Description
Prednisone is a synthetic glucocorticoid and one of the best-characterized substances in pharmacology. The substance was developed in the 1950s and has since been clinical standard for treatment of inflammatory and autoimmune diseases.
Per study reports Prednisone binds to the glucocorticoid receptor and modulates a broad palette of anti-inflammatory and immunosuppressive effects via transcription factors (NF-kB, AP-1): inhibition of cytokine production (IL-1, IL-6, TNF-alpha), reduction of leukocyte migration, inhibition of phospholipase A2 with downstream reduction of prostaglandins and leukotrienes.
Clinically Prednisone is used in many indications: rheumatoid arthritis, asthma, allergies, autoimmune diseases, transplant immunosuppression. The substance is on the WHO list of essential medicines.
Pharmacokinetically orally bioavailable with about 3-4 hour half-life, but biological action duration 18-36 hours (metabolism to active Prednisolone). A once-daily morning dose is clinical standard because endogenous cortisol levels are highest in the morning.
Known effects in studies are dose-dependent and well documented: Cushing symptomatology with longer high dosing (moon face, central adiposity, striae), glucose elevation, hypertension, osteoporosis, cataract, immunosuppression with infection risk, HPA axis suppression with adrenal cortex atrophy. Acute use in low doses is substantially better tolerated.
In recreational research practice Prednisone is less present than other glucocorticoids because the substance is primarily used in clinical indication.
You can order Prednisone as oral tablets in one bottle with 10mg per tablet.
This information is for research and educational purposes only. No medical recommendations.
Risks & Safety
Prednisone is one of the best-characterized glucocorticoids in pharmacology. The documented effects are dose-dependent and broad-ranging. Longer high dosing shifts the risk profile markedly upward.
Documented in clinical studies:
- Immunosuppression: the inhibition of the immune response is both the intended mechanism and a risk, as it raises the infection risk. With longer use this is one of the central points.
- Glucose metabolism: a rise in blood glucose is regularly documented and belongs to the known glucocorticoid profile.
- Bone density: longer use is associated in the literature with osteoporosis and reduced bone density.
- Mood changes: mood swings up to more marked changes are documented.
- HPA axis suppression: with longer use the body’s own cortisol production is suppressed, with adrenal cortex atrophy. Abrupt discontinuation is therefore problematic in the literature; a slow taper is described.
Monitoring via bloodwork is recommended. This classification does not replace medical advice. Risk and responsibility for any actual use lie entirely with the buyer.
Studies
- Antiinflammatory Action of Glucocorticoids - New Mechanisms for Old Drugs - NEJM 2005, Rhen & Cidlowski: NEJM review article on mechanism and pharmacology of glucocorticoids.
- Mechanisms involved in the side effects of glucocorticoids - Pharmacology & Therapeutics 2002, Schäcke et al: comprehensive mechanism review of glucocorticoid side effect profiles.
- Safety of low dose glucocorticoid treatment in rheumatoid arthritis: published evidence and prospective trial data - Annals of the Rheumatic Diseases 2006, Da Silva et al: safety review and prospective data on low-dose glucocorticoids in RA.
- Guidelines for prevention and treatment of glucocorticoid-induced osteoporosis - Bone 2009, Compston: guidelines for prevention of glucocorticoid-induced osteoporosis.
- Safety of low- to medium-dose glucocorticoid treatment in rheumatoid arthritis: myths and reality over the years - Annals of the New York Academy of Sciences 2014, Santiago & Da Silva: updated safety review of low- to medium-dose glucocorticoids in RA.
