment. Chronic overdosage can be managed by temporary dose reduction or alternate day treatment.

Prednisolone is 70-90% protein bound in plasma. Prednisolone typically binds to albumin and corticosteroid binding globulin.

Prednisolone phosphate is indication to a number of conditions including treat allergic states, dermatologic diseases, edematous states, endocrine disorders, gastrointestinal diseases, hematologic disorders, neoplastic diseases, nervous system, ophthalmic diseases, respiratory diseases, rheumatic disorders.

Corticosteroids bind to the glucocorticoid receptor, inhibiting pro-inflammatory signals, and promoting anti-inflammatory signals. Prednisolone has a short duration of action as the half life is 2-4 hours. Corticosteroids have a wide therapeutic window as patients make require doses that are multiples of what the body naturally produces. Patients taking corticosteroids should be counselled regarding the risk of hypothalamic-pituitary-adrenal axis suppression and increased susceptibility to infections.

A group of CORTICOSTEROIDS that affect carbohydrate metabolism (GLUCONEOGENESIS, liver glycogen deposition, elevation of BLOOD SUGAR), inhibit ADRENOCORTICOTROPIC HORMONE secretion, and possess pronounced anti-inflammatory activity. They also play a role in fat and protein metabolism, maintenance of arterial blood pressure, alteration of the connective tissue response to injury, reduction in the number of circulating lymphocytes, and functioning of the central nervous system. (See all compounds classified as Glucocorticoids.)

A 30mg prednisolone oral solution reaches a C_max of 461.33±77.94ng/mL with an AUC of 2426.1±360.0ng\*h/mL. A 30mg prednisolone orally disintegrating tablet reaches a C_max of 420.91±78.28ng/mL with an AUC of 2408.1±361.5ng\*h/mL.|Prednisolone is predominantly eliminated in the urine as sulfate and glucuronide conjugate metabolites.|The volume of distribution of prednisolone phosphate has been reported as 0.22-0.7L/kg.

Prednisolone phosphate undergoes ester hydrolysis to [prednisolone]. After this step, the drug undergoes the normal metabolism of prednisolone.

The half life of prednisolone is 2-4 hours.

The short term effects of corticosteroids are decreased vasodilation and permeability of capillaries, as well as decreased leukocyte migration to sites of inflammation. Corticosteroids binding to the glucocorticoid receptor mediates changes in gene expression that lead to multiple downstream effects over hours to days. Glucocorticoids inhibit neutrophil apoptosis and demargination; they inhibit phospholipase A2, which decreases the formation of arachidonic acid derivatives; they inhibit NF-Kappa B and other inflammatory transcription factors; they promote anti-inflammatory genes like interleukin-10. Lower doses of corticosteroids provide an anti-inflammatory effect, while higher doses are immunosuppressive. High doses of glucocorticoids for an extended period bind to the mineralocorticoid receptor, raising sodium levels and decreasing potassium levels.

Pediapred

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