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Mechanism of Action
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.
Oral administration of single doses of 30 mg prednisolone base equivalent of Orapred ODT (prednisolone sodium phosphate) , and Pediapred Solution to 21 adult volunteers yielded comparable pharmacokinetic data:
Table 1. Comparison of Mean Pharmacokinetic Parameters (%CV)
in Healthy Volunteers Following a Single Dose of 30 mg Orapred ODT (prednisolone sodium phosphate) and Pediapred
|Dose* (30 mg prednisolone base equivalent)||AUC0-∞
(ng•hr/mL) (± S.D.)
|Cmax (ng•hr/mL)** (± S.D.)|
|Pediapred Solution||2426.1 (360.0)||461.33 (77.94)|
|Orapred ODT||2408.1 (361.5)||420.91 (78.28)|
|*Administered under fasting conditions.
**Mean values of 21 normal volunteers
Prednisolone is 70-90% protein-bound in the plasma and the volume of distribution is reported as 0.22 -0.7 L/kg.
Prednisolone is reported to be metabolized mainly in the liver and excreted in the urine as sulfate and glucuronide conjugates.
Prednisolone is eliminated from the plasma with a mean (± SD) half-life of 2.6 (± 0.27) hours.
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 younger (23 to 34 years) and 12 geriatric (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 the 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 6b-hydroxyprednisolone. 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.
Last reviewed on RxList: 8/20/2010
This monograph has been modified to include the generic and brand name in many instances.
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