Cortisyl

Cortisyl Uses, Dosage, Side Effects, Food Interaction and all others data.

Cortisyl was first isolate in 1935 and became more widely researched in 1949. Since then, glucocorticoids such as cortisone acetate have been used to treat a number of inflammatory conditions such as endocrine, rheumatic, collagen, dermatologic, allergic, ophthalmic, respiratory, hematologic, neoplastic, edematous, and gastrointestinal diseases and disorders.

Cortisyl was granted FDA approval on 13 June 1950.

Corticosteroids bind to the glucocorticoid receptor, inhibiting pro-inflammatory signals, and promoting anti-inflammatory signals. The duration of action is moderate as it is generally given once daily. Corticosteroids have a wide therapeutic window as patients may 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.

Cortisyl
Uses
Dosage
Side Effect
Precautions
Interactions
Uses during Pregnancy
Uses during Breastfeeding
Accute Overdose
Food Interaction
Half Life
Volume of Distribution
Clearance
Interaction With other Medicine
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Trade Name	Cortisyl
Generic	Cortisone acetate
Cortisone acetate Other Names	Cortisone acetate, Cortone acetate
Type
Formula	C₂₃H₃₀O₆
Weight	Average: 402.4807 Monoisotopic: 402.204238692
Protein binding	Corticosteroids are generally bound to corticosteroid binding globulin and serum albumin in plasma.
Groups	Approved, Investigational
Therapeutic Class
Manufacturer
Available Country
Last Updated:	September 19, 2023 at 7:00 am

Uses

Cortisyl is a steroid hormone used for the relief of the inflammatory and pruritic manifestations of corticosteroid-responsive dermatoses and endocrine disorders associated with inadequate production of steroid hormones.

Cortisyl is indicated to treat a wide variety of endocrine, rheumatic, collagen, dermatologic, allergic, ophthalmic, respiratory, hematologic, neoplastic, edematous, and gastrointestinal diseases and disorders.

Cortisyl is also used to associated treatment for these conditions: Acne Rosacea, Acute Gouty Arthritis, Adrenal cortical hypofunctions, Adrenocortical Hyperfunction, Ankylosing Spondylitis (AS), Anterior Segment Inflammation, Aspiration Pneumonitis, Asthma, Atopic Dermatitis (AD), Berylliosis, Bullous dermatitis herpetiformis, Bursitis, Chorioretinitis, Choroiditis, Congenital Adrenal Hyperplasia (CAH), Congenital Hypoplastic Anemia, Corneal Inflammation, Cushing's Syndrome, Dermatitis exfoliative generalised, Dermatitis, Contact, Drug hypersensitivity reaction, Epicondylitis, Erythroblastopenia, Hypercalcemia of Malignancy, Idiopathic Thrombocytopenic Purpura, Inflammation, Iridocyclitis, Iritis, Leukemia, Acute, Loeffler's syndrome, Malignant Lymphomas, Mycosis Fungoides (MF), Ophthalmia, Sympathetic, Optic Neuritis, Pemphigus, Perennial Allergic Rhinitis (PAR), Post-traumatic Osteoarthritis, Psoriatic Arthritis, Regional Enteritis, Rheumatoid Arthritis, Rheumatoid Arthritis, Juvenile, Seasonal Allergic Conjunctivitis, Seasonal Allergic Rhinitis, Secondary thrombocytopenia, Serum Sickness, Severe Seborrheic Dermatitis, Stevens-Johnson Syndrome, Synovitis, Systemic Lupus Erythematosus (SLE), Trichinosis, Tuberculosis (TB), Tuberculosis Meningitis, Ulcerative Colitis, Uveitis, Acquired immune hemolytic anemia, Acute nonspecific tenosynovitis, Acute rheumatic carditis, Non-suppurative Thyroiditis, Severe Psoriasis, Symptomatic Sarcoidosis, Varicella-zoster virus acute retinal necrosis

How Cortisyl works

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.

Toxicity

Data regarding acute overdoses of glucocorticoids are rare. Chronic high doses of glucocorticoids can lead to the development of cataract, glaucoma, hypertension, water retention, hyperlipidemia, peptic ulcer, pancreatitis, myopathy, osteoporosis, mood changes, psychosis, dermal atrophy, allergy, acne, hypertrichosis, immune suppression, decreased resistance to infection, moon face, hyperglycemia, hypocalcemia, hypophosphatemia, metabolic acidosis, growth suppression, and secondary adrenal insufficiency. Overdose may be treated by adjusting the dose or stopping the corticosteroid as well as initiating symptomatic and supportive treatment.