Vetdrugs 2.0Cortisone is a naturally occurring glucocorticoid precursor generally supplied medicinally as cortisone acetate. It is converted in the body to cortisol, or hydrocortisone. Its main veterinary application is glucocorticoid replacement in selected dogs with hypoadrenocorticism. The clinical role is endocrine replacement rather than provision of a long-acting depot steroid.
Group
Glucocorticoid replacement
Mechanism of Action
Cortisone is converted to cortisol by 11-beta-hydroxysteroid dehydrogenase, particularly in the liver. Cortisol binds intracellular glucocorticoid receptors and changes transcription of genes regulating metabolism, vascular responsiveness and inflammatory activity. Replacement restores deficient glucocorticoid functions. Cortisol also has mineralocorticoid activity, although the clinical contribution varies with exposure and the patient’s endocrine deficit.
Dose Rates
Dogs
| Use / stage | Dose | Route | Schedule | Instructions |
|---|---|---|---|---|
| Glucocorticoid replacement — Initial | 0.5–1 mg/kg | PO | Every 12–24 h | Oral cortisone acetate during recovery from an adrenal crisis and transition from parenteral replacement; individualize with concurrent mineralocorticoid therapy. The selected source states these are per-administration doses, not an assumed daily total. |
| Glucocorticoid replacement — Maintenance | 0.5 mg/kg | PO | Every 12–24 h | Stable replacement dose; assess clinical response and electrolyte/mineralocorticoid needs. |
Indications
- Glucocorticoid replacement in selected dogs with hypoadrenocorticism.
Contraindications
- Cortisone hypersensitivity
- At supraphysiologic doses: uncontrolled systemic fungal infection
Interactions
- Concurrent NSAIDs increase gastrointestinal injury risk.
- Other immunosuppressants increase infection risk.
- Potassium-depleting medicines, including amphotericin B, furosemide and thiazides, can increase hypokalemia.
- Insulin requirements may rise with glucocorticoid excess.
- Immunosuppressive glucocorticoid dosing can reduce vaccine response and increase risk from live vaccines.
- Warfarin response may change; monitor coagulation.
- Mitotane-induced adrenal insufficiency may require individualized replacement.
Adverse effects
- Polyuria and polydipsia
- Polyphagia
- Muscle wasting
- Adrenal suppression with prolonged excess exposure
Toxicity
Chronic excess produces iatrogenic hyperadrenocorticism; abrupt withdrawal after prolonged treatment can precipitate adrenal insufficiency.
Preparations
| Preparation | Form | Strength | Route |
|---|---|---|---|
| Cortisone acetate tablets 25 mg Strength is cortisone acetate, not hydrocortisone. | Tablet | 25 mg / tablet | PO |
Monitoring and Administration
Individualize replacement to clinical response, electrolytes and concurrent mineralocorticoid treatment.
Increase glucocorticoid support during relevant stress according to an established endocrine plan. Do not abruptly stop chronic replacement.
Cortisone interferes with cortisol assays: obtain diagnostic ACTH-stimulation samples before administration when possible. Interpret thyroid tests, leukograms, glucose and potassium in light of glucocorticoid exposure.
Follow weight, appetite, edema, electrolytes, glucose and growth in immature patients. Store tablets in well-closed containers at 15–30°C.