Di-Adreson
Di-Adreson - General Information
A synthetic anti-inflammatory glucocorticoid derived from cortisone. It is biologically inert and converted to prednisolone in the liver. [PubChem]
Pharmacology of Di-Adreson
Di-Adreson, the most commonly-prescribed corticosteroid, is used to treat allograft rejection, asthma, systemic lupus erythematosus, and many other inflammatory states. Di-Adreson has very little mineralocorticoid activity.
Di-Adreson for patients
Persons who are on immunosuppressant doses of corticosteroids should be warned to avoid exposure to chicken pox or measles. Patients should also be advised if they are exposed, medical advice should be sought without delay.
Di-Adreson Interactions
The pharmacokinetic interactions listed below are potentially clinically important. Drugs that induce hepatic enzymes such as phenobarbital, phenytoin and rifampin may increase the clearance of corticosteroids and may require increases in corticosteroid dose to achieve the desired response. Drugs such as troleandomycin and ketoconazole may inhibit the metabolism of corticosteroids and thus decrease their clearance. Therefore, the dose of corticosteroid should be titrated to avoid steroid toxicity. Corticosteroids may increase the clearance of chronic high dose aspirin. This could lead to decreased salicylate serum levels or increase the risk of salicylate toxicity when corticosteroid is withdrawn. Aspirin should be used cautiously in conjunction with corticosteroids in patients suffering from hypoprothrombinemia. The effect of corticosteroids on oral anticoagulants is variable. There are reports of enhanced as well as diminished effects of anticoagulants when given concurrently with corticosteroids. Therefore, coagulation indices should be monitored to maintain the desired anticoagulant effect.
Di-Adreson Contraindications
Systemic fungal infections and known hypersensitivity to components.
Additional information about Di-Adreson
Di-Adreson Indication: For the treatment of drug-induced allergic reactions, perennial or seasonal allergic rhinitis, serum sickness, giant cell arteritis acute rheumatic or nonrheumatic carditis, systemic dermatomyositis, systemic lupus erythematosus, atopic dermatitis, contact dermatitis, exfoliative dermatitis, bullous dermatitis herpetiformis, severe seborrheic dermatitis, severe (Stevens-Johnson syndrome) erythema multiforme, mycosis fungoides, pemphigus, severe psoriasis, acute adrenocortical insufficiency, Addison's disease, secondary adrenocortical insufficiency, congenital adrenal hyperplasia, hypercalcemia associated with neoplasms, nonsuppurative thyroiditis, ulceratice colitis, Crohn's disease, acquired hemolytic anemia, congenital hypoplastic anemia, erythroblastopenia, adult secondary thrombocytopenia, adult idiopathic thrombocytopenia purpura, acute or subacute bursitis, epicondylitis, acute nonspecific tenosynovitis, acute or chronic lymphocytic leukemia, Hodgkin's or non-Hodgkin's lynphomas, Waldenstrom's macroglobulinemia, primary brain tumors (adjunct), nephrotic syndrome, tuberculous meningitis, multiple sclerosis, myasthenia gravis. cerebral edema, chorioretinitis, diffuse posterior choroiditis, aleergic conjunctivitis, Herpes zoster ophthalmicus, anterior segment inflammation, iridocyclitis, iritis, keratitis, optic neuritis, sympathetic ophthalmia, corneal marginal allergic ulcers, symptomatic sarcoidosis, Loeffler's syndrome not manageable by other means, berylliosis, fulminating or disseminated pulmonary tuberculosis when used concurrently with appropriate antituberculous chemotherapy and aspiration pneumonitis.
Mechanism Of Action: Di-Adreson is a glucocorticoid agonist. It is first metabolized in the liver to its active form, prednisolone. Prednisolone crosses cell membranes and binds with high affinity to specific cytoplasmic receptors. The result includes inhibition of leukocyte infiltration at the site of inflammation, interference in the function of mediators of inflammatory response, suppression of humoral immune responses, and reduction in edema or scar tissue. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes.
Drug Interactions: Itraconazole The imidazole increases the effect and toxicity of the corticosteroid
Ketoconazole The imidazole increases the effect and toxicity of the corticosteroid
Ethotoin The enzyme inducer decreases the effect of the corticosteroid
Fosphenytoin The enzyme inducer decreases the effect of the corticosteroid
Mephenytoin The enzyme inducer decreases the effect of the corticosteroid
Phenytoin The enzyme inducer decreases the effect of the corticosteroid
Rifampin The enzyme inducer decreases the effect of the corticosteroid
Ambenonium The corticosteroid decreases the effect of anticholinesterases
Edrophonium The corticosteroid decreases the effect of anticholinesterases
Neostigmine The corticosteroid decreases the effect of anticholinesterases
Pyridostigmine The corticosteroid decreases the effect of anticholinesterases
Trisalicylate-choline The corticosteroid decreases the effect of salicylates
Salsalate The corticosteroid decreases the effect of salicylates
Salicylate-magnesium The corticosteroid decreases the effect of salicylates
Salicylate-sodium The corticosteroid decreases the effect of salicylates
Aspirin The corticosteroid decreases the effect of salicylates
Bismuth Subsalicylate The corticosteroid decreases the effect of salicylates
Anisindione The corticosteroid alters the anticoagulant effect
Dicumarol The corticosteroid alters the anticoagulant effect
Acenocoumarol The corticosteroid alters the anticoagulant effect
Warfarin The corticosteroid alters the anticoagulant effect
Amobarbital The barbiturate decreases the effect of the corticosteroid
Aprobarbital The barbiturate decreases the effect of the corticosteroid
Butethal The barbiturate decreases the effect of the corticosteroid
Butalbital The barbiturate decreases the effect of the corticosteroid
Butabarbital The barbiturate decreases the effect of the corticosteroid
Heptabarbital The barbiturate decreases the effect of the corticosteroid
Hexobarbital The barbiturate decreases the effect of the corticosteroid
Dihydroquinidine barbiturate The barbiturate decreases the effect of the corticosteroid
Methohexital The barbiturate decreases the effect of the corticosteroid
Methylphenobarbital The barbiturate decreases the effect of the corticosteroid
Pentobarbital The barbiturate decreases the effect of the corticosteroid
Phenobarbital The barbiturate decreases the effect of the corticosteroid
Secobarbital The barbiturate decreases the effect of the corticosteroid
Talbutal The barbiturate decreases the effect of the corticosteroid
Primidone The barbiturate decreases the effect of the corticosteroid
Quinidine barbiturate The barbiturate decreases the effect of the corticosteroid
Chlorotrianisene The estrogenic agent increases the effect of corticosteroid
Clomifene The estrogenic agent increases the effect of corticosteroid
Diethylstilbestrol The estrogenic agent increases the effect of corticosteroid
Estradiol The estrogenic agent increases the effect of corticosteroid
Estriol The estrogenic agent increases the effect of corticosteroid
Conjugated Estrogens The estrogenic agent increases the effect of corticosteroid
Estrone The estrogenic agent increases the effect of corticosteroid
Estropipate The estrogenic agent increases the effect of corticosteroid
Ethinyl Estradiol The estrogenic agent increases the effect of corticosteroid
Mestranol The estrogenic agent increases the effect of corticosteroid
Midodrine Increased arterial pressure
Quinestrol The estrogenic agent increases the effect of corticosteroid
Food Interactions: Avoid alcohol.
Take with food.
Avoid taking with grapefruit juice.
Generic Name: Prednisone
Synonyms: Prednisona [Inn-Spanish]; Prednisonum [Inn-Latin]; PRD; Dehydrocortisone
Drug Category: Antineoplastic Agents; Glucocorticoids; Anti-inflammatory Agents; Adrenergic Agents
Drug Type: Small Molecule; Approved
Other Brand Names containing Prednisone: Delta-cortelan; Delta-cortisone; Delta-cortone; Delta-dome; Adasone; Ancortone; Apo-prednisone; Betapar; Bicortone; Cartancyl; Colisone; Cortan; Cortancyl; Cortidelt; Cotone; Dacorten; Dacortin; Decortancyl; Decortin; Decortisyl; Dekortin; Delcortin; Dellacort; Dellacort A; Delta Cortelan; Delta E; Deltacortene; Deltacortisone; Deltacortone; Deltasone; Deltison; Deltisona; Deltisone; Deltra; Di-Adreson; Diadreson; Econosone; Encorton; Encortone; Enkorton; Fernisone; Fiasone; Hostacortin; In-Sone; Incocortyl; Juvason; Lisacort; Me-Korti; Metacortandracin; Meticorten; Nisona; Nizon; Novoprednisone; Nurison; Orasone; Origen Prednisone; Panafcort; Panasol; Paracort; Parmenison; Pehacort; Precort; Predeltin; Prednicen-M; Prednicorm; Prednicort; Prednicot; Prednidib; Prednilonga; Prednison; Prednisone Intensol; Prednitone; Prednizon; Prednovister; Presone; Pronison; Rectodelt; Retrocortine; Servisone; Sone; Sterapred; Supercortil; Ultracorten; Ultracortene; Winpred; Wojtab; Zenadrid;
Absorption: Readily absorbed from the gastrointestinal tract.
Toxicity (Overdose): Not Available
Protein Binding: Extensively bound to plasma proteins.
Biotransformation: Hepatic.
Half Life: 2 to 3 hours
Dosage Forms of Di-Adreson: Tablet Oral
Chemical IUPAC Name: (8S,9S,10R,13S,14S,17R)-17-hydroxy-17-(2-hydroxyacetyl)-10,13-dimethyl-6,7,8,9,12,14,15,16-octahydrocyclopenta[a]phenanthrene-3,11-dione
Chemical Formula: C21H26O5
Prednisone on Wikipedia: https://en.wikipedia.org/wiki/Prednisone
Organisms Affected: Humans and other mammals