For dogs and cats · Aug 11, 2025
Cortisone works, but the side effects demand a better plan
Glucocorticoids can silence inflammation fast, yet long-term use carries real metabolic, immune, and hormonal costs that every pet owner should understand before saying yes.

Glucocorticoids are among the most effective anti-inflammatory drugs in veterinary medicine, working by inhibiting PLA2, suppressing proinflammatory cytokines, and dampening cell-mediated immunity. They are genuinely warranted for conditions such as atopic dermatitis, inflammatory bowel disease, and Addison’s disease, where survival or quality of life depends on them. The trade-off is real: long-term use carries a urinary tract infection risk of up to 68%, progressive liver enzyme elevation, and immune suppression that raises broader infection susceptibility. Where short-term use is necessary, maintenance dosing at 0.25 mg/kg every 48-72 hours minimises adrenal suppression.
Short-term steroids are basically harmless, it’s only long-term use you need to worry about
I hear this constantly, and I understand why. Vets often reassure owners, rightly, that a short course of prednisolone is far safer than months of continuous use. That’s true as far as it goes, but it has led to a widespread assumption that a two-week course is essentially a free pass. It isn’t.
Research shows that by day 14 of an anti-inflammatory prednisone or prednisolone course, 90% of dogs experienced at least one behavioural or physiological change, polyuria, polydipsia, polyphagia, or increased vocalisation [7]. Those aren’t trivial. They’re signs that the drug is having real, systemic effects on the animal’s physiology, even at standard anti-inflammatory doses.
And the immune suppression is real from day one. Glucocorticoids inhibit virtually the entire inflammatory cascade, PLA2, interleukins, proinflammatory cytokines, leukocyte activity [1], which is precisely why they work, but it also means infection risk opens up immediately, not only after months of use. Long-term use compounds this dramatically: urinary tract infections develop in up to 68% of animals on extended glucocorticoid therapy [9].
Liver enzyme changes begin early too. Alkaline phosphatase, ALT, and gamma-glutamyl transferase rise progressively during glucocorticoid treatment [11], this isn’t a phenomenon reserved for long-term patients.
None of this means a short course is the wrong call. For acute flea-allergy dermatitis, for example, prednisolone can reduce pruritus rapidly [2], and topical hydrocortisone aceponate reduced pruritus by 94% within two days with low systemic exposure [5], a useful option when you want to limit systemic burden. Short-term oral prednisone at 1 mg/kg daily for 14 days caused no significant changes in blood glucose or electrolytes in healthy dogs [6], which is genuinely reassuring.
The point is not to frighten owners away from a course of steroids when it’s warranted. The point is that “short-term equals harmless” is an oversimplification that leads to under-monitoring and under-reporting of side effects. Every course deserves the same respect: lowest effective dose, clear rationale, and eyes open to what the drug is doing to your animal, even in week one.
How glucocorticoids suppress inflammation, and why that’s a double-edged sword
Glucocorticoids work by suppressing virtually every component of the inflammatory process simultaneously. They inhibit phospholipase A2 (PLA2), the enzyme that kicks off the inflammatory cascade, and reduce the synthesis of interleukins and other proinflammatory cytokines. On top of that, they suppress cell-mediated immunity and reduce both the production and activity of leukocytes. The result is broad, rapid dampening of inflammation across the body.
That breadth is precisely what makes them so effective, and so risky with prolonged use.
Because glucocorticoids also act on carbohydrate, protein, and lipid metabolism, supraphysiologic exposure affects far more than just the immune system. The liver accumulates glycogen, causing hepatocellular swelling, with progressive rises in alkaline phosphatase (ALP), ALT, and gamma-glutamyl transferase. In dogs, early ALP increases reflect hepatic enzyme induction; later rises are driven by a distinct cortisone isoenzyme.
Immune suppression comes with a direct infection cost. Long-term use is associated with urinary tract infections in up to 68% of animals, as well as increased rates of pyoderma and pulmonary infections.
Behaviourally, most dogs on short-term prednisone or prednisolone experience polyuria, polydipsia, polyphagia, and increased vocalisation, all predictable consequences of the drug’s systemic hormonal effects.
For Addison’s disease (hypoadrenocorticism), where the adrenal glands fail to produce adequate cortisol, glucocorticoid replacement (typically prednisone) is not optional, it is lifelong and necessary for survival. Most of these patients also require mineralocorticoid replacement with desoxycorticosterone pivalate or fludrocortisone to maintain electrolyte balance.
One specific application worth noting: topical hydrocortisone aceponate reduced pruritus in dogs with flea-allergy dermatitis by 94% within two days, with minimal systemic absorption, a meaningfully different risk profile from oral or injectable glucocorticoids.
Finally, despite their historical use in anaphylaxis, current evidence does not support glucocorticoids as routine treatment. Epinephrine remains the primary intervention; glucocorticoids may have a role only in refractory cases.
How to use cortisone in dogs and cats: What the evidence actually supports
Induction versus maintenance: two distinct phases
For skin and allergic conditions, the research distinguishes clearly between getting a flare under control and keeping it there. An induction period of 5-7 days is used to bring acute inflammation down, after which the dose should be stepped down to the lowest amount that holds the condition, ideally 0.25 mg/kg every 48-72 hours in dogs. Doses should never be given more frequently than every 48 hours once you are in the maintenance phase, specifically to reduce adrenal suppression. [8]
For acute atopic or flea-allergy dermatitis, the anti-inflammatory dose used in dogs is 0.5-1 mg/kg prednisolone per day, and the explicit purpose of this phase is to give you time to find and remove the allergen trigger, not to manage the condition indefinitely. [2]
Topical as an alternative to systemic
Where the condition allows it, topical hydrocortisone aceponate is worth considering before reaching for oral prednisolone. In flea-allergy dermatitis, topical application reduced pruritus by 94% after just two days, with systemic side effects uncommon due to low plasma bioavailability. [5]
Short-term use: what actually happens over 14 days
Fourteen days at 1 mg/kg daily did not produce significant changes in blood glucose or electrolytes in healthy dogs, so short-term use at anti-inflammatory doses carries less metabolic risk than is sometimes assumed. [6] That said, 90% of dogs on a 14-day course showed behavioural changes including increased thirst, urination, appetite, and vocalisation, so warn owners upfront rather than letting them be surprised. [7] The same data confirms that 97% of owners reported the condition was controlled, which tells you the trade-off is often considered worthwhile in the short term. [7]
Long-term use: monitoring is not optional
Long-term systemic glucocorticoid treatment carries a meaningful infection risk, urinary tract infections develop in up to 68% of animals on long-term therapy. Bacteriological culture is recommended every 3-6 months for any animal receiving long-term treatment. [9] Liver enzyme activity (ALP, ALT, gamma-glutamyl transferase) increases progressively during treatment, so liver function should be tracked alongside routine monitoring. [11]
Lifelong use: Addison’s disease
Dogs with hypoadrenocorticism (Addison’s disease) are a distinct category, they require lifelong glucocorticoid replacement, usually prednisone, with most also needing mineralocorticoid replacement (desoxycorticosterone pivalate or fludrocortisone) to maintain electrolyte balance and prevent adrenal crisis. This is replacement therapy, not anti-inflammatory dosing, and it is non-negotiable for survival. [4]
Where cortisone is not the right first choice
In anaphylaxis, the evidence does not support routine glucocorticoid use, epinephrine remains the primary treatment. Glucocorticoids may have a role in refractory anaphylaxis or where concurrent asthma is present, but should not be assumed to be the standard response to acute allergic emergencies. [12]
The principle that runs through all of this
The research is consistent: lowest effective dose, longest dosing interval that controls the condition, shortest course that achieves the goal, and active monitoring the moment treatment extends beyond the short term. [8, 9, 10]
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Frequently asked questions
How does cortisone actually work to reduce inflammation in dogs and cats?
Glucocorticoids suppress inflammation at multiple points simultaneously: they inhibit phospholipase A2 (PLA2), reduce synthesis of interleukins and pro-inflammatory cytokines, suppress cell-mediated immunity, and reduce leukocyte production and activity. That breadth is precisely why they work so well, and why they carry systemic risks. There is no other anti-inflammatory drug that hits as many targets at once.
What side effects can I expect when my dog is on a short course of prednisone?
Even short-term use produces noticeable behavioural changes in most dogs. One study found that by day 14, 90% of dogs on anti-inflammatory doses showed polyuria, polydipsia, polyphagia, or increased vocalisation. That said, 97% of owners in the same study reported the medication controlled the target condition. Short-term oral prednisone at 1 mg/kg daily for 14 days caused no significant changes in blood glucose or electrolytes in healthy dogs.
Does long-term cortisone use increase the risk of infections in pets?
Yes, significantly. Systemic glucocorticoids suppress immune function broadly, and long-term use is associated with urinary tract infections, pyoderma, and pulmonary infections. Urinary tract infections develop in up to 68% of animals on long-term treatment. Vets recommend bacteriological culture every 3-6 months for any animal receiving glucocorticoids long-term. This is one of the strongest arguments for keeping courses as short as possible.
What happens to my dog’s liver during cortisone treatment?
Glucocorticoids cause progressive hepatocellular swelling through glycogen accumulation, with corresponding rises in alkaline phosphatase (ALP), ALT, and gamma-glutamyl transferase. In dogs specifically, the initial ALP rise reflects hepatic enzyme induction, which later shifts to a cortisone-specific isoenzyme. These changes are worth monitoring with blood work, particularly during longer courses.
Can cortisone be used topically to avoid systemic side effects?
Topical formulations can meaningfully reduce systemic exposure. In one study, topical hydrocortisone aceponate reduced pruritus in flea-allergy dermatitis dogs by 94% after just two days, compared with 24% in controls, and systemic side effects were uncommon due to low plasma bioavailability. For localised skin conditions, a topical approach is worth discussing with your vet before moving to oral medication.
Is cortisone ever absolutely necessary long-term, or can it always be replaced?
For Addison’s disease (hypoadrenocorticism), long-term cortisone is not optional, it is life-sustaining. All dogs with Addison’s require lifelong glucocorticoid replacement (typically prednisone), and most also need mineralocorticoid replacement to maintain electrolyte balance and prevent adrenal crises. This is one condition where there is no natural substitute and discontinuation is genuinely dangerous.
Sources
- Corticosteroids in Animals – Pharmacology – Merck Veterinary Manual
- Corticosteroids in Animals – Pharmacology – Merck Veterinary Manual
- Drugs Used to Treat Inflammatory Bowel Disease in Monogastric Animals – Pharmacology – Merck Veterinary Manual
- Management of hypoadrenocorticism (Addison's disease) in dogs – PMC
- Therapeutic efficacy of topical hydrocortisone aceponate in experimental flea-allergy dermatitis in dogs – PubMed
- Effects of short-term anti-inflammatory glucocorticoid treatment on clinicopathologic, echocardiographic, and hemodynamic variables in systemically healthy dogs – American Journal of Veterinary Research
- Perception and usage of short-term prednisone and prednisolone in dogs – PMC
- Hormonal Treatment for Integumentary Disease in Animals – Pharmacology – Merck Veterinary Manual
- Hormonal Treatment for Integumentary Disease in Animals – Pharmacology – Merck Veterinary Manual
- Corticosteroids in Animals – Pharmacology – Merck Veterinary Manual
- Hormonal Treatment for Integumentary Disease in Animals – Pharmacology – Merck Veterinary Manual
- Retrospective evaluation of hypersensitivity reactions and anaphylaxis in dogs (2003-2014): 86 cases – PubMed